感染性急性肺损伤辨治规律研究
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摘要
论文探讨了肺部感染所致急性肺损伤的中医辨证论治规律。通过对古代文献及现代临床、实验资料研究，探讨了感染性急性肺损伤的发病机理、辨证规律及治则治法。
论文提出，感染性急性肺损伤主要致病因素及病理特点为暴感外邪，邪正剧烈交争，病情骤变，导致肺气郁闭，肺体受损，血络瘀滞，瘀血停滞；津液不布，水液停聚；热伤气阴，正气外脱。从肺损伤总的病变过程来看，邪热为病理损伤的始动因素；邪热或热毒蕴肺、肺失宣降为肺损伤的病理基础，并且贯穿病程的始终；痰、饮、瘀等继发性病邪为肺部损伤的重要病理因素；临床表现以肺气郁闭为主要特点。病变早、中期以实为主，病理因素以热毒为主，毒势深重，兼有痰热、瘀血、湿饮，以肺气郁闭为主要特点，临床表现以“急”、“暴”、“闭”为特点；病之后期热伤气阴，病理性质演变为正虚、邪实夹杂，正虚可表现有肺气阴虚、肺肾气虚、肾虚不纳气或正气外脱等；邪实可见痰、饮、瘀等阻于肺。严重者可见肺不主气，正气外脱，化源竭绝证候。
在感染性急性肺损伤辨证中，首先须明确疾病的基本特点。本病由暴感外邪所致，感邪后正邪剧烈交争，邪势深重，导致肺气郁闭，肺体受损。临床以高热，喘憋为基本特点。后期病理变化以邪实正虚或以肺气阴虚、肺肾两虚、正气外脱等为主。邪势炽盛，病势深重者，变化急骤，可致气阴迅速耗伤，急速导致肺不主气，化源速绝，临床表现以呼吸衰竭为主要特征。与普通肺热证比较，具有“急”、“暴”、“闭”的特点。
其次，应辨别疾病卫气营血的浅深层次及病机传变。感邪后可出现短暂肺卫表证，邪不外解，则迅速传入气、营、血分。若邪势较盛，或机体正气不足，病邪也可不拘表里渐次传变，病后即迅速出现病邪内传，见气营(血)两燔证或逆传心包而见窍闭证，或深入营血而见营血分证。后期则以正虚邪实夹杂为主，正虚可表现有肺气阴虚、肺肾气虚、肾虚不纳气或正气外脱等；邪实可见痰、饮、瘀等阻于肺。严重者可见肺不主气，正气外脱，化源竭绝证候。
第三，须辨别病邪性质。急性肺损伤可由多种病邪引起，不同病邪所致者有各自的特殊临床表现。引起本病的病邪包括风热、燥热、暑热、暑湿、湿热等性质病邪，由于病邪多具炎热性质，或为疫邪所感，故致病迅速，病情严重，临床须根据不同特点加以鉴别。
第四，辨析证候虚实及病邪夹杂。在疾病初起，正邪剧烈交争，多表现为实证；随着病程的进展，病邪耗伤气阴，则证候由实致虚，中期可表现为实证夹虚，后期则可表现为虚中夹实，终致以虚为主的证候。另外，在病程发展过程中，还兼夹有痰、饮、瘀血等病理性产物，并可进一步影响肺及全身的病机证候演变。在辨治过程中亦须加以辨析。
最后，还须审疾病发展过程中病邪的脏腑传变。在感染性急性肺损伤的发展过程中，由于邪蕴于肺，肺失宣降，气化失司，通调失职，可致全身各脏腑气机失调；痰、饮、瘀、气闭等病理因素也会影响其它脏腑，从而导致邪传他脏，致多脏器损害发生，病变主要可涉及胃、大肠、肝、心包、肾等脏腑。
根据感染性急性肺损伤病理变化及肺的生理功能特点，确立扶正祛邪，调整脏腑功能为本病的主要治疗原则。在感染性急性肺损伤初期阶段，多以邪实为主，兼有正虚，此时治疗当主以祛邪，兼以扶正；疾病中期阶段，邪气盛，正气损伤，此时当辨清病机侧重，若病机侧重在邪实，则重在攻邪；若正虚明显，则以扶正为主；疾病后期，正气大伤，阴液损伤明显，此时治疗则主以扶正，兼清余邪。并强调在治疗中须正确把握扶正、祛邪与调整脏腑功能三者之间的辨证关系。
在急性肺损伤的发生发展过程中，还多同时出现热毒、痰热、瘀血、水湿等重要病理因素，临床表现以肺气郁闭为主要特点，后期可兼见肺气阴虚、肺肾两虚、正气外脱等证候。因此论文提出，急性肺损伤的治疗以清肺泄热、清解热毒、宣开肺气、化痰除饮、活血化瘀、补肺固脱等为主要治法。由于邪热壅肺、肺失宣降为本病的主要病理基础，故在治疗中清肺为首选治法，贯穿全局，而宣开肺气亦不可或缺，化痰、消饮、活血化瘀、补肺固脱或敛肺救逆固脱等为重要治法。
对现代临床及实验资料研究表明，感染性急性肺损伤西医发病机制主要与过度免疫反应及肺泡上皮细胞的凋亡、修复相关。中医发病机制认识主要与邪热、热毒、痰热、瘀血、气闭等相关。提出以后对于中医药治疗本病的研究须重视中医药对抗病原的作用机制、重视中医药对抗病理损害的作用机制：如药物对肺微血管内皮细胞及肺泡上皮细胞的保护作用、调整循环状态及改善通气功能等、深入研究细胞凋亡在急性肺损伤发病过程中的复杂机制，研究中医不同治法对凋亡过程的调节作用等。
在理论研究的基础上，论文还通过实验研究探讨了开上泄下治法的代表性方剂升降散治疗本病的作用机理，实验研究了升降散对急性肺损伤大鼠肺微血管内皮细胞NF-κB表达的影响及升降散对急性肺损伤大鼠肺终末性细支气管粘膜上皮细胞ICAM-1表达的影响，结果表明，升降散各治疗组可以明显抑制造模后大鼠肺微血管内皮细胞NF-κB表达，结果与模型组比较有显著差异。同时观察了升降散对肺终末性细支气管上皮细胞ICAM-1表达的影响，结果表明，大、中、小剂量组药物对ICAM-1的表达都有明显的抑制作用，与模型组比较有显著性差异，其中大剂量组表达较中、小剂量组低，但三者间无显著性差异。实验结果显示，升降散可以通过抑制肺微血管内皮细胞表达NF-κB及肺组织细胞表达ICAM-1，以抑制炎症反应的放大，调节细胞凋亡，从而起到组织保护，防治急性肺损伤的作用。
The paper discusses the laws of syndrome differentiation and therapeutic rules foracute lung injury caused pulmonary infection in Traditional Chinese Medicine, andelucidates the pathogenesis, syndrome differentiation, therapeutic principles and methodsof infectious acute lung injury based on the ancient medical literatures and modemclinical and experiment data.
