Abstract
An average of 1,100 ml of a 6% solution of dextran in saline was infused into each subject at a mean rate of 54 ml/min. Several minutes after the infusion atropine sulfate was injected intravenously. The pressure-volume relationship of the pulmonary vasculature after dextran reflected a lower dlstensibility than that existing in the control state. The ratio of change in volume to change in transmural pressure in the pulmonary circulation as a whole was 5 ml per m2 per mm Hg. The lung compliance showed a modest but significant reduction. After the injection of atropine the distensibillty of the pulmonary circulation as a whole was considerably greater than that observed after dextran infusion and was close to the control value. The ratio of change in volume to change in pressure was 23 ml per m2 per mm Hg. The lung compliance showed a remarkable increase over both the control and postinfusion levels. The hypothesis is advanced that a reflex may be responsible for the observed changes; it is suggested that the effect of atropine on the pulmonary vessels is mediated through a reduction of the lntravascular pressure, which is ascribed, in turn, to the parasympatholytlc action of the drug that apparently improves the ventricular performance under these circumstances.