摘要
探讨失血性休克再灌注复苏后血浆中降钙素基因相关肽(CGRP)改变的意义,早期使用磷脂酶A2(PLA2)阻断剂、抗氧化剂对CGRP的影响及其与PLA2激活、氧自由基产生的关系。家兔失血性休克维持60分钟后回输自体血液及平衡盐液,血浆中CGRP逐渐升高,复苏后6小时达顶点,同出血前比较有显著性差异(P<0.05);PLA2阻断剂氯喹及ME8101、抗氧化剂黄芪酮于失血后复苏前使用可明显抑制复苏后血浆中CGRP的增高;同时,复苏后家兔平均动脉压(MAP)和血pH值逐渐下降,与CGRP变化没有明显相关(r=0.0040和r=0.0435);假手术造成血浆CGRP水平复苏后逐渐上升,同术前比较差异同样显著(P<0.05),但并不伴随MAP和pH值的下降,氯喹、ME8101及黄芪酮纠正酸中毒、维持血压稳定的作用与抑制CGRP并无明显相关。结果提示:家兔失血性休克后再灌注复苏过程中血浆CGRP水平的上升可能不是pH值和MAP下降的重要因素;
Hemorrhagic shock in rabbits (animal model)was maintained for 60 min followed by infusion of autoblood and saline buffer solution.The plasma calcitonin gene related peptide (CGRP) gradually increased and reached to the peak point at 6hr after resuscitation and was signifficantly higher than that before bloodletting ( P <0 05).The increase of CGRP was obviously blocked by the use of phaspholipase A 2(PLA 2) blocker (chloroquine),ME8101 and antioxidant (TFA) before resuscitation after hemorrhagic shock.At the same time.the mean arterial pressure (MAP) and pH values after resuscitation were decreased gradually but no obvious positive correlation was noted between the changes of MAP,pH and CGRP( r =0 0040 and 0 0435 ).CGRP also was obviously elevated in sham operation group compared with that of before operation( P <0 05),but there was not any decrease in MAP and pH values and the effect of antiacidosis,maitaining MAP by chloroquine,ME8101 and TFA was not found to have a significant correlation with the effect of inhibiting CGRP by them.The above result indicated that elevated plasma CGRP level after hemorrhagic shock/reperfusion resuscitation might not be the main factor of the decrease in MAP and pH.The decrease in plasma CGRP caused by PLA 2 blockers and antioxidant might not correlate with the effect of their antiacidosis and blood pressue maintenance.
出处
《中国危重病急救医学》
CAS
CSCD
1996年第10期582-584,共3页
Chinese Critical Care Medicine
关键词
失血性休克
再灌注损伤
CGRP
氧自由基
酸中毒
hemorrhagic shock/reperfusion injury
calcitonin gene related peptide
phospholipase A 2
oxygenfree radicals
acidosis