The paper puts forward the main pathogenic factor and features include suddenaffection by exopathogen, violent conflict between pathogen and vital Qi and impetuouschange of the morbid condition, and causing blockage of lung Qi, damaging lungparenchyma, stagnating the blood vessels and causing blood stasis; misdistribution ofbody fluid causing water pathogen; collapse of Vital Qi due to heat pathogen damagingYin fluid. In the morbid process of infectious acute lung injury, the pathogenic heat is theprimary factor, the basic pathogeneses of lung injury are pathogenic heat or heat toxinaccumulating in the lung and the lung failing both dispersing and descending, and theyrun through the whole morbid process; the secondary pathogenic factors include phlegm,water pathogen and blood stasis, they are important to the formation of lung injury; themain feature of the clinical manifestation is blockage of the lung Qi. In the early andmiddle stage, the main pathogenic factor is heat toxin, accompanied by phlegm heat,blood stasis, water pathogen and blockage of lung Qi; the main features of the clinicalpresentation include "sudden onset", "violent morbid condition" and "blockage of thelung Qi". At the final stage of the disease, the main pathogenesis of the disease iscoexistence of the deficiency and excess, the deficiency aspect may include lung Qi andYin deficiency, Qi deficiency of lung and kidney, asthenia kidney failing to hold Qi andcollapse of the vital Qi; and the excess aspects include phlegm, water pathogen and bloodstasis stagnating in the lung. In the severe case, the syndrome may be collapse of the vitalQi and lung failing to dominate Qi and control respiration due to the extreme deficiencyof the lung Qi.
In the syndrome differentiation of acute lung injury, we'd better notice the followingaspect. Firstly, understand the basic feature of infectious acute lung injury. ALI is causedby Exopathogen invading suddenly, there is violent conflict between Exopathogen andVital Qi with severe morbid condition, and cause blockage of the lung Qi and damage thelung parenchyma, the clinical manifestation may show high fever, dyspnea andsuppression of the breath. The pathogenesis at final stage may show deficiency typeaccompanied by excess, or lung Qi and Yin deficiency, collapse of the vital Qi. The casewith intense pathogenic heat and severe morbid state can damage Vital Qi and Yinquickly, make the lung failing to dominate Qi and control respiration, cause respiratoryfailure. The syndrome always has the features of "sudden onset", "violent morbidcondition" and "blockage of the lung Qi" compared with common lung-heat syndrome.
Secondly, differentiate the Wei, Qi, Ying and Xue phases and the transference of thedisease. There may be a short time of exterior syndrome at beginning of the disease, thenthe pathogen invade into the Qi, Ying and Xue phases rapidly. If the pathogen is veryintense or the Vital Qi is deficient, the pathogen may transmit disobey the orders, andinvading the interior promptly after occurrence, the syndromes may be intense heat inboth Qi, Ying and Xue phases, or abnormal transmission of the pericardium and causingblockage syndrome of the pericardium, or syndromes of Ying and Xue phases. At thefinal stage of the disease, the main pathogenesis is coexistence of deficiency and excess,the deficiency syndrome may be lung Qi and Y'm deficiency, lung and kidney Qideficiency, asthenia kidney failing to hold Qi or collapse of Vital Qi etc. The excesssyndromes may be phlegm, water pathogen and blood stasis stagnating in the lung.Severe case may show lung failing to dominate Qi, collapse of the Vital Qi and collapseof the origin of the blood and Qi.
Thirdly, differentiate the nature of the pathogen. Acute lung injury may be caused byvarious pathogens, different pathogen can show special clinical manifestation of theirown. The pathogens include wind-heat, dry-heat, summer-heat and damp-heat orpestilential pathogen, they all have the features of scorching nature and causing diseaseswiftly.
Fourthly, differentiate the deficiency and excess of the syndrome and the mixture ofthe pathogen. At the beginning, there is violent conflict between Vital Qi and pathogen,the main syndrome is excess one; along with the morbid progress, the pathogen damage Qi and Yin, the syndrome may be excess accompanied by deficiency in the middle stageof the disease, and deficiency type accompanied by excess, and deficiency type as itsmain aspect at final stage. In addition, in the morbid progress, there may be pathogenicproducts such as phlegm, water pathogen and blood stasis, and these may influence thepathologic changes in the lung and the entire body. So the doctors should consideratethem in the clinical treatment.
Finally, analyze the transmission of the pathogen among the differentZangfu-organs. In the progress of the infectious acute lung injury, the pathogenaccumulate in the lung, cause the lung failing to disperse and descend, and failing ofQi-vary and smoothness of water passages, it may cause disorders of the Qi-movementof the Zangfu-organs and the entire body; and the pathogenic factors, such as phlegm,water pathogen, blood stasis and Qi blockage, may also influence the otherZangfu-organs, and make the pathogen transmit into the other organs, and cause multipleorgans damage. The disease may involve stomach, large intestine, liver, pericardium andkidney, etc.
According to the pathologic changes of the infectious acute lung injury andphysiological function of the lung, the therapeutic principle should be supporting Vital Qiand eliminating pathogens. At the early stage of the infectious acute lung injury, the mainpathogenesis is excess, accompanied with deficiency of the vital Qi, the therapeuticprinciple should be eliminate the pathogen, in the middle stage, intense pathogen damagethe Vital Qi, the therapeutic principle should be made on the basis of differentiating thepathogenesis, if the main aspect is excess type, the principle should be eliminating thepathogen; if the main aspect is deficiency type, the principle should be supporting theVital Qi. At the final stage of the disease, Vital Qi and Yin fluid is damaged distinctly, theprinciple should be supporting the Vital Qi, and combined with eliminating surpluspathogen. The paper stress on coordinating the dialectical relationships amongsupporting Vital Qi, eliminating pathogen and regulating Zangfu-organ.
In the course of the acute lung injury, there may be heat-toxin, phlegm-heat, bloodstasis and water pathogen, the clinical feature of disease is blockage of lung Qi. At finalstage, the syndromes may be lung Qi and Yin deficiency, deficiency of lung and kidneyor collapse of Vital Qi. The paper put forward the therapeutic methods of clearing awaylung heat, eliminating heat-toxin, disperse lung Qi, resolving phlegm and dispelling water pathogen, promoting blood circulation to remove blood stasis and tonifying lungQi to astringe collapse for acute lung injury. Because the main pathogenesis of thedisease is pathogenic heat accumulating in the lung and the lung failing to disperse anddescend, it is the primary method to clear away lung heat running through the entirecourse of disease, dispersing lung Qi is indispensable for treating the disease, andresolving phlegm, eliminating water pathogen, promoting blood circulation to removeblood stasis, tonifying lung Qi to astringe collapse or astringing lung Qi to treat collapseare important methods for treating acute lung injury.
According to modem clinical and experimental studying, the mechanisms ofinfectious acute lung injury are related to the excess immunoreaction and apoptosis andrepair of the alveolar epithelial cells. The mechanisms of the disease are related to thepathogenic heat, heat-toxin, phlegm heat, blood stasis and blockage of Qi. The paper putforward that the study of treating the disease by TCM should focus on the followingfields, i.e. the mechanisms of dispelling pathogen by TCM; the mechanisms ofpreventing pathologic injury to the lung by TCM, such as protecting pulmonarymicrangium endothelial cells and alveolar epithelial cells, improving circulation state andventilatory function; researching on the complex mechanism of apoptosis in the morbidprogress of acute lung injury, and the action of different therapy of TCM on apoptosis.
On the basis of the theoretical studying, the paper discusses the mechanism oftreating the disease by Shengjiang powder, the representative formula for the method ofdispersing the lung and purging the Fu-organs. We observed the influence of Shengiiangpowder on the expression ofNF-κB in pulmonary micrangium endothelial cells and theexpression of ICAM-1 in terminal bronchiolar epithelium, the results show thatShengjiang powder may inhibit the expression of NF-κB in pulmonary micrangiumendothelial cells of model rats, the difference between the treating groups and controlgroup is significant. The experiments also show that the Shengjiang powder withdifferent dose can inhibit the expression of ICAM-1 in terminal bronchiolar epithelialcells obviously, there is significant difference between treating groups and control group,and the effect of the powder with high dose has better effect than middle and low doseone, and there is no significance among three groups. The results shows that Shengjiangpowder can prevent and treat acute lung injury through inhibit inflammatory reaction,preventing apoptosis, protecting lung tissues by inhibiting the expression of NF-κB in pulmonary micrangium and expression of ICAM-1 in bronchiolar epithelium.
