基于五脏应时发病基础的气温骤变诱发脑卒中机制的研究
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摘要
脑卒中(中风)是一种常见的脑血管急症,具有发病率高、死亡率高、致残率高、合并症多及治愈率低等特点。在我国,每年卒中发病率达1.5‰,死亡率达1.2‰,是严重威胁人类健康和生命,影响个人和家庭生活质量的疾病。作为一种重要的“脉络-血管系统病”,其核心病位在心。临床资料显示此类疾病发生具有明显季节性,冬季多发,夏季也可出现一个小高峰,与中医五脏应时发病有相合之处。
1目的
本研究以“脑卒中的季节性发病”作为中医“五脏应时发病”研究的突破口,通过对“脉络-血管系统病季节性发病规律”的理论和冬夏气温骤变诱发高血压大鼠脑卒中发病机制的实验研究,探讨冬夏气温突变诱发脑卒中的发生机制,并观察该现象中发挥主导作用的指标,从而为脑卒中的季节性预防用药提供科学指导,同时也为中医“五脏应时发病”学说的实证研究提供一种途径。
2方法
2.1理论探讨
本研究采用文献资料法和逻辑分析法,探讨季节气候变化对五脏生理病理的影响及“脉络-血管系统病”季节性发病的理论依据,进一步充实“五脏应时发病”的理论内涵。
2.2实验研究
2.2.1模型建立及指标测定
本研究采用改良的黄如训文献报道的方法复制易卒中型肾血管性高血压(RHRSP)大鼠模型,分别放置于人工模拟的夏季气温骤升环境中诱发脑梗塞和冬季气温骤降环境中诱发脑出血。采用血液流变学、放射免疫、酶联免疫、硝酸还原酶法等实验手段主要观察:①夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中血液流变学的动态变化;②夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中凝血-纤溶系统(F1+2、D-dimer)的动态变化;③夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中血管活性因子(ET-1、NO、AngⅡ、AVP)的动态变化;④夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中植物神经因子(E、NE、DA)的动态变化;⑤夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中神经内分泌物质(ACTH、CORT、TSH、T_3、T_4)的动态变化等5个方面的内容。
2.2.2实验结果统计学分析方法
所有数据均用均数±标准差表示,运用SPSS11.5统计软件分析。两两组间比较采用单因素方差分析(One-Way Anova)检验,以P<0.05为差异有显著性。
3结果
3.1理论研究结果
(1)季节气候变化对五脏生理病理具有重要的影响,当五脏精气虚衰不能抵御外界气候变化时,就有可能发生疾病,出现疾病季节性发作。
(2)除风邪外,暑、湿、燥、寒四种外来邪气均可以直接作用于相应的脏腑而发生特异性疾病,并且疾病特征很明显,具有当令节气特点。
(3)疾病的发生与转归有一定的规律可循,基本符合五行生克乘侮规律,但是因疾病存在寒热虚实不同、受到其他脏腑适应性调节和自然环境变幻莫测等多因素的影响,要多方面考虑,不可单一而论。
(4)“脉络—血管系统病”核心病位在心,而其发病规律表现为冬、夏多发,尤以冬季多见,这与五脏气血随季节变化密切相关。
3.2实验研究结果
3.2.1夏季气温骤升易诱发肾性高血压大鼠脑梗塞
①升温时,模型组血液流变学指标(血浆黏度、红细胞压积、红细胞聚集指数、刚性指数、电泳指数)均升高,当升温结束时,上述指标继续升高,其中,模型组的全血黏度、红细胞压积和电泳指数变化最为明显,有显著的统计学意义(P<0.05或P<0.01);②升温时,模型组凝血-纤溶指标(F1+2、D-dimer)水平同时增高;当升温结束时,模型组F1+2持续上升,而D-dimer下降,但高于升温前水平;③升温时,模型组血管活性因子中缩血管物质(ET-1、AngⅡ、AVP)水平均降低,而强舒张血管物质NO水平上升;当升温结束时,模型组ET-1、AVP回升,而AngⅡ水平持续下降、NO水平持续上升,且这4个指标中,模型组升温后NO水平明显高于升温前(P<0.05)和同时间点生理组(P<0.01),④升温时,模型组植物神经因子儿茶酚胺(E、NE、DA)水平上升;当升温结束时,模型组NE、DA水平下降,接近升温前水平,而E仍然处于较高水平,高于升温前(P<0.05)、同时间点生理组和假手术组(P<0.01);⑤升温时,模型组神经内分泌物质中ACTH水平下降,CORT、TSH、T_4水平升高,T_3没有明显变化;当升温结束时,模型组ACTH水平继续下降,低于升温前、同时间点生理组和假手术组(P<0.01),CORT指数仍然维持在一个较高水平,高于升温前和同时间点假手术组(P<0.05),TSH持续上升,T_4明显降低,后者低于升温前、升温中和同时间点的生理组和假手术组(P<0.01)。
