急性高温暴露对清醒非束缚大鼠血液动力学的影响
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摘要
目的观察高温环境对清醒非束缚大鼠血液动力学的影响并探讨其机制。方法选择清洁级SD雄性大鼠30只,随机分为正常对照组和模型组,每组15只,分别暴露于24℃室内和42℃热舱中50 min,在清醒非束缚状态下采用植入式生理信号遥测系统监测体核温度(Tc)、平均动脉压(MAP)、动脉收缩压(SAP)、动脉舒张压(DAP)、心率(HR),以及各组大鼠血清谷草转氨酶(AST)、谷丙转氨酶(ALT)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、尿素氮(BUN)、肌酐(CR)水平,并观察心组织病理改变。结果模型组大鼠入舱10~30 min时,Tc、MAP、SAP、DAP、HR均明显高于正常对照组,30 min达到最高值,差异有统计学意义(P<0.05)。模型组大鼠入舱35、40 min时各指标仍高于正常对照组,但45、50 min时除Tc继续升高外,MAP、SAP、DAP、HR均低于正常对照组,差异有统计学意义(P<0.05)。模型组大鼠血清AST、ALT、ALP、LDH、CK、BUN、CR水平明显高于正常对照组,差异有统计学意义(P<0.05)。结论高温环境引起大鼠血液动力学急剧改变,可能与高温环境导致循环系统功能障碍和多器官衰竭有关。
Objective To understand hemodynamic alteration of heat-exposed rats under conscious unrestrained condition.Methods A total of 30 male anesthetized SD rats of clean degree were randomly divided into control group(n=15) and model group(n=15). The model group rats were exposed to heat(42 ℃ for 50 min) in test module and control group rats were kept at room temperature(24 ℃). Experiment chamber with temperature-controlled water circulation adjusted by DKB-501 S high precision water bath was used, and the indoor temperature was kept at 22-24 ℃, and then the temperature in the chamber was kept at42.0 ℃. Implantable physiological signal telemetry system was used to monitor the core body temperature(Tc), mean arterial pressure(MAP), arterial systolic blood pressure(SAP), artery diastolic pressure(DAP), heart rate(HR). After the thermal damage, blood samples were collected immediately and then the levels of aspertate aminotransferase(AST), alanine aminotransferase(ALT), alkaline phosphatase(ALP), lactate dehydrogenase(LDH), creatine kinase(CK), blood urea nitrogen(BUN), creatinine(CR) in serum of rats were detected. Observation of heart tissue pathological changes was carried out also.Results Compared with control group, all the rats in model group revealed acute hemodynamics alteration.The levels of Tc,MAP, SAP, DAP, HR in heat injury model group increased after exposure to high temperature for 10-30 min(P<0.05). 30 min later, the body core temperature remained at a higher level, while other indicators reduced rapidly. The levels of AST, ALT,ALP, LDH, CK, BUN and CR in model group were higher than those in control group(P<0.05). Conclusion High temperature may cause a tremendous hemodynamic change in rats under conscious unrestrained condition and the change may be related to oxidative stress, dysfunction of the circulatory system and multiple organ failure.
Objective To understand hemodynamic alteration of heat-exposed rats under conscious unrestrained condition.Methods A total of 30 male anesthetized SD rats of clean degree were randomly divided into control group(n=15) and model group(n=15). The model group rats were exposed to heat(42 ℃ for 50 min) in test module and control group rats were kept at room temperature(24 ℃). Experiment chamber with temperature-controlled water circulation adjusted by DKB-501 S high precision water bath was used, and the indoor temperature was kept at 22-24 ℃, and then the temperature in the chamber was kept at42.0 ℃. Implantable physiological signal telemetry system was used to monitor the core body temperature(Tc), mean arterial pressure(MAP), arterial systolic blood pressure(SAP), artery diastolic pressure(DAP), heart rate(HR). After the thermal damage, blood samples were collected immediately and then the levels of aspertate aminotransferase(AST), alanine aminotransferase(ALT), alkaline phosphatase(ALP), lactate dehydrogenase(LDH), creatine kinase(CK), blood urea nitrogen(BUN), creatinine(CR) in serum of rats were detected. Observation of heart tissue pathological changes was carried out also.Results Compared with control group, all the rats in model group revealed acute hemodynamics alteration.The levels of Tc,MAP, SAP, DAP, HR in heat injury model group increased after exposure to high temperature for 10-30 min(P<0.05). 30 min later, the body core temperature remained at a higher level, while other indicators reduced rapidly. The levels of AST, ALT,ALP, LDH, CK, BUN and CR in model group were higher than those in control group(P<0.05). Conclusion High temperature may cause a tremendous hemodynamic change in rats under conscious unrestrained condition and the change may be related to oxidative stress, dysfunction of the circulatory system and multiple organ failure.
