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目的 :观察心肺复苏成功患者血清NO和CO浓度的变化以及颅痛定对这种变化的影响。方法 :把患者随机分为治疗组(20例)和对照组(15例),从心跳骤停到开始复苏时间以15分钟为界进一步把治疗组和对照组分为早期组和晚期组。于心肺复苏成功后第6h、24h、48h、72h抽取病人外周静脉血,用硝酸还原酶法测定血清NO含量,可见分光光度计法测定CO含量。结果 :心肺复苏后6h血清NO浓度上升,24h达高峰,随后又下降,48h降到低谷,然后再次上升。颅通定表现出对NO产生的抑制作用,早期治疗组和对照组NO含量变化曲线几乎平行,两组NO含量差别在6h、24h无显著性,在48h、72h有显著性。晚期治疗组与对照组NO浓度变化方向几乎相反,颅通定也表现出对NO生成的抑制作用,但与对照组无平行关系。晚期治疗组和对照组中任何时间段血清NO含量的差别均无显著性。早期对照组的CO浓度在复苏后6h下降,24h降到低谷,48h略有上升,后又再次下降。而治疗组CO浓度在复苏后6h开始上升,随后急剧下降,48h达到低谷,然后再次上升。早期治疗组和对照组的CO浓度变化曲线几乎呈相反方向。晚期对照组CO浓度在复苏后6h急剧下降,24h降到低谷,随后一直上升。颅通定表现出对CO生成的抑制作用,治疗组从复苏后6h到72h几乎呈直线下降趋势。但无论是早期组或晚期组在各个时间点之间CO浓度差别均无显著性。结论 :颅通定可能通过调控心肺复苏患者体内NO含量发挥抗脑缺血再灌注损伤作用,且在早期复苏(≤15min)患者中作用更明显。而颅通定对心肺复苏患者体内CO含量的影响不明显。
Objective: To observe the changes of serum NO and CO concentrations in patients with successful cardiopulmonary resuscitation (CPR) and the effect of Routine on these changes. Methods: The patients were randomly divided into the treatment group (n = 20) and the control group (n = 15). The treatment group and the control group were further divided into the early group and the late group from the point of cardiac arrest to the start of recovery for 15 minutes. Peripheral venous blood was drawn at 6h, 24h, 48h, 72h after CPR success. The content of NO was determined by nitrate reductase method. The content of CO was measured by spectrophotometer. Results: Serum NO concentration increased 6 h after cardiopulmonary resuscitation, peaked at 24 h, then decreased again, then dropped to low level at 48 h and then rose again. Cranialitia showed NO inhibition, early treatment group and control group NO content curve nearly parallel, the two groups NO content difference at 6h, 24h no significant at 48h, 72h significant. In the late treatment group and the control group, the concentration of NO changed almost in opposite directions. Cranitroprussidine also showed the inhibitory effect on NO production, but had no parallel relationship with the control group. There was no significant difference in serum NO levels between the late treatment group and the control group at any time. The concentration of CO in early control group decreased at 6h after resuscitation, dropped to low level at 24h, increased slightly at 48h and then dropped again. The concentration of CO in the treatment group began to rise at 6h after resuscitation, then dropped sharply, reached a low level at 48h and then rose again. The changes of CO concentration in the early treatment group and the control group showed almost the opposite direction. The concentration of CO in the late control group dropped sharply at 6h after resuscitation and dropped to the lowest level at 24h after resuscitation, and then rose all the way. Intracranialis showed inhibition of CO production, the treatment group from the recovery of 6h to 72h almost straight down trend. However, there was no significant difference in CO concentration between the early and late groups at all time points. Conclusion: CGRP may play an anti-cerebral ischemia-reperfusion injury effect by regulating NO content in patients with cardiopulmonary resuscitation, and plays a more significant role in patients with early resuscitation (≤15min). Cranioparone on the content of CO in patients with cardiopulmonary resuscitation is not obvious.