Abstract
Summary
The left lower lobe of the lung was isolated from the remainder of the pulmonary circulation and was perfused with autologous blood at controlled flow rates. All venous effluent from the lobe was collected into a reservoir. Pulmonary artery and pulmonary venous pressures, systemic arterial pressure and in some cases reservoir level were monitored continuously. In 17 out of 18 experiments in 10 dogs, amyl nitrite inhalation was followed by a decline (av 11%) in pulmonary artery pressure in the presence of constant blood flow. Pulmonary venous pressure was unchanged. Amyl nitrite inhalation was repeated in 6 of the animals after ventricular fibrillation was induced. In this situation systemic arterial pressure remained constant and thereby eliminated; (a) a possible pulmonary reflex response emanating from a sudden change in systemic arterial pressure and (b) an alteration in bronchopulmonary blood flow. The response of the pulmonary vasculature to amyl nitrite in this situation was similar to that before ventricular fibrillation was induced. These results indicate that amyl nitrite exerts a direct dilating effect on pulmonary vessels and decreases pulmonary vascular resistance.
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