阿胶对内毒素性休克狗血液动力学、流变学及微循环的影响

本文报告了阿胶对狗内毒素性休克的治疗作用。实验表明阿胶对休克时血液粘滞性的增加有明显的抑制作用,使微循环障碍改善,动脉血压饺快恢复及稳定。     

Correlation of Plasma Histamine and Catecholamine Levels with Hemodynamic and Microcirculatory Changes in Canine Endotoxin Shock

The plasma histamine concentration was elevated from the controllevel of 1.16±0.28ng/ml to 11.42±5.2ng/ml 2-5 min after intravenousinjection of Serratia marcescens endotoxin to dogs(2mg/kg body wei-ght).and then declined gradually.The level was still slightly hi-gher than the control 4 h later.The plasma norepinephrine(NE)andepinephrin(E)concentrations were increased from the control levelsof 1.13±0.28ng/ml and 1.05±0.32ng/ml to 7.33±1.86ng/ml and 10.04±3.94ng/ml respectively 2-5 min after injection,and 6 h later theywere still significantly elevated.Arterial blood pressure was reducedto 24.16% of the control level 2-5 min after injection and to 69.2%6 h later,and showed a temporal change.Both cardiac output andcardiac index were decreased,but the total peripheral resistance ofsystemic circulation was increased during endotoxin shock.The si-gnificant dilatation of arterioles,venules and capillaries of bulbarconjunctiva microcirculation occurred 1-2 min after endotoxin injec-tion,and the blood flow slowed down at the same time.Five minto six h after endotoxin injection arterioles constricted markedly,but capillaries and venules were still congested and distended.Theinterrelationship of various changes observed in this study in thedevelopment of endotoxin shock was discussed.     

内毒索性休克时血浆组胺、儿茶酚胺的含量与血液动力学和微循环变化的关系

给狗注入灵杆菌内毒素(2mg/kg体重)后2～5 min,血浆组胺含量由对照值的1.16±0.28ng/ml,增高至11.42±5.2ng/ml,以后逐渐下降,至4h仍略高于对照值;血浆去甲肾上腺素(NA)和肾上腺素(Ad)含量,分别由对照值的1.13±0.28ng/ml、1.05±0.32ng/ml,增高至7.33±1.86ng/ml、10.04±3.94ng/ml,至6h仍显著高于对照值。动脉血压在2～5min内降至对照值的24.16％,至6h仍为对照值的69.2％,血压呈时相性变化;在休克过程中心输出量、心脏指数均降低,体循环总阻力增高;球结膜微循环在注入内毒素后1～2min即可见微动脉、微静脉和毛细血管明显扩张、血流缓慢,5min以后的6h内,微动脉明显收缩,而毛细血管和微静脉仍扩张、淤血。根据实验结果,讨论了所得各种变化在内毒素性休克发生发展过程中的关系。注入内毒素后很快地促使组胺大量释放,引起微循环扩张、淤血,外周阻力下降,回心血量减少,导致动脉血压急剧降低,反射性地NA和Ad释放增多,使微动脉、小动脉收缩,外周阻力升高,血压有所回升。但由于微静脉和毛细血管持续性扩张、淤血,因此血压和心输出量在实验过程中始终是降低的,甚至导致动物死亡。     

电解毁损与红藻氨酸微量注入大鼠下丘脑外侧视前区诱发急性肺水肿的比较—对神经源性肺水肿发病机理的探讨

用电解毁损和红藻氨酸微量注入大鼠下丘脑外侧视前区均能引起急性肺水肿,二组大鼠的肺病变程度很相似。红藻氨酸组的动脉血压及内脏大神经放电频率增值大,变化迅速;电解毁损组的血压及放电频率增值相对较小,变化缓慢。根据红藻氨酸的神经药理作用特点,实验结果提示了下丘脑外侧视前区的损伤     

电解毁损与红藻氨酸微量注入大鼠下丘脑外侧视前区诱发急性肺水肿的比较——对神经源性肺水肿发病机理的探讨

用电解毁损和红藻氨酸微量注入大鼠下丘脑外侧视前区均能引起急性肺水肿,二组大鼠的肺病变程度很相似。红藻氨酸组的动脉血压及内脏大神经放电频率增值大,变化迅速;电解毁损组的血压及放电频率增值相对较小,变化缓慢。根据红藻氨酸的神经药理作用特点,实验结果提示了下丘脑外侧视前区的损伤与肺水肿发生有一定内在联系。并探讨了血液动力学的变化在神经源性肺水肿发病机理中的地位。