Energy metabolism of vascular smooth muscle and circulating vasoactive substances in hemorrhagic shock in the dog

Metabolic and endocrine alterations were compared in control dogs and dogs subjected to hemorrhagic shock. The latter animals were hemorrhaged and the mean arterial blood pressure maintained at 35-40 mmHg until 30% of the maximal shed blood volume was spontaneously taken up by the animal. At the point of 30% uptake, the remaining shed blood was infused. The experiments were terminated when the mean arterial pressure fell 10-20 mmHg below that after reinfusion. The following alterations were found as compared to corresponding values in control animals. Arterial blood PO₂ and PCO₂ showed biphasic reciprocal changes and returned to control level at the end of the experiments. There was pronounced acidosis throughout the experiments. Blood glucose concentration was increased threefold during the early stages of hypotension. Thereafter, it returned to control levels at the point of 30% uptake and pronounced hypoglycemia was observed at the end of the experiments. Plasma catecholamines were increased 250-fold during the early stages of hypotension and gradually decreased to ninefold elevation above control at the end of the experiments. Plasma renin activity (PRA) and aldosterone concentration increased about ten times in the early stages of hypotension. While PRA remained elevated, aldosterone fell to control levels at the end of the experiments. Plasma bradykinin (BK) was elevated only at the point of 30% uptake. Thoracic aorta and small branches of mesenteric arteries were removed at the end of the experiments, and the rates of O₂ uptake and adenosine triphosphate (ATP) formation by homogenates of aortic intima-media strips and mesenteric arteries were measured by succinate oxidation. Oxygen consumption, ATP formation and P/O ratio did not differ from corresponding values in control nonhemorrhaged animals. It is concluded that hemorrhagic shock does not results in permanent damage to vascular smooth muscle mitochondrial respiration. However, the development of pronounced acidosis and hypoglycemia may adversely affect the energy metabolism of blood vessels in vivo and thereby contribute to the development of irreversible shock. The pattern of changes in the vasoactive systems suggests that progression to the irreversible stage of shock correlates with decline in the intensity of the sympathoadrenal activation and with the increase in plasma BK levels.