3.2.2冬季气温骤降易诱发肾性高血压大鼠脑出血
①降温时,模型组血液流变学指标(全血黏度、血浆黏度、红细胞压积、红细胞聚集指数、刚性指数、电泳指数)均下降;降温结束时,前5项指标持续下降,红细胞电泳指数回升。其中,模型组的低切全血黏度、血浆黏度、红细胞聚集指数3项指标变化最显著,有统计学意义(P<0.05);②降温时,模型组凝血-纤溶指标(F1+2、D-dimer)水平同时下降,低于降温前(P<0.05);降温结束时,F1+2与D-dimer水平回升;③降温时,模型组血管活性因子中缩血管物质(ET-1、AngⅡ、AVP)水平均上升,而强舒张血管物质NO水平下降;当降温结束时,模型组大鼠ET-1、AngⅡ、AVP指数回落,NO水平升高。其中,模型组的AVP变化更为显著,降温中明显高于降温前(P<0.01)和同时间点生理组(P<0.05),降温后明显高于降温前和同时间点假手术组(P<0.01);④降温时,模型组植物神经因子(E、NE)水平上升,高于同时间点生理组和假手术组(P<0.01),DA变化不明显;降温结束时,模型组NE水平下降,E水平继续升高,高于降温前(P<0.01)、降温中(P<0.01)和同时间点假手术组(P<0.01);⑤降温时,模型组神经内分泌物质(ACTH、CORT、TSH、T_3、T_4)水平均升高;降温结束时,模型组ACTH、CORT水平持续上升,并且都与降温前、降温中、同时间点生理组和假手术组相比有非常显著的统计学意义(P<0.05或P<0.01),TSH也继续升高,高于降温前(P<0.01)和同时间点生理组(P<0.05)。
4结论4.1冬夏季节气温骤变诱发。肾性高血压大鼠脑卒中的发病机制
(1)长期高血压上调机体的内稳态水平、紊乱机体自我调节功能、减弱机体自我恢复能力。
(2)夏季气温骤升诱发高血压机体脑梗塞的发病机制:应激系统被外界高温刺激启动,神经递质E释放,影响血管内皮细胞的分泌,NO的分泌量急遽上升,血管发生明显扩张,血压降低会影响血流速度,血液黏度可增高;同时外界高温,机体通过出汗调节体温,血容量减少,血流减慢,血液黏度升高,进而使血液流动更慢,容易形成血栓,导致发生脑梗塞。
(3)冬季气温骤降诱发高血压机体脑出血的发病机制:相比夏季高温,机体应激系统对冬季寒冷气候更敏感,E、ACTH、CORT和TSH大量释放,上述神经递质作用于血管,影响血管内皮细胞的分泌,AVP的分泌量迅速增加,其与受体V1的结合激活蛋白激酶C而加重血管收缩,血管内壁压力增大,血压升高;同时,寒冷刺激使机体血液黏度降低,凝血因子减少,机体又处于易出血状态,当血压上升超过血管壁能承受的压力时,血管就可能破裂出血。
4.2作为“脉络-血管系统病”之一的脑卒中病具有明显的季节性发病特点,通过实验,发现外界环境导致血管状态、血液成份和血细胞功能发生改变,提示“五脏应时发病”具有一定科学依据和物质基础。
Stroke,a frequent acute disease of cerebral vessels,has the characteristic of high attack rate, high fatality,high disability rate,complex complication and low cure rate.In our country,stoke threatens the health and life of people and influences the quality of individual and family life,with the incidence and fatality of 1.5‰and 1.2‰respectively.Stroke is a disease of meridian and vascular system,its core location of disease is the heart.Clinical data indicates that attack of stroke have seasonal characteristics,it usually attacks in winter and secondly in summer.It coincides with the theory of the attack of disease of five viscera proper to the season.
