摘要
目的 研究兔肝缺血 再灌过程中肝组织氧分压 (PtiO2 ) ,二氧化碳分压 (PtiCO2 )和酸碱度 (pHti)变化规律、原因及其临床意义。方法 将麻醉后的大白兔阻断肝十二指肠韧带 45min后开放 ,观察 12 0min。持续监测PtiO2 ,PtiCO2 和pHti值 ,并取肝组织行病理检查。结果 肝门阻断后 15minPtiO2 急剧下降至 4mmHg以下 ,PtiCO2 急剧升高至 (149 6 3± 9 80 )mmHg(P <0 .0 0 1) ,pHti急剧下降至 (7 0 5± 0 0 9) (P <0 .0 0 1)。肝门开放后 ,PtiO2 迅速回升 ,并于 6 0min后稳定在 (16 4± 4 7)mmHg ,PtiCO2 下降并稳定在 (6 0 6 0± 6 6 6 )mmHg ,pHti上升并稳定在 (7 40± 0 12 )。病理观察 (光镜、电镜 )发现肝门阻断 15min以上 ,肝细胞显微及亚显微结构损害明显重于阻断 15min以内。结论 15min可能是兔肝门阻断的安全时限 ,4mmHg可能是兔肝门阻断的临界氧分压。肝组织PtiO2 ,PtiCO2
Objective To study the causes, significance of alteration of PtiO 2, PtiCO 2 and pHti in liver tissue during liver ischemia reperfusion (I R). Methods After rabbits were anesthetized, liver ischemia was induced by complete occlusion of the hepatoduodenal ligment for 45 min, then the portal and arterial flow were released, and observed for 120 min for measuring the PtiO 2, PtiCO 2 and pHti in liver tissue and the pathology of the liver during ischemia reperfusion. Results After 15 min of hepatic vascular occlusion, PtiO 2 decreased to 4 mmHg, PtiCO 2 increased fast to (149.63±9.80) mmHg (P<0.001), pHti decreased to (7.05±0.09) (P<0.001). After hepatic vascular released, PtiO 2 increased to (16.4±4.7) mmHg, PtiCO 2 decreased to (60.60±6.66) mmHg (P<0.001), pHti increased to (7.40±0.12) (P<0.001). Histopathologic findings (microscopy and electron microscopy) indicated that when the occlusion was more than 15 minutes the liver damage was significantly severer than that the occlusion with in 15 min. Conclusions The maximum period of hepatic vascular occlusion in rabbits liver may be 15 minutes, and 4 mmHg may be the boundary of liver tissue PtiO 2 in ischemia. Measurement of PtiO 2, PtiCO 2 and pHti in liver tissue may be a predictive indicator of liver I R injury.
出处
《中国普通外科杂志》
CAS
CSCD
2001年第4期331-333,共3页
China Journal of General Surgery
