The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Abstract

Pulmonary arterial pressure increases in dogs exposed to alveolar hypoxia or intravascular infusion of 5-hydroxytryptamine (serotonin). Although most investigators believe that this increase in pressure reflects a vasoconstriction in the pulmonary vascular bed, the site of vasoconstriction, whether venular, capillary, or arteriolar, is controversial. Interpretations have been based previously upon measurements of pressure and flow at various sites in the pulmonary circulation and have been handicapped by the inability to measure the volumes of the segments under study (1-3). MethodsEleven mongrel dogs weighing 12.3 to 17.7 kg were used in the experiments. They were anesthetized with sodium pentobarbital in a dosage of 26 mg per kg body weight. An 8F or 9F Cournand cardiac catheter 1 was introduced into the external jugular vein, and under fluoroscopic guidance its tip was placed within the pulmonary artery. A second catheter was placed so that its tip lay within the superior vena cava. A pediatric 7F Brockenbrough left heart catheter 1 was introduced into the femoral vein and the atrial septum punctured so that the tip of the catheter lay free in the left atrial cavity. The femoral artery was cannulated with polyethylene tubing 25 cm in length and 2 mm in diameter in such a way that its tip lay in the distal aorta. The animal was enclosed within a horizontal Plexiglas body plethysmograph (4), then paralyzed with succinylcholine and ventilated with a Starling pump. Intravascular pressures were measured by strain gauges 2 balanced to a reference pressure level 9.8 cm above the surface of the dog board. Plethysmographic pressure was measured by a differential strain gauge.3 A direct-writing instrument 4 recorded pressures from the strain gauges, the electrocardiogram, and dye concentration from a cuvette densitometer.5The plethysmograph was calibrated by injection and withdrawal of 10 ml of air with a syringe, and this produced a deflection of 20 to 30 mm on the record. The pulmonary arterial pressure was monitored while the catheter was pulled back slowly until a ventricular pressure tracing was recorded, and then the tip of the catheter was advanced to the point where a pulmonary arterial pressure tracing was again recorded from a position just beyond the pulmonic valve. A 0.5-ml volume of solution, containing 0.1 ml of ether in 0.4 ml of alcohol, was instilled into the catheter to be flushed into the animal by 5 ml of saline. In several experiments designed to determine whether C02 evolution rate was affected, 0.5 ml of a 0.5 M lactic acid solution was instilled into the catheter to be flushed into the animal by 5 ml of saline, or 5 ml of a 0.9 M sodium bicarbonate solution was placed into the catheter and connecting tubing, and this was also ad-

Differential reactivity in the pulmonary circulation

“…Several studies have shown venous constriction (14,15), whereas others have found predominant arterial constriction (16,17). Our findings help explain many of the seemingly conflicting results in the literature.…”

Aggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine.

“…Introduction 5-Hydroxytryptamine (serotonin) contracts canine and human isolated intrapulmonary vascular preparations (1)(2)(3)(4) and elevates pulmonary vascular resistance in intact organisms (5)(6)(7)(8)(9)(10) or vascularly isolated perfused lungs (1 1-13). Microembolization or in situ aggregation of platelets produces an elevation of pulmonary vascular resistance, leading to pulmonary hypertension, which can be attributed in part to the release of vasoactive substances (5,(14)(15)(16)(17)(18)(19).…”

Sites of pulmonary vasomotor reactivity in the dog during alveolar hypoxia and serotonin and histamine infusion

“…9). It is apparent from the most recent reviews (13,14) that the sites of action for alveolar hypoxia, histamine (15), and serotonin (16,17) are very much in doubt.…”