1 Objective
According to the experimental study on changes of blood composition of stroke rat with hypertension induced by cataclysm of temperature in winter and summer and theoretical study of seasonal onset rule of disease of meridian and vascular system,to provide scientific instruction to seasonal preventive medication for stroke,to reveal the important role of changes of weather in attack of disease of meridian and vascular system and to provide an new way to modern study on theory of the attack of disease of five viscera proper to the season.
2 Method
2.1 Theoretical study
On basis of literature data and logic analytic method,the study is to approach the effect of seasonal and climatic change on physiology and pathology of five viscera,and enrich the theoretical connotation of the attack of disease of five viscera proper to the season.
2.2 Experimental study
2.2.1 Establishing model and detecting indexes
RHRSP model was established according to the modified method on basis of HUANG Ru-xun's, the model rats were placed in the artificial environment with sharp increase and..decrease of ambient temperature to induce cerebral infarction and cerebral hemorrhage respectively.The hemorrheology,radioimmunity,ELISA and NR were used to observe the dynamic changes of stroke RHRSP rat induced by sharp increase and decrease of temperature in summer and winter respectively from following aspects:①the hemorrheology②the Fl+2 and D-dimer;③the ET-1,NO,AngⅡand AVP;④the E,NE and DA;⑤the ACTH,CORT,TSH,T3 and T4.
2.2.2 Statistics
Data are presented as group mean values_S.E.M.The data analyzed with one-way ANOVA. The SPSS statistical package(version 11.5) was used in the analyses.The significance was set at pb0.05.
3 Results
3.1 Theoretical results
(1) Seasonal climatic changes had important influence on physiology and pathology of five viscera.The disease attacked in condition of deficiency of essence and qi of five viscera,with characteristic of attacked and aggravated seasonally.
(2) Except wind evil,the other four kinds of evil,such as summer-heat,damp,dryness and cold,can act on corresponding zang and fu to induce special disease with obvious genius morbi and seasonal feature.
(3) The onset and transmission had certain rule,and in accordance with inter-generation and inter-restriction among five elements in some extent.But other factors should be considered during the progress of disease,such as the cold,heat,excessive and deficient nature of disease,changes of physical environment,inter-regulation among zang and fu.
(4) Heart was the core location of disease of meridian and vascular system;which usually attacked in winter and summer,especially in winter,and it correlated with the change of qi and blood of five viscera following the change of seasons.
3.2 Experimental results
3.2.1 Cerebral infarction was induced by sharp increase of temperature in summer
①during and after the course of temperature increase,the viscosity of blood plasma,HCT, index of erythrocyte aggregation,ERI and ionophoresis in model group increased,especially the viscosity of WB,VPC and index of ionophoresis(P＜0.05;P0.01);②during the course of temperature increase,the level of Fl+2 and D-dimer in model group increased,after the course of temperature increase,the level of Fl+2 increased continually and the level of D-dimer decreased, but was still higher than that before the increase of temperature;③during the course of temperature increase,the level of ET-1,AngⅡand AVP decreased,but the NO increased;after the course of temperature increase,the level of ET-1 and AVP rebounded,but the level of AngⅡreduced and the NO increased persistently.The level of NO in model group after the increase of temperature was higher than that before and higher than that in normal group at the same time point.④in the course of increase of temperature,the level of E,NE and DA increased;after the increase of temperature,the levels of NE and DA reduced and closed to those before the course of increase of temperature,but the level of E was still higher than that before increase of temperature (P＜0.05) and than that in normal group and sham-operation group respectively(P＜0.01);⑤during the course of temperature increase,the level of ACTH descended,but the levels of CORT, TSH,T_4 increased,the level of T_3 had no change;after the course of temperature increase,the level of ACTH descended persistently and was lower than that in normal and sham-operation groups respectively at the same time point(P＜0.01),the level of CORT was higher than that in sham-operation group(P＜0.05),the level of TSH increased continually,the level of T_4 decreased obviously and was lower than that in normal group and sham-operation before and during the course of temperature increase and at the same time point.
