Effect of acute isovolemic anemia on cardiac output and estimated hepatic blood flow in the conscious dog

Abstract

The effect of acute isovolemic anemia induced by Dextran 70 exchange (40 ml/kg body weight) on estimated hepatic blood flow, cardiac output, and related variables was studied in 27 experiments on 24 unsedated dogs. Experiments were performed 5-10 days after implantation of an electromagnetic flow transducer around the aorta and catheters in the hepatic vein, jugular vein, and carotid artery. Bromsulphalein infusion was used to measure estimated hepatic blood flows, and electromagnetic measurements of stroke volume and cardiac output were calibrated using a simultaneous dye dilution curve. With a mean fall in hematocrit from 34.8 to 17.0 ml/100 ml, estimated hepatic blood flow rose from 53.6 ± 15.3 (SD) to 76.3 ± 21.1 ml/min Kg-1 and splanchnic vascular resistance fell from 119± 41 to 93 ± 38 mm Hg/liter min-1 (P<0.01). These changes were proportionately smaller than the increase in cardiac output (182 ± 80 to 350 ± 146 ml/min Kg-1) and the fall in systemic vascular resistance (37.0 ± 4.9 to 21.7 ± 4.9 mm Hg/liter min-1), leading to a fall in the ratio of estimated hepatic blood flow to cardiac output from 34.3 to 25.7%. Bromsulphalein extraction ratio was significantly decreased, but bromsulphalein clearance increased 44%. Splanchnic oxygen consumption did not change. Beta receptor blockade in 6 dogs (propranolol 0.5 mg/kg body weight) failed to prevent or attenuate the increase in estimated hepatic blood flow or cardiac output when the blocking agent was given before induction of acute isovolemic anemia. Sixty minutes after accomplishment of anemia, estimated hepatic blood flow and cardiac output had returned toward but not to control levels. Induction of β receptor blockade in the anemic dog did not influence the effects of time on estimated hepatic blood flow or cardiac output. It is concluded that acute isovolemic anemia leads to a significant increase in estimated hepatic blood flow that is essentially independent of β receptor stimulation.