论文提出，感染性急性肺损伤主要致病因素及病理特点为暴感外邪，邪正剧烈交争，病情骤变，导致肺气郁闭，肺体受损，血络瘀滞，瘀血停滞；津液不布，水液停聚；热伤气阴，正气外脱。从肺损伤总的病变过程来看，邪热为病理损伤的始动因素；邪热或热毒蕴肺、肺失宣降为肺损伤的病理基础，并且贯穿病程的始终；痰、饮、瘀等继发性病邪为肺部损伤的重要病理因素；临床表现以肺气郁闭为主要特点。病变早、中期以实为主，病理因素以热毒为主，毒势深重，兼有痰热、瘀血、湿饮，以肺气郁闭为主要特点，临床表现以“急”、“暴”、“闭”为特点；病之后期热伤气阴，病理性质演变为正虚、邪实夹杂，正虚可表现有肺气阴虚、肺肾气虚、肾虚不纳气或正气外脱等；邪实可见痰、饮、瘀等阻于肺。严重者可见肺不主气，正气外脱，化源竭绝证候。
在感染性急性肺损伤辨证中，首先须明确疾病的基本特点。本病由暴感外邪所致，感邪后正邪剧烈交争，邪势深重，导致肺气郁闭，肺体受损。临床以高热，喘憋为基本特点。后期病理变化以邪实正虚或以肺气阴虚、肺肾两虚、正气外脱等为主。邪势炽盛，病势深重者，变化急骤，可致气阴迅速耗伤，急速导致肺不主气，化源速绝，临床表现以呼吸衰竭为主要特征。与普通肺热证比较，具有“急”、“暴”、“闭”的特点。
其次，应辨别疾病卫气营血的浅深层次及病机传变。感邪后可出现短暂肺卫表证，邪不外解，则迅速传入气、营、血分。若邪势较盛，或机体正气不足，病邪也可不拘表里渐次传变，病后即迅速出现病邪内传，见气营(血)两燔证或逆传心包而见窍闭证，或深入营血而见营血分证。后期则以正虚邪实夹杂为主，正虚可表现有肺气阴虚、肺肾气虚、肾虚不纳气或正气外脱等；邪实可见痰、饮、瘀等阻于肺。严重者可见肺不主气，正气外脱，化源竭绝证候。
第三，须辨别病邪性质。急性肺损伤可由多种病邪引起，不同病邪所致者有各自的特殊临床表现。引起本病的病邪包括风热、燥热、暑热、暑湿、湿热等性质病邪，由于病邪多具炎热性质，或为疫邪所感，故致病迅速，病情严重，临床须根据不同特点加以鉴别。
第四，辨析证候虚实及病邪夹杂。在疾病初起，正邪剧烈交争，多表现为实证；随着病程的进展，病邪耗伤气阴，则证候由实致虚，中期可表现为实证夹虚，后期则可表现为虚中夹实，终致以虚为主的证候。另外，在病程发展过程中，还兼夹有痰、饮、瘀血等病理性产物，并可进一步影响肺及全身的病机证候演变。在辨治过程中亦须加以辨析。
最后，还须审疾病发展过程中病邪的脏腑传变。在感染性急性肺损伤的发展过程中，由于邪蕴于肺，肺失宣降，气化失司，通调失职，可致全身各脏腑气机失调；痰、饮、瘀、气闭等病理因素也会影响其它脏腑，从而导致邪传他脏，致多脏器损害发生，病变主要可涉及胃、大肠、肝、心包、肾等脏腑。
根据感染性急性肺损伤病理变化及肺的生理功能特点，确立扶正祛邪，调整脏腑功能为本病的主要治疗原则。在感染性急性肺损伤初期阶段，多以邪实为主，兼有正虚，此时治疗当主以祛邪，兼以扶正；疾病中期阶段，邪气盛，正气损伤，此时当辨清病机侧重，若病机侧重在邪实，则重在攻邪；若正虚明显，则以扶正为主；疾病后期，正气大伤，阴液损伤明显，此时治疗则主以扶正，兼清余邪。并强调在治疗中须正确把握扶正、祛邪与调整脏腑功能三者之间的辨证关系。
在急性肺损伤的发生发展过程中，还多同时出现热毒、痰热、瘀血、水湿等重要病理因素，临床表现以肺气郁闭为主要特点，后期可兼见肺气阴虚、肺肾两虚、正气外脱等证候。因此论文提出，急性肺损伤的治疗以清肺泄热、清解热毒、宣开肺气、化痰除饮、活血化瘀、补肺固脱等为主要治法。由于邪热壅肺、肺失宣降为本病的主要病理基础，故在治疗中清肺为首选治法，贯穿全局，而宣开肺气亦不可或缺，化痰、消饮、活血化瘀、补肺固脱或敛肺救逆固脱等为重要治法。
对现代临床及实验资料研究表明，感染性急性肺损伤西医发病机制主要与过度免疫反应及肺泡上皮细胞的凋亡、修复相关。中医发病机制认识主要与邪热、热毒、痰热、瘀血、气闭等相关。提出以后对于中医药治疗本病的研究须重视中医药对抗病原的作用机制、重视中医药对抗病理损害的作用机制：如药物对肺微血管内皮细胞及肺泡上皮细胞的保护作用、调整循环状态及改善通气功能等、深入研究细胞凋亡在急性肺损伤发病过程中的复杂机制，研究中医不同治法对凋亡过程的调节作用等。
在理论研究的基础上，论文还通过实验研究探讨了开上泄下治法的代表性方剂升降散治疗本病的作用机理，实验研究了升降散对急性肺损伤大鼠肺微血管内皮细胞NF-κB表达的影响及升降散对急性肺损伤大鼠肺终末性细支气管粘膜上皮细胞ICAM-1表达的影响，结果表明，升降散各治疗组可以明显抑制造模后大鼠肺微血管内皮细胞NF-κB表达，结果与模型组比较有显著差异。同时观察了升降散对肺终末性细支气管上皮细胞ICAM-1表达的影响，结果表明，大、中、小剂量组药物对ICAM-1的表达都有明显的抑制作用，与模型组比较有显著性差异，其中大剂量组表达较中、小剂量组低，但三者间无显著性差异。实验结果显示，升降散可以通过抑制肺微血管内皮细胞表达NF-κB及肺组织细胞表达ICAM-1，以抑制炎症反应的放大，调节细胞凋亡，从而起到组织保护，防治急性肺损伤的作用。
The paper discusses the laws of syndrome differentiation and therapeutic rules foracute lung injury caused pulmonary infection in Traditional Chinese Medicine, andelucidates the pathogenesis, syndrome differentiation, therapeutic principles and methodsof infectious acute lung injury based on the ancient medical literatures and modemclinical and experiment data.
The paper puts forward the main pathogenic factor and features include suddenaffection by exopathogen, violent conflict between pathogen and vital Qi and impetuouschange of the morbid condition, and causing blockage of lung Qi, damaging lungparenchyma, stagnating the blood vessels and causing blood stasis; misdistribution ofbody fluid causing water pathogen; collapse of Vital Qi due to heat pathogen damagingYin fluid. In the morbid process of infectious acute lung injury, the pathogenic heat is theprimary factor, the basic pathogeneses of lung injury are pathogenic heat or heat toxinaccumulating in the lung and the lung failing both dispersing and descending, and theyrun through the whole morbid process; the secondary pathogenic factors include phlegm,water pathogen and blood stasis, they are important to the formation of lung injury; themain feature of the clinical manifestation is blockage of the lung Qi. In the early andmiddle stage, the main pathogenic factor is heat toxin, accompanied by phlegm heat,blood stasis, water pathogen and blockage of lung Qi; the main features of the clinicalpresentation include "sudden onset", "violent morbid condition" and "blockage of thelung Qi". At the final stage of the disease, the main pathogenesis of the disease iscoexistence of the deficiency and excess, the deficiency aspect may include lung Qi andYin deficiency, Qi deficiency of lung and kidney, asthenia kidney failing to hold Qi andcollapse of the vital Qi; and the excess aspects include phlegm, water pathogen and bloodstasis stagnating in the lung. In the severe case, the syndrome may be collapse of the vitalQi and lung failing to dominate Qi and control respiration due to the extreme deficiencyof the lung Qi.
