失血性休克再灌注复苏后血浆降钙素基因相关肽的变化

Alteration of calcitonin gene related peptide after resusciatation of hemorrhagic shock and reperfusion/

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.