实验性肝脏撞击伤后家兔心肌收缩功能和动脉血气的变化

目的探讨肝脏撞击伤对家兔心肌收缩功能和动脉血气的影响。方法建立肝脏撞击伤动物模型,分别在伤前,伤后即刻、0.5、1、2h或死亡前测定家兔心肌收缩功能和动脉血气变化。结果肝脏损伤后,心率(HR)、左室收缩压(LVSP)、左室内压最大变化速率(±dp/dtmax)均显著下降,左室舒张末压(LVEDP)差异无显著性。伤后pH值降低,HCO-3显著下降,细胞外液剩余碱(BEecf)负值逐渐增大,表现为渐进性代谢性酸中毒;动脉血二氧化碳分压(PaCO2)伤前与伤后差异无显著性,动脉血氧分压(PaO2)逐渐降低,但伤后0.5h及1h与伤前比较差异无显著性。结论肝脏撞击伤后,心肌收缩功能下降,酸碱平衡紊乱,表现为代谢性酸中毒。

Experimental study on changes in myocardial systolic function and arterial blood gases after impact injury to liver in rabbits

OBJECTIVE: To explore the effects of impact injury of liver on myocardial systolic function and arterial blood gases in rabbits. METHODS: A model of hepatic impact injury was reproduced in rabbits by hitting the xiphoid area with two falling steel balls. Myocardial systolic function and arterial blood gases were measured respectively before injury, immediately and 0.5, 1, 2 hours after injury, and before the death. RESULTS: After injury, heart rate (HR), left ventricular systolic pressure (LVSP), the maximum change rate of left ventricular pressure rise and fall (+/-dp/dt max) descended significantly, while left ventricular end-diastolic pressure (LVEDP) showed no statistically significant change. At the same time, blood pH and HCO(3)(-) fell gradually, and negative base excess (BEecf) showed a significant increase, indicating metabolic acidosis gradually developed. There was no obvious significant difference in partial pressure of carbon dioxide in artery (PaCO(2)) between the values before and after injury. Partial pressure of oxygen in artery (PaO(2)) decreased gradually, but no significant differences were found between the values of 0.5 hour and 1 hour after injury and that before injury. CONCLUSION: After hepatic impact injury, myocardial systolic function deteriorates, metabolic acidosis appears.