In the syndrome differentiation of acute lung injury, we'd better notice the followingaspect. Firstly, understand the basic feature of infectious acute lung injury. ALI is causedby Exopathogen invading suddenly, there is violent conflict between Exopathogen andVital Qi with severe morbid condition, and cause blockage of the lung Qi and damage thelung parenchyma, the clinical manifestation may show high fever, dyspnea andsuppression of the breath. The pathogenesis at final stage may show deficiency typeaccompanied by excess, or lung Qi and Yin deficiency, collapse of the vital Qi. The casewith intense pathogenic heat and severe morbid state can damage Vital Qi and Yinquickly, make the lung failing to dominate Qi and control respiration, cause respiratoryfailure. The syndrome always has the features of "sudden onset", "violent morbidcondition" and "blockage of the lung Qi" compared with common lung-heat syndrome.
Secondly, differentiate the Wei, Qi, Ying and Xue phases and the transference of thedisease. There may be a short time of exterior syndrome at beginning of the disease, thenthe pathogen invade into the Qi, Ying and Xue phases rapidly. If the pathogen is veryintense or the Vital Qi is deficient, the pathogen may transmit disobey the orders, andinvading the interior promptly after occurrence, the syndromes may be intense heat inboth Qi, Ying and Xue phases, or abnormal transmission of the pericardium and causingblockage syndrome of the pericardium, or syndromes of Ying and Xue phases. At thefinal stage of the disease, the main pathogenesis is coexistence of deficiency and excess,the deficiency syndrome may be lung Qi and Y'm deficiency, lung and kidney Qideficiency, asthenia kidney failing to hold Qi or collapse of Vital Qi etc. The excesssyndromes may be phlegm, water pathogen and blood stasis stagnating in the lung.Severe case may show lung failing to dominate Qi, collapse of the Vital Qi and collapseof the origin of the blood and Qi.
Thirdly, differentiate the nature of the pathogen. Acute lung injury may be caused byvarious pathogens, different pathogen can show special clinical manifestation of theirown. The pathogens include wind-heat, dry-heat, summer-heat and damp-heat orpestilential pathogen, they all have the features of scorching nature and causing diseaseswiftly.
Fourthly, differentiate the deficiency and excess of the syndrome and the mixture ofthe pathogen. At the beginning, there is violent conflict between Vital Qi and pathogen,the main syndrome is excess one; along with the morbid progress, the pathogen damage Qi and Yin, the syndrome may be excess accompanied by deficiency in the middle stageof the disease, and deficiency type accompanied by excess, and deficiency type as itsmain aspect at final stage. In addition, in the morbid progress, there may be pathogenicproducts such as phlegm, water pathogen and blood stasis, and these may influence thepathologic changes in the lung and the entire body. So the doctors should consideratethem in the clinical treatment.
Finally, analyze the transmission of the pathogen among the differentZangfu-organs. In the progress of the infectious acute lung injury, the pathogenaccumulate in the lung, cause the lung failing to disperse and descend, and failing ofQi-vary and smoothness of water passages, it may cause disorders of the Qi-movementof the Zangfu-organs and the entire body; and the pathogenic factors, such as phlegm,water pathogen, blood stasis and Qi blockage, may also influence the otherZangfu-organs, and make the pathogen transmit into the other organs, and cause multipleorgans damage. The disease may involve stomach, large intestine, liver, pericardium andkidney, etc.
According to the pathologic changes of the infectious acute lung injury andphysiological function of the lung, the therapeutic principle should be supporting Vital Qiand eliminating pathogens. At the early stage of the infectious acute lung injury, the mainpathogenesis is excess, accompanied with deficiency of the vital Qi, the therapeuticprinciple should be eliminate the pathogen, in the middle stage, intense pathogen damagethe Vital Qi, the therapeutic principle should be made on the basis of differentiating thepathogenesis, if the main aspect is excess type, the principle should be eliminating thepathogen; if the main aspect is deficiency type, the principle should be supporting theVital Qi. At the final stage of the disease, Vital Qi and Yin fluid is damaged distinctly, theprinciple should be supporting the Vital Qi, and combined with eliminating surpluspathogen. The paper stress on coordinating the dialectical relationships amongsupporting Vital Qi, eliminating pathogen and regulating Zangfu-organ.
In the course of the acute lung injury, there may be heat-toxin, phlegm-heat, bloodstasis and water pathogen, the clinical feature of disease is blockage of lung Qi. At finalstage, the syndromes may be lung Qi and Yin deficiency, deficiency of lung and kidneyor collapse of Vital Qi. The paper put forward the therapeutic methods of clearing awaylung heat, eliminating heat-toxin, disperse lung Qi, resolving phlegm and dispelling water pathogen, promoting blood circulation to remove blood stasis and tonifying lungQi to astringe collapse for acute lung injury. Because the main pathogenesis of thedisease is pathogenic heat accumulating in the lung and the lung failing to disperse anddescend, it is the primary method to clear away lung heat running through the entirecourse of disease, dispersing lung Qi is indispensable for treating the disease, andresolving phlegm, eliminating water pathogen, promoting blood circulation to removeblood stasis, tonifying lung Qi to astringe collapse or astringing lung Qi to treat collapseare important methods for treating acute lung injury.
According to modem clinical and experimental studying, the mechanisms ofinfectious acute lung injury are related to the excess immunoreaction and apoptosis andrepair of the alveolar epithelial cells. The mechanisms of the disease are related to thepathogenic heat, heat-toxin, phlegm heat, blood stasis and blockage of Qi. The paper putforward that the study of treating the disease by TCM should focus on the followingfields, i.e. the mechanisms of dispelling pathogen by TCM; the mechanisms ofpreventing pathologic injury to the lung by TCM, such as protecting pulmonarymicrangium endothelial cells and alveolar epithelial cells, improving circulation state andventilatory function; researching on the complex mechanism of apoptosis in the morbidprogress of acute lung injury, and the action of different therapy of TCM on apoptosis.
On the basis of the theoretical studying, the paper discusses the mechanism oftreating the disease by Shengjiang powder, the representative formula for the method ofdispersing the lung and purging the Fu-organs. We observed the influence of Shengiiangpowder on the expression ofNF-κB in pulmonary micrangium endothelial cells and theexpression of ICAM-1 in terminal bronchiolar epithelium, the results show thatShengjiang powder may inhibit the expression of NF-κB in pulmonary micrangiumendothelial cells of model rats, the difference between the treating groups and controlgroup is significant. The experiments also show that the Shengjiang powder withdifferent dose can inhibit the expression of ICAM-1 in terminal bronchiolar epithelialcells obviously, there is significant difference between treating groups and control group,and the effect of the powder with high dose has better effect than middle and low doseone, and there is no significance among three groups. The results shows that Shengjiangpowder can prevent and treat acute lung injury through inhibit inflammatory reaction,preventing apoptosis, protecting lung tissues by inhibiting the expression of NF-κB in pulmonary micrangium and expression of ICAM-1 in bronchiolar epithelium.