引文
[1]冯雷,李旭东.高温热浪对人类健康影响的研究进展[J].环境与健康杂志,2016,33(2):182-188.
[2]Bouchama A,Knochel JP.Heat stroke[J].N Engl J Med,2002,346:1978-1988.
[3]范辉,王小红,沈云志.P-selectin、IVAM-1和ICAM-1在大鼠重症急性胰腺炎并发急性心肌损害中的作用机制[J].世界华人消化杂志,2011,19(30):3122-3129.
[4]Lin MT,Chang CP.The neuropharmacological basis of heat intolerance and its treatment[J].J Ther Biol,2004,29:463-469.
[5]Hsu SF,Niu KC,Lin CL,et al.Brain cooling causes attenuation of cerebral oxidative stress,systemic inflammation,activated coagulation,and tissue ischemia/injury during heatstroke[J].Shock,2006,26:210-220.
[6]Chou YT,Lai ST,Lee CC,et al.Hypothermia attenuates circulatory shock and cerebral ischemia in experimental heatstroke[J].Shock,2003,19:388-393.
[7]Lee JJ,Lin MT,Wang NL,et al.Platonin,a cyanine photosensitizing dye,causes attenuation of circulatory shock,hypercoagulable state,and tissue ischemia during heat stroke[J].Shock,2005,24:577-582.
[8]Chen SH,Niu KC,Lin MT.Cerebrovascular dysfunction is an attractive target for therapy in heat stroke[J].Clin Exp Pharmacol Physiol,2006,33:663-672.
[9]Sharma HS,Alm P.Nitric oxide synthase inhibitors influence dynorphin A(1-17)immunoreactivity in the rat brain following hyperthermia[J].Amino Acids,2002,23:247-259.
[10]Dematte JE,O’Mara K,Buescher J,et al.Near-fatal heat stroke during the 1995 heat wave in Chicago[J].Ann Intern Med,1998,129:173-181.
[11]Hall DM,Buettner GR,Oberley LW,et al.Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia[J].Am J Physiol Heart Circ Physiol,2001,280:509-521.
[12]Leon LR,Du Bose DA,Mason CW.Heat stress induces a biphasic thermoregulatory response in mice[J].Am J Physiol Regul Integrat Comp Physiol,2005,288:197-204.
[13]Chatterjee S,Premachandran S,Sharma D,et al.Therapeutic treatment with L-arginine rescues mice from heat stroke-induced death:physiological and molecular mechanisms[J].Shock,2005,24:341-347.
[14]Leon LR,Blaha MD,Du Bose DA.Time course of cytokine,corticosterone,and tissue injury responses in mice during heat strain recovery[J].J Appl Physiol,2006,100:1400-1409.
[15]Bouchama A,Roberts G,Al Mohanna F,et al.Inflammatory,hemostatic,and clinical changes in a baboon experimental model for heatstroke[J].J Appl Physiol,2005,98:697-705.
[16]高俊涛,万朋,王春艳,等.芩丹颗粒对热损伤大鼠心功能的保护作用[J].环境与健康杂志,2016,33(1):73-75.
[17]耿瑶,朱玲勤,刘法东,等.高温高湿环境对自发性高血压大鼠胸主动脉细胞凋亡的影响[J].环境与健康杂志,2017,34(10):847-850.
[18]井然,钱捷,弓景波,等.热应激大鼠心脏损伤与血淋巴细胞热休克蛋白70的关系[J].环境与健康杂志,2012,29(10):881-883.
[19]Chen SH,Lin MT,Chang CP.Ischemic and oxidative damage to the hypothalamus may be responsible for heat stroke[J].Curr Neur,2013,11:129-140.
[20]Leon LR,Dineen S,Blaha MD,et al.Attenuated thermoregulatory,metabolic,and liver acute phase protein response to heat stroke in TNF receptor knockout mice[J].Am J Physiol Regul Integr Comp Physiol,2013,305:1421-1432.
[21]Shen KH,Lin CH,Chang HK,et al.Premarin can act via estrogen receptors to rescue mice from heatstroke-induced lethality[J].Shock,2008,30:668-674.
[22]Lin MT,Liu HH,Yang YL.Involvement of interleukin-1 receptor mechanisms in development of arterial hypotension in rat heatstroke[J].Am J Physiol,1997,273:2072-2077.
[23]Helwig BG,Leon LR.Tissue and circulating expression of IL-1family members following heat stroke[J].Physiol Genomics,2011,43:1096-1104.
[24]Lin XJ,Mei GP,Liu J,et al.The rapeutic effects of melatonin on heatstroke-induced multiple organ dysfunction syndrome in rats[J].2011,50:436-444.
[25]Rodriguez-Fernandez M,Grosman B,Yuraszeck TM,et al.Modeling the intra-and extracellular cytokine signaling pathway under heat stroke in the liver[J].PLo S One,2013,8:73393.
