Hemodynamic Response in Lung Transplantation as a Model of Total Lung Denervation

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Abstract
As a means to approach the question regarding the exact effect of lung denervation, hemodynamic studies were carried out in 49 dogs which had undergone either unilateral or bilateral lung autotransplantation. In 14 chronically survived animals of 20 with unilateral lung reimplant, unilateral pulmonary artery occlusion test was carried out. In the 29 with either one-stage or two-stage bilateral lung reimplants, serial hemodynamic studies were performed along with histologic examinations of the transplanted lung at autopsy. In the chronic survivors with the bilateral transplants, rapid and continuing infusion of 3, 000 ml of plasma expander was performed within 10 min through intraatrial catheter and various hemodynamic values were measured simultaneously. The animals with one-stage bilateral lung reimplants showed a varying degree of pulmonary edema in both lungs in the early postoperative period, and some of them succumbed to respiratory failure with a gradual decease in PaO2 but the other animals recovered from these pathologic states within 10 postoperative days and survived chronically. Hemodynamics of those longterm survivors showed high pulmonary vascular resistance early after surgery but this value returned nearly to the preoperative level in a distant postoperative period. On occlusion of contralateral pulmonary artery in unilateral lung replantation an increase in pulmonary arterial pressure was invariably observed. Their relationship was steep and almost linear against a given increment of cardiac output when cardiac output vs. pulmonary arterial pressure was plotted in each animal. These facts suggest that transplant differs from the normal lung in tolerance of the vasculature in an event of an increase in pulmonary blood flow. In the plasma expander infusion test, the dog with bilateral lung autotransplants demonstrated that pulmonary arterial pressure showed a parallel and linear increase with an increase in cardiac output until lung transplant became edematous, while in the control animal total pulmonary vascular resistance decreased with an increment in pulmonary arterial pressure during the course of increasing cardiac output. It can be interpreted from these results that changes have occurred in mechanism of pulmonary circulation of the transplant; the transplanted lungs cannot vasodilate totally with an increase in blood flow.

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