引文
1. Bauer TT, Monton C, Torres A, et al. Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome severe pneumonia and controls. Thorax, 2000, 55: 46
2．张灵恩．急性肺损伤的诊治．小儿急救医学，2000，7(3)：164～165
3．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
4．赵景民，周光德，孙艳玲等．1例地方非典型肺炎病例病理及病原学发现．解放军医学杂志，2003，28(5)：379～382
5．赵景民，周光德，孙艳玲等．重症急性呼吸综合征肺外器官的病理学观察研究．解放军医学杂志，2003，28(6)：480～481
6．蔡柏蔷，呼吸内科学，北京：中国北京协和医科大学出版社，2000：632～645
7．夏媛，金晓毛，庞玉英．IL和TNF-α与急性下呼吸道感染的关系，疾病控制杂志，2003，7(2)：112
8. Monton C, Torres A, Ebiary M, et al. Cytokin expression in severe pneumonia [J]. Crit Care Med, 1999, 27: 1745-1753
9. Bont L, Heijneu CJ, Kowelaars A, et al. Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis [J]. Eur Respir J, 1999, 14: 144-149
10．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
11．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
12．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
13．耿耘，魏星．急性肺损伤、急性呼吸窘迫综合征的中医发病机理探讨．江西中医药，2002，33(5)：11～12
14．江学成，张育才，徐德明等．大剂量654-2、硝普钠、和丹参注射液辅助呼吸支持治疗ARDS．徐州医学院学报，1999，19(4)：316～319
15．曹珉，沈祖法．脉络宁治疗新生儿成人型呼吸窘迫综合征．现代中西医结合杂志，2000，(1)：38
16．刘哲峰，杨明会，孙艳等．生脉注射液对放射性肺损伤防治作用的临床研究．解放军药学学报，2005，21(2)：112～115
17．刘福成，薛芳，崔志永等．大承气汤治疗严重创伤呼吸窘迫综合征的临床研究．河北中医，1994，16(5)：2～3
18．刘世坤，谭琛，钟筱英等．牛珀至宝丹及参麦液对内毒素休克大鼠肺损伤的保护作用．中国中医急症，1999，8(2)：77～79
19．任继学．毒邪肺热病辨证论治．中医药通讯，2005，4(6)：8
20．杨进．温病学．北京：人民卫生出版社，2003：31～32
21．罗会明，何剑峰，汤洪伟．SARS的流行病学特征．华南预防医学，2004，30(1)：61～64
22．沈华浩，张根生．从炎症本质看急性肺损伤／急性呼吸窘迫综合征．中华急诊医学杂志，2006，15(11)：965～966
23．李荣成，王今达，崔乃杰等．清心泻肝法治疗急性呼吸窘迫综合征22例临床观察．中西医结合实用临床急救，1997，4(10)：453
24．薛芳．急性呼吸窘迫综合征和阳明腑实喘满证．辽宁中医杂志，1982，9(4)：10～11
25．陈正堂．急性呼吸窘迫综合征发病机制及诊治进展．中国急救医学，1999，19(4)：255
26．阎田玉．病毒性肺炎与血瘀证．中医杂志，1991，(4)：48
27．龚婕宁．论温病肺热证与清肺活血法．中国中医基础医学杂志，1997，4(2)：8
28．丁慧芬．中医肺与争性肺损伤发病关系初探．辽宁中医杂志，2004，31(10)：823～824
29．任继学，张志强．毒邪肺热病辨证论治．中医药通报，2005，4(6)：7～10
30．杨进．温病学．北京：人民卫生出版社，2003：118
31．张宁，刘世巍，李方洁等．SARS的鉴别诊断与早期中医症状学特征．中国医药学报，2003，18(11)：676
32．郝瑞福，唐启盛，林谦等．178例SARS恢复期患者中医证候观察．中国中医药信息杂志，2004，11(6)：516～517
33．霍娜，陆海英，徐小元等．45例SAPS病例早期临床特点及疗效的初步分析．北京大学学报(医学版)，2003，35(S1)：19～22
34．刘明芳，聂秀红，王烁等．严重急性呼吸综合征患者血小板的动态变化及意义．临床荟萃，2004，19(22)：1274～1276
35．李群，蓝雨，徐翠玲等．一例孕妇感染禽流感病毒(H5N1)死亡的调查．中华流行病学杂志，2006，27(4)：288～292
36．王淑玲．“肺肾相关”的物质基础．中国中医基础医学杂志，2002，8(4)：9～10、18
37．王淑玲，宗全和．中西医结合探讨“肺肾相关”．中国医药学报，2002，17(4)：221～223
38．孙瑛，孙仁宇，杜烨玮等．银杏叶提取物对衰老大鼠急性肺损伤和肾功能受损的保护作用．中华老年医学杂志，2004，23(5)：324～327
39．任继学，张志强．毒邪肺热病辨证论治．中医药通报，2005，4(6)：7～10
40．彭胜权．温病学．北京：人民卫生出版社，2000：187
41．吴斌龙，杨涛．热饮浅识．浙江中医杂志，2001，(8)：332
42．刘涛．王灿晖教授论传染性非典型肺炎的病变规律和防治要点．江苏中医药，2003，24(6)：5～7
43．单书健，陈子华．古今名医临证金鉴·咳喘肺胀卷(下)，北京：中国中医药出版社，1999：45～49
44．杨进．新编温病学．北京：学苑出版社，2003：361
45. Bauer TT, Monton C, Torres A, et al. Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome severe pneumonia and controls [J]. Thorax, 2000, 55: 46
46．张灵恩．急性肺损伤的诊治．小儿急救医学，2000，7(3)：164～165
47．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
48．曾其毅．炎症反应综合征与急性肺损伤．实用儿科临床杂志，2002，17(2)：139-141
49. Kurahashi K, Kajikawa O, Sawa T, et al. Pathogenesis of septic shock in pseudomonas aeruginosa pneumonia [J]. J Clin Invest, 1999, 104: 743-750
50. Martin TR. Lung cytokines and ARDS. Chest, 1999, 116.. S2～S8
51．徐军，张梅，刘学民等．TNF-α基因表达在大鼠急性重症胰腺炎肺损伤中的作用．西安交通大学学报(医学版)，2004，25(4)：388～392
52．夏燕亮，刘昕．丹参对大鼠脓毒症急性肺损伤发生中TNF-α的影响及对肺的保护作用．中药药理与临床，2004，20(6)：14～17
53．夏媛，金晓毛，庞玉英．IL和TNF-α与急性下呼吸道感染的关系，疾病控制杂志，2003，7(2)：112
54. Monton C, Torres A, Ebiary M, et al. Cytokin expression in severe pneumonia [J]. Crit Care Med, 1999, 27: 1745-1753
55. Bont L, Heijneu CJ, Kowelaars A, et al. Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis [J]. Eur Respir J, 1999, 14: 144-149
56．刘继英，李瑾，王学谦．神农33对急性肺损伤大鼠白介素-1β基因表达的影响．中国中西医结合外科杂志，2001，7(3)：151～154
57．史或，王崇伟．油酸-内毒素序贯致新生大鼠急性肺损伤IL-18水平的变化．南京医科大学学报(自然科学版)，2006，26(10)941～944
