Cardiac function after hepatic ischemia-anoxia and reperfusion injury

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Abstract
During liver transplantation, reperfusion of the donor liver and in the clinical setting, end-stage liver disease, have occasionally resulted in profound cardiovascular disturbances. The etiology of hepatic injury-induced myocardial dysfunction is still unclear. In this study, the aims were to develop an experimental model that would facilitate the study of the effects of hepatic failure on myocardial function and to determine whether hepatic ischemia or anoxia and reperfusion injury of similar duration would result in the same degree of hepatic failure. Seventy male Sprague-Dawley rats were used as organ donors. Three simultaneous liver-heart perfusions (corresponding to three groups) were established using a modified Krebs-Henseleit buffer with 2% bovine albumin, membrane oxygenation, and a peristaltic pump. Group 1 (n = 10) and group 2 (n = 15) experiments consisted of liver-heart perfusions after 90 mins of normothermic hepatic ischemia or 90 mins of hepatic anoxia, respectively, followed by reoxygenation and 60 mins of reperfusion. Group 3 (n = 8) experiments consisted of sham liver-heart perfusions studied over the same experimental time period (60 mins). Myocardial function variables, liver function tests, arterial blood gases, and electrolytes were measured at baseline and at 3-, 10-, 30-, and 60-min intervals during reperfusion in all experiments. Ischemia or anoxia-induced hepatic failure resulted in a similar degree of hepatic dysfunction. Both forms of acute hepatic failure caused significant increases in liver function tests, a reduction in heart rate (p less than .05), coronary flow (p less than .05), and an increase in calculated coronary vascular resistance (p less than .05). There were no changes in buffer pH, CO2, or ionized calcium that could explain the coronary vasoconstriction. Hepatic dysfunction induced by ischemia or anoxia of similar duration results in a similar hepatic metabolic profile during reperfusion and can cause direct myocardial dysfunction of the isolated perfused rat heart.

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