3.2.2 Cerebral hemorrhage was induced by sharp decrease of temperature
①during the course of temperature decrease,the viscosity of blood plasma and WB,HCT, index of erythrocyte aggregation,ERIand ionophoresis in model group decreased,especially the viscosity of WB and blood plasma and index of erythrocyte aggregation(P＜0.05);and after the course of temperature decrease,the index of erythrocyte ionophoresis rebounded;②during the course of temperature decrease,the levels of F1+2 and D-dimer in model group decreased(P＜0.05), after the course of temperature decrease,the levels of F1+2 and D-dimer rebounded;③during the course of temperature decrease,the level of ET-1,AngⅡincreased and the level of AVP in model group was higher than that before temperature decrease(P＜0.01);and higher than that in normal group at the same time point(P＜0.05),but the NO decreased;after the course of temperature decrease,the level of ET-1,AngⅡand AVP decreased,but the level of NO increased. The level of AVP in model group after the course of temperature decrease was higher than that before the course of temperature decrease and that in sham-operation group at the same time point (P＜0.01);④in the course of decrease of temperature,the levels of E,NE in model group increased and were higher than those in normal group and sham-operation group respectively at the same time piont(P＜0.01);the level of DA had no significant change;after the decrease of temperature,the levels of NE reduced,but the level of E ascended continually and was higher than that before and during the course of temperature decrease and in sham-operation group(P＜0.01);⑤during the course of temperature decrease,the level of ACTH,CORT,TSH,T_4 and T_3 in model group increased;compared with before and during the course of temperature decrease,the level of ACTH and CORT after the course of temperature decrease ascended persistently(P＜0.05) and was higher than that in normal and sham-operation groups respectively at the same time point (P＜0.01);Compared with before the course of temperature decrease,level of TSH increased continually after the temperature decrease and was higher than that in normal group(P＜0.05 )
4 Conclusion
4.1 Possible mechanism of stroke attack in RHRSP rats induced by sharp change of temperature in winter and summer
4.1.1 Hypertension lasted chronically can regulate up the level of entatic state,and result in disorder of self-regulation function and reduction of the self-recovery capability of the organism.
4.1.2 Possible mechanism of cerebral infarction in RHRSP rats induced by sharp increase of temperature in summer was following circuit:stress was induced by high temperature;release of neurotransmitter acted on blood vessel and influenced the release of VEC;release of NO with a sudden increase;the blood vessel expanded obviously;blood pressure decreased and influenced the blood flow rate,and then the viscosity of blood increased;At the same time,the high temperature outside caused the organism to regulate self-temperature by sweating,the blood volume reduced,the blood flow step down,the blood viscocity ascended and then influenced the blood flow,the thrombus formed and the cerebral infarction attacked.
4.1.3 Possible mechanism of cerebral hemorrhage in RHRSP rats induced by sharp decrease of temperature in winter was following circuit:the organism was sensitive to cold weather,the release of E,ACTH,CORT and TSH increased,those neurotransmitter acted on blood vessel and influenced the release of VEC;release of AVP with a sudden increase and bind with Vl,then PKC was activated to increase the vasoconstriction,the pressure of inner wall of blood vessel ascended and blood pressure increased;On the other hand,stimulation of cold weather decreased the blood viscosity,blood coagulation factor decreased,then cerebral hemorrhage attacked when the blood pressure exceeded the tension that vessel wall can bear.
