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探讨出血性休克及复苏过程中肝脏局部组织PtiO2 、PtiCO2 和pHti变化规律、原因及其意义。方法 家兔麻醉并放血至MAP =40mmHg ,6 0分钟后复苏至MAP =80mmHg ,维持 30分钟。持续监测肝脏组织氧分压 (PtiO2 )、二氧化碳分压 (PtiCO2 )及酸碱度 (pHti)。结果 休克过程中 ,PtiO2 逐渐下降至 0 ;PtiCO2 升高至 41 2± 15 6mmHg(P <0 0 0 1) ;pHti降至7 41± 0 0 9(P <0 0 0 1)。复苏后PtiO2 迅速上升并稳定在 11 0± 2 0mmHg ,PtiCO2 逐渐下降至 39 1± 14 7mmHg(P <0 0 0 1) ,pHti逐渐升高至 7 46± 0 0 8(P <0 0 0 1)。结论 严重长时间出血性休克可导致肝脏缺氧 ,CO2 蓄积和组织酸中毒。复苏后 ,组织缺氧 ,CO2 蓄积及酸中毒可部分减轻 ,但难以在短时间内恢复至正常。肝组织PtiO2 、PtiCO2 和pHti可能是评价缺血性休克严重程度及复苏有效性的有用指标
To investigate the changes of PtiO2, PtiCO2 and pHti in local tissues during hemorrhagic shock and resuscitation, the reasons and their significance. Methods The rabbits were anesthetized and bleed to MAP = 40mmHg. After 60 minutes, they recovered to MAP = 80mmHg for 30 minutes. Continuous monitoring of liver tissue PO2, PtiCO2 and pHti. Results During the course of shock, PtiO2 decreased gradually to 0; PtiCO2 increased to 41 2 ± 15 6mmHg (P <0.01); pHti decreased to 7 41 ± 0 0 9 (P 0 001). After recovery, PtiO2 increased rapidly and stabilized at 11 0 ± 20 mmHg, PtiCO2 decreased gradually to 39 1 ± 14 7mmHg (P <0.01), and pHti increased gradually to 7 46 ± 0 0 8 (P 0 01 0 ). Conclusion Serious prolonged hemorrhagic shock can lead to liver hypoxia, CO2 accumulation and tissue acidosis. After recovery, tissue hypoxia, CO2 accumulation and acidosis may be partially alleviated, but it is difficult to return to normal within a short period of time. Liver tissue PtiO2, PtiCO2 and pHti may be useful indicators for assessing the severity of ischemic shock and the effectiveness of resuscitation