[2]Bouchama A,Knochel JP.Heat stroke[J].N Engl J Med,2002,346:1978-1988.
[3]范辉,王小红,沈云志.P-selectin、IVAM-1和ICAM-1在大鼠重症急性胰腺炎并发急性心肌损害中的作用机制[J].世界华人消化杂志,2011,19(30):3122-3129.
[4]Lin MT,Chang CP.The neuropharmacological basis of heat intolerance and its treatment[J].J Ther Biol,2004,29:463-469.
[5]Hsu SF,Niu KC,Lin CL,et al.Brain cooling causes attenuation of cerebral oxidative stress,systemic inflammation,activated coagulation,and tissue ischemia/injury during heatstroke[J].Shock,2006,26:210-220.
[6]Chou YT,Lai ST,Lee CC,et al.Hypothermia attenuates circulatory shock and cerebral ischemia in experimental heatstroke[J].Shock,2003,19:388-393.
[7]Lee JJ,Lin MT,Wang NL,et al.Platonin,a cyanine photosensitizing dye,causes attenuation of circulatory shock,hypercoagulable state,and tissue ischemia during heat stroke[J].Shock,2005,24:577-582.
[8]Chen SH,Niu KC,Lin MT.Cerebrovascular dysfunction is an attractive target for therapy in heat stroke[J].Clin Exp Pharmacol Physiol,2006,33:663-672.
[9]Sharma HS,Alm P.Nitric oxide synthase inhibitors influence dynorphin A(1-17)immunoreactivity in the rat brain following hyperthermia[J].Amino Acids,2002,23:247-259.
[10]Dematte JE,O’Mara K,Buescher J,et al.Near-fatal heat stroke during the 1995 heat wave in Chicago[J].Ann Intern Med,1998,129:173-181.
[11]Hall DM,Buettner GR,Oberley LW,et al.Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia[J].Am J Physiol Heart Circ Physiol,2001,280:509-521.
[12]Leon LR,Du Bose DA,Mason CW.Heat stress induces a biphasic thermoregulatory response in mice[J].Am J Physiol Regul Integrat Comp Physiol,2005,288:197-204.
[13]Chatterjee S,Premachandran S,Sharma D,et al.Therapeutic treatment with L-arginine rescues mice from heat stroke-induced death:physiological and molecular mechanisms[J].Shock,2005,24:341-347.
[14]Leon LR,Blaha MD,Du Bose DA.Time course of cytokine,corticosterone,and tissue injury responses in mice during heat strain recovery[J].J Appl Physiol,2006,100:1400-1409.
[15]Bouchama A,Roberts G,Al Mohanna F,et al.Inflammatory,hemostatic,and clinical changes in a baboon experimental model for heatstroke[J].J Appl Physiol,2005,98:697-705.
[16]高俊涛,万朋,王春艳,等.芩丹颗粒对热损伤大鼠心功能的保护作用[J].环境与健康杂志,2016,33(1):73-75.
[17]耿瑶,朱玲勤,刘法东,等.高温高湿环境对自发性高血压大鼠胸主动脉细胞凋亡的影响[J].环境与健康杂志,2017,34(10):847-850.
[18]井然,钱捷,弓景波,等.热应激大鼠心脏损伤与血淋巴细胞热休克蛋白70的关系[J].环境与健康杂志,2012,29(10):881-883.
[19]Chen SH,Lin MT,Chang CP.Ischemic and oxidative damage to the hypothalamus may be responsible for heat stroke[J].Curr Neur,2013,11:129-140.
[20]Leon LR,Dineen S,Blaha MD,et al.Attenuated thermoregulatory,metabolic,and liver acute phase protein response to heat stroke in TNF receptor knockout mice[J].Am J Physiol Regul Integr Comp Physiol,2013,305:1421-1432.
[21]Shen KH,Lin CH,Chang HK,et al.Premarin can act via estrogen receptors to rescue mice from heatstroke-induced lethality[J].Shock,2008,30:668-674.
[22]Lin MT,Liu HH,Yang YL.Involvement of interleukin-1 receptor mechanisms in development of arterial hypotension in rat heatstroke[J].Am J Physiol,1997,273:2072-2077.
[23]Helwig BG,Leon LR.Tissue and circulating expression of IL-1family members following heat stroke[J].Physiol Genomics,2011,43:1096-1104.
[24]Lin XJ,Mei GP,Liu J,et al.The rapeutic effects of melatonin on heatstroke-induced multiple organ dysfunction syndrome in rats[J].2011,50:436-444.
[25]Rodriguez-Fernandez M,Grosman B,Yuraszeck TM,et al.Modeling the intra-and extracellular cytokine signaling pathway under heat stroke in the liver[J].PLo S One,2013,8:73393.