4.2 Stroke,a kind of disease of meridian and blood vascular system,attacked seasonally,the experiment results revealed that the environmental changes outside can influence the blood composition and provided scientific and material bases to theory of the attack of disease of five viscera proper to the season.
1目的
本研究以“脑卒中的季节性发病”作为中医“五脏应时发病”研究的突破口,通过对“脉络-血管系统病季节性发病规律”的理论和冬夏气温骤变诱发高血压大鼠脑卒中发病机制的实验研究,探讨冬夏气温突变诱发脑卒中的发生机制,并观察该现象中发挥主导作用的指标,从而为脑卒中的季节性预防用药提供科学指导,同时也为中医“五脏应时发病”学说的实证研究提供一种途径。
2方法
2.1理论探讨
本研究采用文献资料法和逻辑分析法,探讨季节气候变化对五脏生理病理的影响及“脉络-血管系统病”季节性发病的理论依据,进一步充实“五脏应时发病”的理论内涵。
2.2实验研究
2.2.1模型建立及指标测定
本研究采用改良的黄如训文献报道的方法复制易卒中型肾血管性高血压(RHRSP)大鼠模型,分别放置于人工模拟的夏季气温骤升环境中诱发脑梗塞和冬季气温骤降环境中诱发脑出血。采用血液流变学、放射免疫、酶联免疫、硝酸还原酶法等实验手段主要观察:①夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中血液流变学的动态变化;②夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中凝血-纤溶系统(F1+2、D-dimer)的动态变化;③夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中血管活性因子(ET-1、NO、AngⅡ、AVP)的动态变化;④夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中植物神经因子(E、NE、DA)的动态变化;⑤夏季气温骤升、冬季气温骤降诱发RHRSP大鼠脑卒中神经内分泌物质(ACTH、CORT、TSH、T_3、T_4)的动态变化等5个方面的内容。
2.2.2实验结果统计学分析方法
所有数据均用均数±标准差表示,运用SPSS11.5统计软件分析。两两组间比较采用单因素方差分析(One-Way Anova)检验,以P<0.05为差异有显著性。
3结果
3.1理论研究结果
(1)季节气候变化对五脏生理病理具有重要的影响,当五脏精气虚衰不能抵御外界气候变化时,就有可能发生疾病,出现疾病季节性发作。
(2)除风邪外,暑、湿、燥、寒四种外来邪气均可以直接作用于相应的脏腑而发生特异性疾病,并且疾病特征很明显,具有当令节气特点。
(3)疾病的发生与转归有一定的规律可循,基本符合五行生克乘侮规律,但是因疾病存在寒热虚实不同、受到其他脏腑适应性调节和自然环境变幻莫测等多因素的影响,要多方面考虑,不可单一而论。
(4)“脉络—血管系统病”核心病位在心,而其发病规律表现为冬、夏多发,尤以冬季多见,这与五脏气血随季节变化密切相关。
3.2实验研究结果
3.2.1夏季气温骤升易诱发肾性高血压大鼠脑梗塞
①升温时,模型组血液流变学指标(血浆黏度、红细胞压积、红细胞聚集指数、刚性指数、电泳指数)均升高,当升温结束时,上述指标继续升高,其中,模型组的全血黏度、红细胞压积和电泳指数变化最为明显,有显著的统计学意义(P<0.05或P<0.01);②升温时,模型组凝血-纤溶指标(F1+2、D-dimer)水平同时增高;当升温结束时,模型组F1+2持续上升,而D-dimer下降,但高于升温前水平;③升温时,模型组血管活性因子中缩血管物质(ET-1、AngⅡ、AVP)水平均降低,而强舒张血管物质NO水平上升;当升温结束时,模型组ET-1、AVP回升,而AngⅡ水平持续下降、NO水平持续上升,且这4个指标中,模型组升温后NO水平明显高于升温前(P<0.05)和同时间点生理组(P<0.01),④升温时,模型组植物神经因子儿茶酚胺(E、NE、DA)水平上升;当升温结束时,模型组NE、DA水平下降,接近升温前水平,而E仍然处于较高水平,高于升温前(P<0.05)、同时间点生理组和假手术组(P<0.01);⑤升温时,模型组神经内分泌物质中ACTH水平下降,CORT、TSH、T_4水平升高,T_3没有明显变化;当升温结束时,模型组ACTH水平继续下降,低于升温前、同时间点生理组和假手术组(P<0.01),CORT指数仍然维持在一个较高水平,高于升温前和同时间点假手术组(P<0.05),TSH持续上升,T_4明显降低,后者低于升温前、升温中和同时间点的生理组和假手术组(P<0.01)。