58．杨光，李鸣真，叶望云等．白细胞介素8和一氧化氮在家兔内毒素性急性肺损伤中的作用．中国病理生理杂志，1998，14(1)：86
59．余追，许友芝，周晓阳等．大鼠急性肺损伤时iNOS mRNA和eNOS mRNA表达的时相变化．武汉大学学报(医学版)，2003，24(1)：24～27
60．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
61．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
62. Le Tulzo l, Shenkar R, Kaneko D, et al. Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappa B regulation and cytokine expression [J]. Clinlnvest, 2003, 99 (7): 1516
63．王建春，姜鹏，谢艳萍等．急性肺损伤大鼠肺组织NF-κB表达的研究．中国现代医学杂志，2006，16(16)：2448～2452
64．农凌波，肖正伦．急性肺损伤中的细胞凋亡及凋亡调控．国外医学·呼吸系统分册，2002，22(3)：149-151
65. Hengarther M O. The biochemistry of apoptosis [J]. Nature, 2000, 407 (6805): 770～776
66. Tesfaigzi J, Wood M B, Johnson N F, et al. Apoptosis is a pathway responsible for the resolution ofendotoxin-induced alveolar type Ⅱ cell hyperplasia in the rat[J]. Int J Exp Pathol, 1998, 79: 303～311
67．黎檀实，尹明，冯丽洁等．急性肺损伤中肺泡Ⅱ型细胞凋亡机制的研究现状．中国危重病急救医学，2002，14(3)：185～187
68．窦志芳．细胞凋亡在急性肺损伤中的作用．甘肃科技，2004，20(4)：143～144，59
69．宋勇，毛宝龄，钱桂生等．急性肺损伤大鼠肺组织细胞凋亡及Fas／FasL系统表达改变及其意义．中国危重病急救医学，1999，11(11)：662～665
70．顾俭勇，黄培志．脂多糖致急性肺损伤后Bax／Bcl-2变化．中国基层医药，2006，13(10)：1585～1586
71．耿耘，魏星．急性肺损伤、急性呼吸窘迫综合征的中医发病机理探讨．江西中医药，2002，33(5)：11～12
72．叶汉兰，潘可欣．中西医结合治疗成人呼吸窘迫综合征20例．北京中医药大学学报，1998，21(1)：48～49
73．陈天琪，葛正行．浅谈中医对急性肺损伤的认识．贵阳中医学院学报，2006，28(5)：7
74．葛金文，闻晓东，袁长津等．严重急性呼吸综合症(SARS)的中医病名及病因病机研究．湖南中医学院学报，2003，23(5)：59～61
75．刘福成，薛芳，崔志永等．大承气汤治疗严重创伤呼吸窘迫综合征的临床研究．河北中医，1994，16(5)：2～3
76．李志文，张风敏，莫顺景等．中西医结合治疗急性肺损伤疗效观察．中国中医急症，2004，13(9)：574～575
77．李伟，罗彦英，李继坤等．开肺陷胸汤对大鼠胰源性肺损伤的防治效应．中国中西医结合外科杂志，2002，8(3)：195～197
78．韩恩昆，吴咸中．大承气汤和活血清胰汤对重型急性胰腺炎肺损伤治疗的实验研究．中国中西医结合外科杂志，2004，10(2)：90～92
79．李春盛，何新华，桂培春．大黄对急性肺损伤大鼠血浆和支气管肺泡灌洗液中炎症细胞因子表达的影响．中国中西医结合急救杂志，2005，12(5)：306～308
80．李春盛，桂培春，何新华等．大黄对内毒素诱导急性肺损伤大鼠的保护作用．基础医学与临床，2001，21(1)：65～68
81．杨光，李鸣真，黄光英等．热毒清对家兔内毒素性DIC急性肺损伤的保护作用．中国中西医结合外科杂志，1996，(6)：455-459
82．杨明炜，陆付耳，李鸣真等．热毒清对内毒素体内、外诱生肿瘤坏死因子的影响．中国中医基础医学杂志，2000，6(8)：19～21
83．李风雷，刘晓晴，柳青等．鱼腥草对油酸性急性肺损伤大鼠肺组织TNF-α表达的影响．中国病理生理杂志，2003，19(4)：547～548
84．王波涌，张宗林，郭鹏程．痰热清注射液对急性胰腺炎肺损伤的疗效观察．中国药师，2006，9(3)：225-226
85．李澎涛，张娜，朱晓磊等．痰热清注射液抗内毒素所致急性肺损伤的实验研究．中国药学杂志，2005，40(7)：518-521
86．刘秀芳，王炳胜，张佩等．益气活血中药防治放射性肺损伤的临床观察．中国中医药信息杂志，2004，11(12)：1085～1086
87．沈炳玲，徐燕燕，齐虹．复方丹参注射液对兔油酸型呼吸窘迫综合征影响的实验研究．天津医药，2000，28(5)：293-294
88．曹春水，黄亮，肖金娥．复方丹参对急性肺损伤6-keto-PGF_(1a)、TXB_2的影响．岭南急诊医学杂志，2004，9(1)：1～3
89．夏燕亮，刘昕．丹参对大鼠脓毒症急性肺损伤发生中TNF-α的影响及对肺的保护作用．中药药理与临床，2004，20(6)：14～17
90．吴山，盛延良，蒋志学．丹参对肺水肿大鼠白细胞介素-8和内皮素的影响．辽宁中医杂志，2003，30(10)：796～797
91．陈畅，夏中元，孟庆涛．赤芍对大鼠内毒素性急性肺损伤保护作用机制的研究．中国急救医学，2005，25(1)：38～40
92．刘哲峰，杨明会，孙艳等．生脉注射液对放射性肺损伤防治作用的临床研究．解放军药学学 报，2005，21(2)：112～115
93．何新华，李春盛，桂培春．生脉饮对内毒素诱导急性肺损伤大鼠一氧化氮及其合酶的影响
94．李瑜，李琳章，王世端等．黄芪对兔内毒素性急性肺损伤的保护作用．山东医药主，2006，46(11)：63～64
95．黄翠萍，杨和平，张珍祥．参麦注射液对脂多糖诱导大鼠急性肺损伤防护机制探讨．中华结核和呼吸杂志，2005，28(1)：67～68
96．艾宇航，彭鎏，张丽娜．参附注射液对内毒素所致肺损伤的保护作用．中国急救医学，2006，26(4)：285～287
97．刘克玄，柳垂亮，吴伟康等．四逆汤预先给药对大鼠肠缺血／再灌注所致急性肺损伤的作用．中华麻醉学杂志，2004，24(7)：511-514
98．曹慧玲，吕士杰，姜艳霞等．清开灵注射液对大鼠急性肺损伤中氧自由基的干预作用．现代中西医结合杂志，2006，15(18)：2465～2467
99．廖欣，杨爱莲，杜少辉等．牛珀至宝微丸对内毒素急性肺损伤MDA和SOD的影响．深圳中西医结合杂志．2006，16(4)：196～198
100．黎晖，刘望姣，李志新等．牛珀至宝微丸对内毒素急性肺损伤胶原纤维表达的影响．深圳中西医结合杂志．2004，14(4)：196～198
1．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
2．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
3．孙立．“百病生于气”与升降散之应用．浙江中医杂志，2004，(10)：425
4．刘建军，孙向党．升降散加减治疗重症肺炎11例观察．中医药学刊，2001，19(2)：149
5．李际强，张春学，胡溪柳等．升降散抗小鼠流感病毒性肺炎的实验研究．实用中医内科杂志，2004，18(1)：28
6．彭燕．孙定隆副教授应用升降散加减治疗小儿重症肺炎经验．疑难病杂志，2004，3(3)：179
1. Ley K. Molecular mechanisms of leukocyte recruitment in the inflammatory process[J]. Cardiovascular Research, 1996, 32:733～742
2．佟振月，侯立新，马跃文等．肺纤维化细胞间粘附分子1基因产物表达的作用．中华结核和呼吸杂志，2000，23(6)：363～365
3．刘小丽，顾大勇，马布仁等．LPS直接诱导的肺微血管内皮细胞与PMN的粘附作用及核因子κB调控机理的实验研究．青海医药杂志，2003，33(1)：2～6
