Semler, Herbert J.

The effect of exercise on the pulmonary circulation was studied in a group of 6 intact dogs and in a second group of 4 subjected to ligation and division of the left pulmonary artery. Observations were made with the dogs standing and running on a horizontal treadmill up to the maximal speed they could maintain for periods of at least 2 minutes, usually 12 or 14 km./hr. Continuous records were made of the difference in pressure between the main pulmonary artery (PA) and a pulmonary-artery wedge (PAW) position. Cardiac output was determined by the indicator-dilution method, with injection of indocyanine (cardiogreen) dye into the main pulmonary artery and continuous sampling from the root of the aorta. The mean transit time of indicator betweell the pulmonary and aortic valves was obtained from the dilution curves, a correction being made for the transit time through the sampling apparatus. From these measurements the blood volume of the lungs and left heart chambers was derived. In the intact dogs, cardiac output increased approximately threefold from rest to severe exercise. There was an increase of only 12 per cent to 50 per cent in PA minus PAW pressure. Thus a continued fall occurred in pulmonary vascular resistance. The blood volume of the lungs and left heart of 3 intact dogs was measured. In 2 it did not change through the range of activity, and in the third the increase with maximal exercise was 18 per cent. The dogs with ligated left pulmonary artery also showed a threefold increase in output with severe exercise. Since the entire output passed through a single lung, the effect on the pulmonary vessels was comparable to that of a sixfold increase in output in a normal dog. Despite such large flows, in 3 of 4 dogs the difference between PA and PAW pressure rose only 37 per cent to 50 per cent. The volume of blood in the lungs and left heart was unchanged between rest and 8 km./hr., and at higher speeds showed a 0 per cent to about 20 per cent increase.

It has been suggested that the pressor effect of hypertonic solutions of sodium chloride on the Pulmonary circulation results from spasm of the pulmonary veins at their junction with the left atrium. These studies demonstrate that the increased resistance in the pulmonary vessels develops upstream to this site and that it may result primarily from mechanical blockage of vessels by clumped erythrocytes rather than from vasoconstriction.

Survival following surgical correction of congenital cardiovascular defects is unlikely if pulmonary hypertension cannot be decreased significantly. Infusions of acetylcholine decreased pulmonary vascular resistance in 6 of 11 patients having pulmonary hypertension associated with atrial or ventricular septal defects. When the acetylcholine was combined with the breathing of oxygen, resistance decreased further. These findings are consistent with the theory that, at some stage, the pulmonary hypertension in cases of congenital heart disease is maintained at least in part by vasoconstriction and therefore is potentially reversible.

Changes in pulmonary vascular (arteriolar) resistance were estimated in 58 patients with mitral stenosis following mitral valvotomy and during exercise. Evidence is presented that changes in "resistance" reflect active changes in the caliber of the vessels due to alteration in their smooth muscle tone, valvotomy being followed by a decrease in tone and exercise by an increase.