Perspectives of Total Artificial Heart Research as a Valuable Modelling System for General Physiology and Pathophysiology

Electronmicroscopic Changes in Selected Vital Organs After Long‐Term Total Artificial Heart Pumping in Animal Experiments

“…In the treated group, the aim of the antihypertensive treatment was to decrease both the CVP and the arterial pressure, which, after a prolonged TAH pumping, can seriously damage the vital organs, especially the organ microcirculatory structures. The effect of this treatment could be observed in the decrease of the CVP values in the treated group and partially in the protection of the liver tissue from extensive microcirculatory damage, which was, on the other hand, observed by the means of light microscopy in the untreated animals (5,7,10). Also, the prolongation of survival was evident in the treated group.…”

“…Especially in the liver, the changes were mainly caused by the increased CVP with concomitant subsequent stasis in the liver microcirculation with hypoxic damage of the hepatic tissue. The pathogenesis of the CVP increase in the TAH animals has been published elsewhere, and based on this pathogenetic background, we also could perform an essentially successful pathophysiological treatment (5,7,10–12). Due to this treatment and also partly due to the systemic antimineralization treatment aimed at the prevention of mineralization of driving diaphragms, we could substantially increase the length of survival (1,2).…”

“…The materials and methods concerning the type of the TAH implanted in our long‐term experiments and the arrangement of the experiments in our 66 animals (65 calves and 1 goat) were published elsewhere (5–10). In this study, dealing with the evaluation of the EM changes of 3 vital organs (liver, kidney, and lungs) in 51 long‐term survivors, we evaluated the EM findings in 22 animals (21 calves and 1 goat) with the antihypertensive treatment (average survival 162 days of pumping, mean ± 59.2 SD; the longest survival 293 days) and in the untreated group.…”

Total Artificial Heart: The Adaptation and Pathophysiological Deviations in the Recipient

“…To increase the survival of the animals as much as possible, we have elaborated the measures for the treatment of the arterial and venous hypertension that was manifested during the experiments by the increase of the central venous pressure (CVP), which finally caused a serious hepatomegaly with an extensive tissue damage (hemorrhages, fibroses) leading to death (6,7). This form of hypertension is caused by the removal of the heart ventricles where the Bezold‐Jarisch reflex secures the decrease of the vascular tone and bradycardia in the intact hearts.…”

“…were regularly performed in all the experiments. Details of these tests are published elsewhere (4–8).…”