Isolated dog hearts were perfused while time heart weight was electrically recorded. Arterialized blood was pumped into a coronary perfusion reservoir either from the femoral artery of a donor dog or from the arterial outlet of various oxygenators. The right heart was widely open. The presence of myocardial edema and the rate of fluid accumulation in heart muscle were observed from the slopes of tile weight registration and from the difference of the directly measured heart weights before and after an experiment. Blood hold-up was measured in three experiments with tagged red cells: it accounted for 15 per cent or less of the observed weight gain. When the heart was perfused from a donor dog and was not otherwise injured, myocardial edema fluid did not accumulate unless the coronary pressure exceeded 200 mm. Hg. Myocardial edema also formed when blood was diluted with Ringer's solution or after cardiac injury; the rate of edema formation was then dependent on the coronary perfusion pressure. Edematous hearts could often be made to lose weight (i.e., edema fluid) when perfused at pressures below 100 mm.Hg. Perfusion with blood from a disposable bag oxygenator initiated inyocardial edema formation almost immediately.
Working toward a completely implantable total artificial heart, we have designed an eccentric roller type total artificial heart. The actuator of this artificial heart is a drum type eccentric roller that squeezes the blood chambers. The blood chambers are made of silicone rubber and are torus in shape. The shape of the artificial heart is an almost circular cylinder, and its length and diameter are 10 cm and 8 cm, respectively. The 2 main characteristics of this artificial heart are that it discharges blood in a pulsatile mode and that it requires no reversing of the motor. Because we have not completed the artificial heart yet, we have tested the eccentric roller mechanism on the prototype with an overflow type mock circulation with a 100 mm Hg afterload. The prototype worked at the roller speeds of 50, 100, and 150 rpm with flow rates of 1.7, 3.7, and 5.4 L/min, respectively. Next the prototype was connected to a Donovan type mock circulatory system and worked at roller speeds of 88-214 rpm with flow rates of 3.0-8.4 L/min against mean afterloads of 82-120 mm Hg.
The left lower lobe of anesthetized, heparinized dogs was excised, weighed, and cannulated. Another lobe of the same dog was excised for control purposes. The cannulated lobe was perfused by a system of adjustable reservoirs which was fed with fresh blood from a donor dog. The perfused lobe was mounted on an electronic balance so that weight changes could be recorded together with the pressures in the inflow and outflow conduits and in the bronchus. When the per fusion pressures were varied within normal limits, the weight of the lobes reached stable plateaus. Abnormally high perfusion pressures caused a continuous, steady increase in lobe weight, which was evident from the slope of the weight registration. Blood holdup in the lobe was measured by comparing the hemoglobin content of the control lobe with that of the experimental specimen taken at the end of an experiment. Blood holdup accounted for only about 10 per cent of the weight increase of edematous lobes. Initial observations were made in collapsed lobes; in the course of some experiments these lobes were inflated and the static airway pressures were then kept at varying levels. Irrespective of the perfusion pressures, transudate did not issue from the airway as long as the lobe was collapsed. Abnormal perfusion pressures caused the accumulation of fluid, which continued as long as the perfusion pressures were constant. The rate of transudation was determined by the perfusion pressures and was not influenced by inflation of the collapsed lobe nor by variations of the static airway pressure. When a collapsed lobe had become edematous anti was then inflated, transudate issued from the airway. Increases of the static airway pressure did not decrease the rate of fluid accumulation, but only confined the transudate to the lung and prevented its discharge from the airway.
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