2．张灵恩．急性肺损伤的诊治．小儿急救医学，2000，7(3)：164～165
3．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
4．赵景民，周光德，孙艳玲等．1例地方非典型肺炎病例病理及病原学发现．解放军医学杂志，2003，28(5)：379～382
5．赵景民，周光德，孙艳玲等．重症急性呼吸综合征肺外器官的病理学观察研究．解放军医学杂志，2003，28(6)：480～481
6．蔡柏蔷，呼吸内科学，北京：中国北京协和医科大学出版社，2000：632～645
7．夏媛，金晓毛，庞玉英．IL和TNF-α与急性下呼吸道感染的关系，疾病控制杂志，2003，7(2)：112
8. Monton C, Torres A, Ebiary M, et al. Cytokin expression in severe pneumonia [J]. Crit Care Med, 1999, 27: 1745-1753
9. Bont L, Heijneu CJ, Kowelaars A, et al. Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis [J]. Eur Respir J, 1999, 14: 144-149
10．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
11．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
12．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
13．耿耘，魏星．急性肺损伤、急性呼吸窘迫综合征的中医发病机理探讨．江西中医药，2002，33(5)：11～12
14．江学成，张育才，徐德明等．大剂量654-2、硝普钠、和丹参注射液辅助呼吸支持治疗ARDS．徐州医学院学报，1999，19(4)：316～319
15．曹珉，沈祖法．脉络宁治疗新生儿成人型呼吸窘迫综合征．现代中西医结合杂志，2000，(1)：38
16．刘哲峰，杨明会，孙艳等．生脉注射液对放射性肺损伤防治作用的临床研究．解放军药学学报，2005，21(2)：112～115
17．刘福成，薛芳，崔志永等．大承气汤治疗严重创伤呼吸窘迫综合征的临床研究．河北中医，1994，16(5)：2～3
18．刘世坤，谭琛，钟筱英等．牛珀至宝丹及参麦液对内毒素休克大鼠肺损伤的保护作用．中国中医急症，1999，8(2)：77～79
19．任继学．毒邪肺热病辨证论治．中医药通讯，2005，4(6)：8
20．杨进．温病学．北京：人民卫生出版社，2003：31～32
21．罗会明，何剑峰，汤洪伟．SARS的流行病学特征．华南预防医学，2004，30(1)：61～64
22．沈华浩，张根生．从炎症本质看急性肺损伤／急性呼吸窘迫综合征．中华急诊医学杂志，2006，15(11)：965～966
23．李荣成，王今达，崔乃杰等．清心泻肝法治疗急性呼吸窘迫综合征22例临床观察．中西医结合实用临床急救，1997，4(10)：453
24．薛芳．急性呼吸窘迫综合征和阳明腑实喘满证．辽宁中医杂志，1982，9(4)：10～11
25．陈正堂．急性呼吸窘迫综合征发病机制及诊治进展．中国急救医学，1999，19(4)：255
26．阎田玉．病毒性肺炎与血瘀证．中医杂志，1991，(4)：48
27．龚婕宁．论温病肺热证与清肺活血法．中国中医基础医学杂志，1997，4(2)：8
28．丁慧芬．中医肺与争性肺损伤发病关系初探．辽宁中医杂志，2004，31(10)：823～824
29．任继学，张志强．毒邪肺热病辨证论治．中医药通报，2005，4(6)：7～10
30．杨进．温病学．北京：人民卫生出版社，2003：118
31．张宁，刘世巍，李方洁等．SARS的鉴别诊断与早期中医症状学特征．中国医药学报，2003，18(11)：676
32．郝瑞福，唐启盛，林谦等．178例SARS恢复期患者中医证候观察．中国中医药信息杂志，2004，11(6)：516～517
33．霍娜，陆海英，徐小元等．45例SAPS病例早期临床特点及疗效的初步分析．北京大学学报(医学版)，2003，35(S1)：19～22
34．刘明芳，聂秀红，王烁等．严重急性呼吸综合征患者血小板的动态变化及意义．临床荟萃，2004，19(22)：1274～1276
35．李群，蓝雨，徐翠玲等．一例孕妇感染禽流感病毒(H5N1)死亡的调查．中华流行病学杂志，2006，27(4)：288～292
36．王淑玲．“肺肾相关”的物质基础．中国中医基础医学杂志，2002，8(4)：9～10、18
37．王淑玲，宗全和．中西医结合探讨“肺肾相关”．中国医药学报，2002，17(4)：221～223
38．孙瑛，孙仁宇，杜烨玮等．银杏叶提取物对衰老大鼠急性肺损伤和肾功能受损的保护作用．中华老年医学杂志，2004，23(5)：324～327
39．任继学，张志强．毒邪肺热病辨证论治．中医药通报，2005，4(6)：7～10
40．彭胜权．温病学．北京：人民卫生出版社，2000：187
41．吴斌龙，杨涛．热饮浅识．浙江中医杂志，2001，(8)：332
42．刘涛．王灿晖教授论传染性非典型肺炎的病变规律和防治要点．江苏中医药，2003，24(6)：5～7
43．单书健，陈子华．古今名医临证金鉴·咳喘肺胀卷(下)，北京：中国中医药出版社，1999：45～49
44．杨进．新编温病学．北京：学苑出版社，2003：361
45. Bauer TT, Monton C, Torres A, et al. Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome severe pneumonia and controls [J]. Thorax, 2000, 55: 46
46．张灵恩．急性肺损伤的诊治．小儿急救医学，2000，7(3)：164～165
47．中华医学会重症医学分会．急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南(2006)．中国实用外科杂志，2007，27(1)：1～6
48．曾其毅．炎症反应综合征与急性肺损伤．实用儿科临床杂志，2002，17(2)：139-141
49. Kurahashi K, Kajikawa O, Sawa T, et al. Pathogenesis of septic shock in pseudomonas aeruginosa pneumonia [J]. J Clin Invest, 1999, 104: 743-750
50. Martin TR. Lung cytokines and ARDS. Chest, 1999, 116.. S2～S8
51．徐军，张梅，刘学民等．TNF-α基因表达在大鼠急性重症胰腺炎肺损伤中的作用．西安交通大学学报(医学版)，2004，25(4)：388～392
52．夏燕亮，刘昕．丹参对大鼠脓毒症急性肺损伤发生中TNF-α的影响及对肺的保护作用．中药药理与临床，2004，20(6)：14～17
53．夏媛，金晓毛，庞玉英．IL和TNF-α与急性下呼吸道感染的关系，疾病控制杂志，2003，7(2)：112
54. Monton C, Torres A, Ebiary M, et al. Cytokin expression in severe pneumonia [J]. Crit Care Med, 1999, 27: 1745-1753
55. Bont L, Heijneu CJ, Kowelaars A, et al. Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis [J]. Eur Respir J, 1999, 14: 144-149
56．刘继英，李瑾，王学谦．神农33对急性肺损伤大鼠白介素-1β基因表达的影响．中国中西医结合外科杂志，2001，7(3)：151～154
57．史或，王崇伟．油酸-内毒素序贯致新生大鼠急性肺损伤IL-18水平的变化．南京医科大学学报(自然科学版)，2006，26(10)941～944
58．杨光，李鸣真，叶望云等．白细胞介素8和一氧化氮在家兔内毒素性急性肺损伤中的作用．中国病理生理杂志，1998，14(1)：86
