Vasků J, Vasků J, Cerný J, Dostál M, Dolezel S, Vasků A, Guba P, Urbánek P, Petrzilka J, Sotolová O
Institute of Pathophysiology, Faculty of Medicine, J.E. Purkynĕ University, Brno, CSSR.
Int J Artif Organs. 1989 Apr;12(4):242-51.
Vasomotor disregulation, preponderantly expressed by a pathological increase of central venous pressure (CVP) in calves with total artificial heart (TAH), starts to be evident from about the 50th day of pumping. The main cause of this state is an imbalance in cardiac receptor areas. Ventricular vasodepressor mechanisms are eliminated with the ventricular tissue, which is replaced by the artificial blood pump. In the stumps of both atria, which remain in situ, all neural elements disappear immediately after TAH implantation, but within two months they are fully regenerated. Regenerated atrial receptors are the starting points of afferent neural stimuli, which in the vasomotor center of the brainstem, increase the activity of the vasoconstricting functional component. A general tendency to vasoconstriction, now not well counterbalanced, increases, and the progressive venous hypertension causes loss of liver function and morphology. Two therapeutic approaches were tried: afferent therapy by atrial electrical stimulation, and efferent therapy by the administration of antihypertensives. Both kinds of this therapy were sufficiently effective in reducing CVP, protecting the liver, and prolonging average survival.
血管舒缩失调主要表现为植入全人工心脏（TAH）的小牛中心静脉压（CVP）病理性升高，从开始泵血约第50天起就开始明显。这种状态的主要原因是心脏受体区域失衡。心室血管减压机制随心室组织一同被去除，取而代之的是人工血泵。在原位保留的双侧心房残端，TAH植入后所有神经元件立即消失，但在两个月内它们会完全再生。再生的心房受体是传入神经刺激的起始点，这些刺激在脑干的血管舒缩中枢增加血管收缩功能成分的活性。血管收缩的总体趋势（现在没有得到很好的平衡）增强，进行性静脉高压导致肝功能和形态学丧失。尝试了两种治疗方法：通过心房电刺激进行传入治疗，以及通过给予抗高血压药物进行传出治疗。这两种治疗方法在降低CVP、保护肝脏和延长平均生存期方面都有足够的效果。
