PLASMA SUBSTITUTES 



77 



the patients with mitral \alvular disease, the pressure 

 in the pulmonary arteries increased more rapidly and 

 more markedly than in the normal subjects for the 

 same increase of plasma volume and right atrial pres- 

 sure. As in normal subjects, a variable relation was 

 found between right heart filling pressure and cardiac 

 output, stroke volume, or right ventricular stroke 

 work. With the expansion of the plasma volume 

 cardiac output increased at times, but not always. 

 Hemoglobin concentration in these studies was never 

 below 10 g/ioo ml of blood and thus anemia could 

 not be expected to have affected the cardiac output. 



Studies of hemodynamic effects of de.xtran infusion 

 have also been made in animals. Gowdey & Young 

 (38) infused 6*^ dextran at a rate of i ml per kg per 

 min into dogs. In these animals increases of right 

 atrial pressure and of cardiac output were observed; 

 however, there was no consistent relationship between 

 rise in right atrial pressure and increase of cardiac 

 output. Usually the cardiac output continued to rise 

 as the infusion progressed until a \olume of dextran 

 equivalent to about lo'i of body weight had been 

 given. With further infusion high output heart failure 

 suddenly developed and the animal died within a few 

 minutes. Heart failure was defined here as a state in 

 which the increased cardiac output had begun to fall 

 and continued to fall while right atrial pressure ro.se 

 abruptly. During the early stages of infusion arterial 

 oxygen transport was maintained, the increasing 

 cardiac output compensating for the decreasing 

 arterial oxygen content; however, when the 

 hematocrit level had fallen below 20 '"o the arterial 

 oxygen transport was reduced; when cardiac failure 

 occurred, oxygen transport was markedly reduced. 

 Arteriovenous oxygen differences grew progressively 

 smaller throughout the infusion. Systemic arterial 

 blood pressure either did not change appreciably or 

 rose with the infusion. The total peripheral resistance 

 invariably decreased, often to 50 % of control values, 

 until the cardiac output ceased to rise and then the 

 total peripheral resistance began to increase. The 

 pulse rate showed no consistent response to infusion, 

 but usually decreased with cardiac failure. Fowler and 

 associates (32) studied the hemodynamic effects of 

 dextran infusion in hypervolemic and normovolemic 

 dogs. Eleven clogs were given three separate infusions 

 of 6 % dextran, totaling 8 % of the body weight. Ten 

 other dogs were bled 6 % of body weight and the blood 

 removed was replaced with 6% iso-oncotic dextran. 

 Cardiac output increased significantly after infusions 

 in both the bled (normovolemic) and unbled (hyper- 

 volemic) animals. Significant increase in cardiac 



output was seen when the hemoglobin was lowered to 

 between 7.7 and 10 g%. Significant decrease in 

 hematocrits was observed in both groups of dogs. 

 Right atrial mean pressure showed no increase in bled 

 dogs, but did show an increase in unbled dogs. Both 

 groups of dogs showed significant increases in pulmo- 

 nary arterial pressure. There was no positive associa- 

 tion between right atrial mean pressure increase and 

 increase of cardiac output. Cardiac output increased 

 comparably with similar degrees of anemia in hyper- 

 volemic and normovolemic animals. In a further 

 study. Fowler and associates (33) rendered 21 dogs 

 hypervolemic without anemia either by the infusion 

 of red cells suspended in dextran or by the infusion of 

 fresh whole blood, each animal receiving a total in- 

 fusion equivalent to 8 % of body weight. The hyper- 

 volemic animals showed no increase in cardiac output 

 and no striking changes in mean arterial blood pres- 

 sure 20 min after the infusion, although outputs did 

 increase during the infusion. Pulmonary arterial 

 pressure rose moderately in both groups of dogs and 

 right atrial pressure rose slightly. Ten animals which 

 had received fresh whole blood equivalent to 8 % of 

 body weight were then bled 700 to 1000 ml with 

 simultaneous replacement of the blood removed with 

 an equal volume of 6 % dextran. After bleeding and 

 dextran infusion there was a slight rise in both pulmo- 

 nary arterial and right atrial pressure, and striking 

 increase in cardiac output. These studies suggested 

 that the increase in cardiac output following dextran 

 infusion was related to the anemia produced thereby 

 and not to the expansion of whole blood volume or to 

 the increase of cardiac filling pressure. No relation- 

 ship between changes in stroke volume and right 

 heart filling pressure was shown in these studies. In 

 later studies Fowler and associates (31) studied the 

 effect of dextran-induced anemia in hypovolemic 

 dogs. Dogs were rendered hypovolemic by bleeding 

 20 ml, kg. Hypovolemic anemia then was produced 

 by further bleeding of 60 ml/kg w'ith simultaneous 

 dextran volume replacement, the dextran used being 

 6 % iso-oncotic dextran in normal saline. The mean 

 blood volumes were decreased 15.5% during hypo- 

 volemic anemia. The mean of hematocrits was 48.4% 

 in the control period and 16.2 % in the anemic period. 

 During hypovolemic anemia there was an increase of 

 cardiac output, stroke volume and right ventricular 

 stroke work, but no increase of right atrial transmural 

 pressure. The rise in cardiac output during hypo- 

 volemic anemia aboxe that of the hypovolemic period 

 was due to increase in both stroke volume and in heart 

 rate. The increase of cardiac output over control, 