59．余追，许友芝，周晓阳等．大鼠急性肺损伤时iNOS mRNA和eNOS mRNA表达的时相变化．武汉大学学报(医学版)，2003，24(1)：24～27
60．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
61．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
62. Le Tulzo l, Shenkar R, Kaneko D, et al. Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappa B regulation and cytokine expression [J]. Clinlnvest, 2003, 99 (7): 1516
63．王建春，姜鹏，谢艳萍等．急性肺损伤大鼠肺组织NF-κB表达的研究．中国现代医学杂志，2006，16(16)：2448～2452
64．农凌波，肖正伦．急性肺损伤中的细胞凋亡及凋亡调控．国外医学·呼吸系统分册，2002，22(3)：149-151
65. Hengarther M O. The biochemistry of apoptosis [J]. Nature, 2000, 407 (6805): 770～776
66. Tesfaigzi J, Wood M B, Johnson N F, et al. Apoptosis is a pathway responsible for the resolution ofendotoxin-induced alveolar type Ⅱ cell hyperplasia in the rat[J]. Int J Exp Pathol, 1998, 79: 303～311
67．黎檀实，尹明，冯丽洁等．急性肺损伤中肺泡Ⅱ型细胞凋亡机制的研究现状．中国危重病急救医学，2002，14(3)：185～187
68．窦志芳．细胞凋亡在急性肺损伤中的作用．甘肃科技，2004，20(4)：143～144，59
69．宋勇，毛宝龄，钱桂生等．急性肺损伤大鼠肺组织细胞凋亡及Fas／FasL系统表达改变及其意义．中国危重病急救医学，1999，11(11)：662～665
70．顾俭勇，黄培志．脂多糖致急性肺损伤后Bax／Bcl-2变化．中国基层医药，2006，13(10)：1585～1586
71．耿耘，魏星．急性肺损伤、急性呼吸窘迫综合征的中医发病机理探讨．江西中医药，2002，33(5)：11～12
72．叶汉兰，潘可欣．中西医结合治疗成人呼吸窘迫综合征20例．北京中医药大学学报，1998，21(1)：48～49
73．陈天琪，葛正行．浅谈中医对急性肺损伤的认识．贵阳中医学院学报，2006，28(5)：7
74．葛金文，闻晓东，袁长津等．严重急性呼吸综合症(SARS)的中医病名及病因病机研究．湖南中医学院学报，2003，23(5)：59～61
75．刘福成，薛芳，崔志永等．大承气汤治疗严重创伤呼吸窘迫综合征的临床研究．河北中医，1994，16(5)：2～3
76．李志文，张风敏，莫顺景等．中西医结合治疗急性肺损伤疗效观察．中国中医急症，2004，13(9)：574～575
77．李伟，罗彦英，李继坤等．开肺陷胸汤对大鼠胰源性肺损伤的防治效应．中国中西医结合外科杂志，2002，8(3)：195～197
78．韩恩昆，吴咸中．大承气汤和活血清胰汤对重型急性胰腺炎肺损伤治疗的实验研究．中国中西医结合外科杂志，2004，10(2)：90～92
79．李春盛，何新华，桂培春．大黄对急性肺损伤大鼠血浆和支气管肺泡灌洗液中炎症细胞因子表达的影响．中国中西医结合急救杂志，2005，12(5)：306～308
80．李春盛，桂培春，何新华等．大黄对内毒素诱导急性肺损伤大鼠的保护作用．基础医学与临床，2001，21(1)：65～68
81．杨光，李鸣真，黄光英等．热毒清对家兔内毒素性DIC急性肺损伤的保护作用．中国中西医结合外科杂志，1996，(6)：455-459
82．杨明炜，陆付耳，李鸣真等．热毒清对内毒素体内、外诱生肿瘤坏死因子的影响．中国中医基础医学杂志，2000，6(8)：19～21
83．李风雷，刘晓晴，柳青等．鱼腥草对油酸性急性肺损伤大鼠肺组织TNF-α表达的影响．中国病理生理杂志，2003，19(4)：547～548
84．王波涌，张宗林，郭鹏程．痰热清注射液对急性胰腺炎肺损伤的疗效观察．中国药师，2006，9(3)：225-226
85．李澎涛，张娜，朱晓磊等．痰热清注射液抗内毒素所致急性肺损伤的实验研究．中国药学杂志，2005，40(7)：518-521
86．刘秀芳，王炳胜，张佩等．益气活血中药防治放射性肺损伤的临床观察．中国中医药信息杂志，2004，11(12)：1085～1086
87．沈炳玲，徐燕燕，齐虹．复方丹参注射液对兔油酸型呼吸窘迫综合征影响的实验研究．天津医药，2000，28(5)：293-294
88．曹春水，黄亮，肖金娥．复方丹参对急性肺损伤6-keto-PGF_(1a)、TXB_2的影响．岭南急诊医学杂志，2004，9(1)：1～3
89．夏燕亮，刘昕．丹参对大鼠脓毒症急性肺损伤发生中TNF-α的影响及对肺的保护作用．中药药理与临床，2004，20(6)：14～17
90．吴山，盛延良，蒋志学．丹参对肺水肿大鼠白细胞介素-8和内皮素的影响．辽宁中医杂志，2003，30(10)：796～797
91．陈畅，夏中元，孟庆涛．赤芍对大鼠内毒素性急性肺损伤保护作用机制的研究．中国急救医学，2005，25(1)：38～40
92．刘哲峰，杨明会，孙艳等．生脉注射液对放射性肺损伤防治作用的临床研究．解放军药学学 报，2005，21(2)：112～115
93．何新华，李春盛，桂培春．生脉饮对内毒素诱导急性肺损伤大鼠一氧化氮及其合酶的影响
94．李瑜，李琳章，王世端等．黄芪对兔内毒素性急性肺损伤的保护作用．山东医药主，2006，46(11)：63～64
95．黄翠萍，杨和平，张珍祥．参麦注射液对脂多糖诱导大鼠急性肺损伤防护机制探讨．中华结核和呼吸杂志，2005，28(1)：67～68
96．艾宇航，彭鎏，张丽娜．参附注射液对内毒素所致肺损伤的保护作用．中国急救医学，2006，26(4)：285～287
97．刘克玄，柳垂亮，吴伟康等．四逆汤预先给药对大鼠肠缺血／再灌注所致急性肺损伤的作用．中华麻醉学杂志，2004，24(7)：511-514
98．曹慧玲，吕士杰，姜艳霞等．清开灵注射液对大鼠急性肺损伤中氧自由基的干预作用．现代中西医结合杂志，2006，15(18)：2465～2467
99．廖欣，杨爱莲，杜少辉等．牛珀至宝微丸对内毒素急性肺损伤MDA和SOD的影响．深圳中西医结合杂志．2006，16(4)：196～198
100．黎晖，刘望姣，李志新等．牛珀至宝微丸对内毒素急性肺损伤胶原纤维表达的影响．深圳中西医结合杂志．2004，14(4)：196～198
1．莫红缨．NF-kB及iNOS与肺部疾病．国外医学呼吸系统分册，2000，20(3)：160
2．叶进燕．核因子kB与肺部疾病．国外医学内科学分册，2004，31(1)：29
3．孙立．“百病生于气”与升降散之应用．浙江中医杂志，2004，(10)：425
4．刘建军，孙向党．升降散加减治疗重症肺炎11例观察．中医药学刊，2001，19(2)：149
5．李际强，张春学，胡溪柳等．升降散抗小鼠流感病毒性肺炎的实验研究．实用中医内科杂志，2004，18(1)：28
6．彭燕．孙定隆副教授应用升降散加减治疗小儿重症肺炎经验．疑难病杂志，2004，3(3)：179
1. Ley K. Molecular mechanisms of leukocyte recruitment in the inflammatory process[J]. Cardiovascular Research, 1996, 32:733～742
2．佟振月，侯立新，马跃文等．肺纤维化细胞间粘附分子1基因产物表达的作用．中华结核和呼吸杂志，2000，23(6)：363～365
3．刘小丽，顾大勇，马布仁等．LPS直接诱导的肺微血管内皮细胞与PMN的粘附作用及核因子κB调控机理的实验研究．青海医药杂志，2003，33(1)：2～6
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