3.2.2冬季气温骤降易诱发肾性高血压大鼠脑出血
①降温时,模型组血液流变学指标(全血黏度、血浆黏度、红细胞压积、红细胞聚集指数、刚性指数、电泳指数)均下降;降温结束时,前5项指标持续下降,红细胞电泳指数回升。其中,模型组的低切全血黏度、血浆黏度、红细胞聚集指数3项指标变化最显著,有统计学意义(P<0.05);②降温时,模型组凝血-纤溶指标(F1+2、D-dimer)水平同时下降,低于降温前(P<0.05);降温结束时,F1+2与D-dimer水平回升;③降温时,模型组血管活性因子中缩血管物质(ET-1、AngⅡ、AVP)水平均上升,而强舒张血管物质NO水平下降;当降温结束时,模型组大鼠ET-1、AngⅡ、AVP指数回落,NO水平升高。其中,模型组的AVP变化更为显著,降温中明显高于降温前(P<0.01)和同时间点生理组(P<0.05),降温后明显高于降温前和同时间点假手术组(P<0.01);④降温时,模型组植物神经因子(E、NE)水平上升,高于同时间点生理组和假手术组(P<0.01),DA变化不明显;降温结束时,模型组NE水平下降,E水平继续升高,高于降温前(P<0.01)、降温中(P<0.01)和同时间点假手术组(P<0.01);⑤降温时,模型组神经内分泌物质(ACTH、CORT、TSH、T_3、T_4)水平均升高;降温结束时,模型组ACTH、CORT水平持续上升,并且都与降温前、降温中、同时间点生理组和假手术组相比有非常显著的统计学意义(P<0.05或P<0.01),TSH也继续升高,高于降温前(P<0.01)和同时间点生理组(P<0.05)。
4结论4.1冬夏季节气温骤变诱发。肾性高血压大鼠脑卒中的发病机制
(1)长期高血压上调机体的内稳态水平、紊乱机体自我调节功能、减弱机体自我恢复能力。
(2)夏季气温骤升诱发高血压机体脑梗塞的发病机制:应激系统被外界高温刺激启动,神经递质E释放,影响血管内皮细胞的分泌,NO的分泌量急遽上升,血管发生明显扩张,血压降低会影响血流速度,血液黏度可增高;同时外界高温,机体通过出汗调节体温,血容量减少,血流减慢,血液黏度升高,进而使血液流动更慢,容易形成血栓,导致发生脑梗塞。
(3)冬季气温骤降诱发高血压机体脑出血的发病机制:相比夏季高温,机体应激系统对冬季寒冷气候更敏感,E、ACTH、CORT和TSH大量释放,上述神经递质作用于血管,影响血管内皮细胞的分泌,AVP的分泌量迅速增加,其与受体V1的结合激活蛋白激酶C而加重血管收缩,血管内壁压力增大,血压升高;同时,寒冷刺激使机体血液黏度降低,凝血因子减少,机体又处于易出血状态,当血压上升超过血管壁能承受的压力时,血管就可能破裂出血。
4.2作为“脉络-血管系统病”之一的脑卒中病具有明显的季节性发病特点,通过实验,发现外界环境导致血管状态、血液成份和血细胞功能发生改变,提示“五脏应时发病”具有一定科学依据和物质基础。
Stroke,a frequent acute disease of cerebral vessels,has the characteristic of high attack rate, high fatality,high disability rate,complex complication and low cure rate.In our country,stoke threatens the health and life of people and influences the quality of individual and family life,with the incidence and fatality of 1.5‰and 1.2‰respectively.Stroke is a disease of meridian and vascular system,its core location of disease is the heart.Clinical data indicates that attack of stroke have seasonal characteristics,it usually attacks in winter and secondly in summer.It coincides with the theory of the attack of disease of five viscera proper to the season.
