Abstract
If oxygen uptake in the tissues of the body is to remain unaltered when the concentration of hemoglobin in the circulating blood is reduced, either cardiac output must increase to maintain the amount of oxyhemo-globin delivered to the tissues per minute or the extraction of oxygen from the available hemoglobin must be increased, or both mechanisms must operate.
Studies in animals and man have shown that cardiac output is increased in anemia (1-6), but the relative importance of all the factors which may influence the output has not been established. With the exception of the studies by Fowler and associates (1) and of Murray and co-workers (4), few measurements have been made on the relation of changes in total blood volume to changes in cardiac output in anemia. The present studies were therefore designed to assess in dogs the cardiovascular changes which accompany acute anemia and hypervolemia when these conditions are imposed singly or in combination.
Methods. Experiments were carried out in 21 dogs anesthetized with sodium pentobar-bital (25 mg/kg) and in 3 conscious dogs. The dogs weighed from 9.4 to 19 kg.
Six dogs were made hypervolemic and anemic by transfusions at body temperature of 4 aliquots of 250 ml of 6% dextran (75,000 molecular weight) in normal saline. Each aliquot was transfused over a 5-minute period. Four more dogs had similar treatment, one after cardiac denervation(7), two after cardiac denervation and bilateral thora-coabdominal sympathectomy, and one after receiving atropine and pentolinium.
In 6 dogs normovolemic anemia was achieved by establishing a temporary extracorporeal bypass connected to a reservoir which was initially filled with dextran. The volume of the reservoir was kept constant. The bypass allowed a progressive equilibrium between the animal's blood and the dextran, resulting in anemia with little or no change in blood volume. By substituting fresh reservoirs of dextran, step-wise reductions in hematocrit were achieved.
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