A NEW EXPERIMENTAL-MODEL OF SPECIFIC LIVER HYPOXIA USING MEMBRANE-OXYGENATOR

The present study introduces a new experimental canine model of hepati c arterial deoxygenation using a membrane oxygenator to investigate th e influence of hepatic arterial hypoxia on hepatic hemodynamics and en ergy metabolism. Eighteen mongrel dogs weighing 10 kg each were random ly divided into three groups: group A served as a control (118.0+/-9.0 mmHg of hepatic arterial O-2 content), group B as a moderately deoxyg enated group (40 mmHg of hepatic arterial O-2 content), and group C as a severely deoxygenated group (25 mmHg of hepatic arterial O-2 conten t). Deoxygenation was achieved by perfusion of a gas mixture of O-2 an d N-2 through the membrane oxygenator, which was interposed between th e femoral artery and the proper hepatic artery, for 60 min. In group C , hypoxia decreased the mean systemic arterial blood pressure and hepa tic arterial blood flow. Arterial blood ketone body ratio (AKBR=acetoa cetate/3-hydroxybutyrate), which reflects the hepatic mitochondrial re dox state, rapidly decreased prior to the significant increase of glut amate oxaloacetate transminase, glutamate pyruvate transminase, and la ctate dehydrogenase after the initiation of hypoxia. Hepatic arterial deoxygenation to 25 mmHg for 60 min induced injury to hepatic hemodyna mics, resulting in the deterioration of systemic hemodynamics even aft er the termination of liver hypoxia. This in vivo temporal hepatic art erial hypoxic model without alteration of inflow volume might be usefu l for investigating the mechanism of hypoxic injury and the critical p oint of liver hypoxia on hepatic and/or systemic hemodynamics and live r viability.