1 Objective
According to the experimental study on changes of blood composition of stroke rat with hypertension induced by cataclysm of temperature in winter and summer and theoretical study of seasonal onset rule of disease of meridian and vascular system,to provide scientific instruction to seasonal preventive medication for stroke,to reveal the important role of changes of weather in attack of disease of meridian and vascular system and to provide an new way to modern study on theory of the attack of disease of five viscera proper to the season.
2 Method
2.1 Theoretical study
On basis of literature data and logic analytic method,the study is to approach the effect of seasonal and climatic change on physiology and pathology of five viscera,and enrich the theoretical connotation of the attack of disease of five viscera proper to the season.
2.2 Experimental study
2.2.1 Establishing model and detecting indexes
RHRSP model was established according to the modified method on basis of HUANG Ru-xun's, the model rats were placed in the artificial environment with sharp increase and..decrease of ambient temperature to induce cerebral infarction and cerebral hemorrhage respectively.The hemorrheology,radioimmunity,ELISA and NR were used to observe the dynamic changes of stroke RHRSP rat induced by sharp increase and decrease of temperature in summer and winter respectively from following aspects:①the hemorrheology②the Fl+2 and D-dimer;③the ET-1,NO,AngⅡand AVP;④the E,NE and DA;⑤the ACTH,CORT,TSH,T3 and T4.
2.2.2 Statistics
Data are presented as group mean values_S.E.M.The data analyzed with one-way ANOVA. The SPSS statistical package(version 11.5) was used in the analyses.The significance was set at pb0.05.
3 Results
3.1 Theoretical results
(1) Seasonal climatic changes had important influence on physiology and pathology of five viscera.The disease attacked in condition of deficiency of essence and qi of five viscera,with characteristic of attacked and aggravated seasonally.
(2) Except wind evil,the other four kinds of evil,such as summer-heat,damp,dryness and cold,can act on corresponding zang and fu to induce special disease with obvious genius morbi and seasonal feature.
(3) The onset and transmission had certain rule,and in accordance with inter-generation and inter-restriction among five elements in some extent.But other factors should be considered during the progress of disease,such as the cold,heat,excessive and deficient nature of disease,changes of physical environment,inter-regulation among zang and fu.
(4) Heart was the core location of disease of meridian and vascular system;which usually attacked in winter and summer,especially in winter,and it correlated with the change of qi and blood of five viscera following the change of seasons.
3.2 Experimental results
3.2.1 Cerebral infarction was induced by sharp increase of temperature in summer
①during and after the course of temperature increase,the viscosity of blood plasma,HCT, index of erythrocyte aggregation,ERI and ionophoresis in model group increased,especially the viscosity of WB,VPC and index of ionophoresis(P＜0.05;P0.01);②during the course of temperature increase,the level of Fl+2 and D-dimer in model group increased,after the course of temperature increase,the level of Fl+2 increased continually and the level of D-dimer decreased, but was still higher than that before the increase of temperature;③during the course of temperature increase,the level of ET-1,AngⅡand AVP decreased,but the NO increased;after the course of temperature increase,the level of ET-1 and AVP rebounded,but the level of AngⅡreduced and the NO increased persistently.The level of NO in model group after the increase of temperature was higher than that before and higher than that in normal group at the same time point.④in the course of increase of temperature,the level of E,NE and DA increased;after the increase of temperature,the levels of NE and DA reduced and closed to those before the course of increase of temperature,but the level of E was still higher than that before increase of temperature (P＜0.05) and than that in normal group and sham-operation group respectively(P＜0.01);⑤during the course of temperature increase,the level of ACTH descended,but the levels of CORT, TSH,T_4 increased,the level of T_3 had no change;after the course of temperature increase,the level of ACTH descended persistently and was lower than that in normal and sham-operation groups respectively at the same time point(P＜0.01),the level of CORT was higher than that in sham-operation group(P＜0.05),the level of TSH increased continually,the level of T_4 decreased obviously and was lower than that in normal group and sham-operation before and during the course of temperature increase and at the same time point.
