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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



changed. In contrast to its direct depressant effect 

 on the isolated perfused heart, a C0 2 concentration 

 in the respired air of the open-chest dog of at least 8 

 per cent has a stimulating influence on the myocar- 

 dium for the contractile force may not be lowered and 

 myocardial function curves are not depressed (267). 

 Presumably, this arises from its stimulating influence 

 on the sympatho-adrenal system since acidotic heart 

 failure in the heart-lung preparation can be reversed 

 by administration of sympathomimetic amines. The 

 divergent results with hypercapnia may, therefore, 

 merely express the variable weighting of the antago- 

 nistic effects on the intact animal circulation, of a 

 direct depressant effect on the myocardium and 

 smooth muscle of the coronary vessels, and of an 

 indirect stimulating effect on the same structures 

 through the sympatho-adrenal system. In the intact 

 dog, hypocapnia (arterial C0 2 less than 35 vol per 

 cent) is without effect on systemic and coronary 

 hemodynamics and the ventricular function curve is 

 unaltered (1 14, 267). 



In the isolated heart doing no work, alkalosis in- 

 duced by varying the bicarbonate concentration of 

 the perfusing solution, or following CO» administra- 

 tion, depresses inotropic and chronotropic cardiac 

 activities but increases coronary flow. These changes 

 in cardiac function are effected only when the pH of 

 the perfusate is altered (248). Sodium bicarbonate 

 infusion in the intact anesthetized dog stimulates 

 both systemic and coronary hemodynamics. In the 

 presence of an essentially constant heart rate and 

 arterial blood pressure, and a marked increase in 

 cardiac output, the coronary flow and oxygen usage 

 per minute and per heart beat are elevated consider- 

 ably (134). The mechanisms concerned are not 

 known. Nor has it been established whether these 

 effects of acidosis and alkalosis on the coronary cir- 

 culation in the intact dog arise from changes in pCO>, 

 HC0 3 , or from the resulting change in pH, since in no 

 instance has the pH been separately controlled. 



potassium, calcium. There has not been sufficient 

 experimentation to determine the role, if any, of the 

 electrolytes in regulating the coronary circulation. 

 Increased potassium concentration (150%) in the 

 blood perfusing the fibrillating heart of the Langen- 

 dorff preparation increases coronary flow, while 

 larger intracoronary concentrations in the open- 

 chest dog also produce similar increases (88). In the 

 heart-lung preparation, isolated heart, or heart within 

 the chest, very large potassium concentrations suffi- 

 cient to arrest the heart reduce coronary inflow (249, 



259). In the latter instance, the oxygen usage is also 

 greatly reduced as a result of a decreased flow and 

 oxygen extraction. In the open-chest dog, upon the 

 addition of pharmacological amounts of Ca gluconate, 

 coronary flow and oxygen consumption increase and 

 oxygen extraction decreases without much change in 

 blood pressure and heart rate (115). 



Transfusion 



Augmentation of ventricular load by increasing 

 venous return, and, hence, circulating blood volume 

 through infusion has a clinical counterpart in the load 

 placed upon the human heart by transfusion or by an 

 aortacaval fistula. During transfusion, systolic and 

 diastolic heart size, ventricular stroke volume and 

 stroke work, atrial and ventricular end-diastolic 

 pressures and arterial blood pressure all increase as 

 the heart rate slows considerably. When the coronary 

 arteries are perfused at a constant pressure or with a 

 normal pulsatile aortic pressure, an increase in the 

 cardiac output or cardiac work through augmentation 

 of venous return to the heart beating in situ augments 

 moderately the coronary flow and oxygen usage per 

 minute and per heart beat while the aortic pressure 

 rises (46, 90, 152, 153). The increasing coronary flow 

 is partially explainable on a mechanical basis since 

 the slowing of the heart should increase coronary 

 flow per beat and per minute by increasing the dia- 

 stolic time period during which coronary flow is 

 greater. The coronary flow and oxygen are used 

 economically, for the ratio of stroke cardiac work to 

 stroke oxygen consumption increases. However, it 

 has been repeatedly shown in the denervated heart 

 and heart-lung preparation that coronary arterial 

 inflow and coronary sinus outflow are reduced some- 

 what or unchanged by alterations in cardiac output 

 as long as the resistance against which the ventricles 

 contract is unaltered (10). These findings have been 

 extended to the open-chest dog in which coronary 

 flow and oxygen usage may not change or may rise 

 only slightly in the presence of a constant arterial 

 blood pressure and marked increase in cardiac out- 

 put (46). In the isolated supported heart, the coronary 

 flow and oxygen usage per minute and per heart 

 beat can be made to decrease in response to a lowering 

 of arterial blood pressure, achieved by release of an 

 aortic constriction during the augmentation of cardiac 

 output which follows an increase in venous return 



(334)- 



Since the average individual is transfused only on 



rare occasions, it is not known whether such, informa- 



