THE EFFECT OF CYCLOPROPANE ON CARDIAC WORK CAPACITY

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Abstract
Expts. were performed on intact dogs and on dog heart-lung preparations to determine the effect of cyclopropane on cardiac work capacity. Seven intact dogs were anesthetized with 15-20 mg./kg. of thiopental. The trachea was attached to a Foregger anesthesia apparatus. The abdominal aorta was cannulated and attached to a stabilizer; heparinized blood was administered from a donor animal through a cannula inserted in the jugular or femoral vein. Artificial respiration was maintained with a Starling pump. After the animals recovered from the thiopental anesthesia, cyclopropane-O2 mixtures were administered. Pressure-loading of the heart was accomplished by elevating the pressure in the reservoir attached to the abdominal aorta by increments of 20 mm. of Hg until marked elevation of the right auricular pressure occurred. Right auricular pressure was recorded by a water manometer attached to a cannula inserted into the right auricle through the right external jugular vein. When the blood cyclopropane level was 10 mg.%, increasing the work of the heart by 60% (elevation of the aortic pressure from 86 to 108 mm. of Hg ) elevated the right auricular pressure from 50 to 96 mm. of H2O. With a cyclopropane level of 20.5 mg.% and a comparable work load, the right auricular pressure increased from 69 to 173 mm. of H2O. Decreasing the blood cyclopropane level to 4 mg.% and injecting 10 mg./kg. of pentobarbital Na intraven., the response of the heart to increased work load was greatly improved. Further injn. of pentobarbital to the point of respiratory arrest caused little further impairment of cardiac work capacity. Five expts. were performed in heart-lung prepns. In these expts. the control response of the heart to increased work load could be determined in environment free of anesthetic drugs. In 3 expts. the loading was accomplished by elevating the cardiac output against unchanged arterial resistance, and also by elevating the arterial resistance while the cardiac output was kept constant. In 2 other expts. only the cardiac output against constant resistance was increased. When the work of the left ventricle was increased 180% by "volume" loading the decrease in the cardiac work capacity (as measured by the right and left auricular pressure) was relatively slight in the control period, marked during exposure to "20%" cyclopropane, and still greater when the cyclopropane concn. in the system was 40 vol.%. Comparable work increments produced by "pressure loading" (elevation of arterial resistance) caused greater changes in the work capacity of the heart. In all cases the changes produced in the heart-lung prepns. by cyclopropane were reversible. The above expts. indicate that a significant reduction of cardiac reserve occurs with a cyclopropane blood concn. corresponding to 15 vol.% of cyclopropane in the inhaled atmosphere. The reduction of cardiac reserve was severe when the cyclopropane concn. was raised to 25-35 vol.%.
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