Cardiac and hepatic metabolism in spontaneously hypertensive rats following acute blood loss

Abstract

Seven spontaneously hypertensive rats (SHRs) and eight Wistar-ST rats were used to assess the influence of hemorrhage on myocardial and hepatic energy metabolism. They received 2% halothane and pancuronium, 0.3 mg·kg⁻¹, during preparation. After discontinuation of halothane, blood (2 ml·100g body welght⁻¹) was gradually withdrawn over a 5 min period from a femoral artery. Thirty min after induction of hemorrhage, the heart and liver were removed and myocardial and hepatic metabolites (ATP, lactate, pyruvate and glycogen) were measured by the enzymatic methods. Acidosis and decreased hematocrit were noted in the both groups after hemorrhage. Mean arterial pressure (MAP) in SHR was significantly higher than that in Wistar rat before hemorrhage. However, there were no significant differences in MAP and heart rate between the two groups after hemorrhage. Although there were no significant differences in cardiac metabolites, a significant decrease of hepatic ATP and an increase of hepatic lactate/pyruvate ratio were found in SHR when compared with Wistar rat. These results suggest that human hypertensive disease may run a high risk in connection with acute hemorrhage.