3.2.2 Cerebral hemorrhage was induced by sharp decrease of temperature
①during the course of temperature decrease,the viscosity of blood plasma and WB,HCT, index of erythrocyte aggregation,ERIand ionophoresis in model group decreased,especially the viscosity of WB and blood plasma and index of erythrocyte aggregation(P＜0.05);and after the course of temperature decrease,the index of erythrocyte ionophoresis rebounded;②during the course of temperature decrease,the levels of F1+2 and D-dimer in model group decreased(P＜0.05), after the course of temperature decrease,the levels of F1+2 and D-dimer rebounded;③during the course of temperature decrease,the level of ET-1,AngⅡincreased and the level of AVP in model group was higher than that before temperature decrease(P＜0.01);and higher than that in normal group at the same time point(P＜0.05),but the NO decreased;after the course of temperature decrease,the level of ET-1,AngⅡand AVP decreased,but the level of NO increased. The level of AVP in model group after the course of temperature decrease was higher than that before the course of temperature decrease and that in sham-operation group at the same time point (P＜0.01);④in the course of decrease of temperature,the levels of E,NE in model group increased and were higher than those in normal group and sham-operation group respectively at the same time piont(P＜0.01);the level of DA had no significant change;after the decrease of temperature,the levels of NE reduced,but the level of E ascended continually and was higher than that before and during the course of temperature decrease and in sham-operation group(P＜0.01);⑤during the course of temperature decrease,the level of ACTH,CORT,TSH,T_4 and T_3 in model group increased;compared with before and during the course of temperature decrease,the level of ACTH and CORT after the course of temperature decrease ascended persistently(P＜0.05) and was higher than that in normal and sham-operation groups respectively at the same time point (P＜0.01);Compared with before the course of temperature decrease,level of TSH increased continually after the temperature decrease and was higher than that in normal group(P＜0.05 )
4 Conclusion
4.1 Possible mechanism of stroke attack in RHRSP rats induced by sharp change of temperature in winter and summer
4.1.1 Hypertension lasted chronically can regulate up the level of entatic state,and result in disorder of self-regulation function and reduction of the self-recovery capability of the organism.
4.1.2 Possible mechanism of cerebral infarction in RHRSP rats induced by sharp increase of temperature in summer was following circuit:stress was induced by high temperature;release of neurotransmitter acted on blood vessel and influenced the release of VEC;release of NO with a sudden increase;the blood vessel expanded obviously;blood pressure decreased and influenced the blood flow rate,and then the viscosity of blood increased;At the same time,the high temperature outside caused the organism to regulate self-temperature by sweating,the blood volume reduced,the blood flow step down,the blood viscocity ascended and then influenced the blood flow,the thrombus formed and the cerebral infarction attacked.
4.1.3 Possible mechanism of cerebral hemorrhage in RHRSP rats induced by sharp decrease of temperature in winter was following circuit:the organism was sensitive to cold weather,the release of E,ACTH,CORT and TSH increased,those neurotransmitter acted on blood vessel and influenced the release of VEC;release of AVP with a sudden increase and bind with Vl,then PKC was activated to increase the vasoconstriction,the pressure of inner wall of blood vessel ascended and blood pressure increased;On the other hand,stimulation of cold weather decreased the blood viscosity,blood coagulation factor decreased,then cerebral hemorrhage attacked when the blood pressure exceeded the tension that vessel wall can bear.
4.2 Stroke,a kind of disease of meridian and blood vascular system,attacked seasonally,the experiment results revealed that the environmental changes outside can influence the blood composition and provided scientific and material bases to theory of the attack of disease of five viscera proper to the season.
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