Redistribution of Cardiac Output during Hemorrhage in the Unanesthetized Monkey

Regional flow measurements were made, using the Rudolph and Heymann microsphere technique, before and after 10, 30, and 50% of the previously measured blood volume was withdrawn from five unanesthetized rhesus monkeys restrained in horizontally tilted primate chairs. Measurements at similar time intervals were also made in seven control monkeys. Systemic arterial and central venous pressures, cardiac output, stroke volume, and hematocrit decreased progressively at each level of bleeding. Heart rate (until severe hemorrhage), respiratory rate, and blood levels of α-glucosidase rose; bradykinin levels in arterial blood were unchanged. The fraction of cardiac output was found to be progressively increased to brain, heart, adrenal gland, and hepatic artery vascular bed at the expense of skin, spleen, and pancreas. The hepatic artery vascular bed was the only one that showed significant vasodilatation at either 30 or 50% hemorrhage. During acute endotoxin shock in monkeys, we have previously found a similar fall in systemic arterial pressure due to a decrease in total peripheral resistance and a different pattern of regional blood flow changes. The lack of bradykinin production, the integrity of cardioregulatory mechanisms, and the fall of hematocrit levels found during hemorrhage may help account for some of the hemodynamic differences between these two types of shock.