内源性一氧化碳/一氧化氮在失血性休克中的作用

目的探讨内源性一氧化碳(CO)／一氧化氮(NO)在失血性休克(HS)中的变化及其意义。方法14头体重为14～17kg的健康雄性家猪，随机分成两组：失血性休克组(H组)和对照组(C组)，每组7头。H组按照Wigger’s改良法制作失血性休克模型，经股动脉快速放血使MAP降至40mmHg，维持90min，然后回输血液及等量的复方乳酸钠。C组处理同实验组，但不放血。各组分别在休克前、休克末、复苏末、复苏后0．5、1、2、4h分别记录MAP、HR、PAP、PCWP、CVP，测定股动脉血、肺动脉血中CO含量，以及动脉血乳酸盐浓度和血浆中N0水平。结果H组休克后MAP、PAP和CVP降低而HR升高，PCWP无显著变化。休克后肺动脉血CO水平逐渐增加，复苏后2h显著高于休克前，并高于C组，此后逐渐下降；股动脉血CO水平无显著变化；血浆NO水平在休克后逐渐升高，复苏后1h显著高于休克前和对照组水平。乳酸盐浓度在失血后显著升高，休克末达峰值，显著高于休克前和C组，以后逐渐下降，至4h恢复到休克前水平。结论HS后肺动脉血中CO水平增加，与NO共同参与HS的病理生理过程。

The role of endogenous carbon monoxide/nitric oxide in hemorrhagic shock in piglets

Objective To study the changes of carbon monoxide (CO) and nitric oxide(NO)and explore the possible involvement of NO/CO in the development of hemorrhagic shock. Methods Fourteen male healthy piglets weighing 14-17 kg were anesthetized and randomly divided into two groups:hemorrhagic shock group(group H,n = 7) and control group(group C,n=7). The shock state (MAP=40 mmHg) was induced by controlled bleeding and maintained for 90 min,then the shed blood was returned,followed by the infusion of lactated Ringer's solution euqal to the shed-blood volume. The animals in group C were anesthetized and instrumented for 90 min,but did not undergo hemorrhage. MAP,HR,CVP,MPAP and PCWP were monitored. The concentrations of CO in pulmonary artery and femoral artery were determined before and after shock,immediately after resuscitation and at 0. 5,1,2 and 4 h after resuscitation. The plasma concentrations of NO and lactate were detected at the same time-points. Results After withdrawal of blood, MAP, MPAP and CVP decreased in group H, while HR increased and PCWP remained at the same level as before shock. Significant difference of NO in hemodynamic values was seen in group C. There was a tendency of increase of pulmonary artery CO at 2 h after resuscitation in group H, and then declined. The plasma level of NO was markedly elevated 1 h after resuscitation,and remained higher levels. The concentration of lactate was markedly increased at the end of shock,and then declined. Conclusion It is suggested that an increased of CO in pulmonary artery might play an important role in the pathogenesis of hemorrhagic shock.