Although it has been recognized for some time that anoxia may result in an elevation of the pressure in the pulmonary artery, the mechanism of this response has not been satisfactorily explained.Von Euler and Liljestrand (1) in 1946 demonstrated in anesthetized cats that breathing 10%o to 11 %7o oxygen in nitrogen caused a rise in pulmonary artery pressure which was not affected by vagotomy or excision of the stellate ganglia, and which they therefore attributed to a direct effect of anoxia on the pulmonary vessels. Although left atrial pressure was sometimes recorded directly (2), no measurements of cardiac output were made, so that the pressor effects of changes in vascular resistance could not be separated conclusively from those due to variations in blood flow.Motley and his associates (3) in 1947 demonstrated the pulmonary hypertensive effect of anoxia in five unanesthetized human subjects, using the technique of cardiac catheterization. A slight fall in cardiac output occurred simultaneously with the rise in pulmonary arterial pressure and an inverse relationship between the two was suggested. Nevertheless, the two possible mechanisms of (a) stasis in the smaller pulmonary vessels associated with a decreased output of the left ventricle, or (b) pulmonary arteriolar constriction, could not be segregated except by inference.Recent reviews (4-6) of the pulmonary circulation in general, have accepted the role of anoxia in the pathogenesis of pulmonary hypertension, and have implied that the mechanism involved is pulmonary vasoconstriction. However, vasoconstric- tion with an increase in the pressure gradient and resistance to blood flow across the human pulmonary vascular bed has heretofore not been conclusively demonstrated to result from anoxia.The study of pressure in any closed fluid system requires not only a quantitative knowledge of the flow through the system, but an understanding of the resistance to that flow. In analyzing the resistance to the flow of blood from the pulmonary artery through the lungs to the left ventricle, the factor of left atrial or pulmonary venous pressure must be segregated from pulmonary vascular resistance. Without knowledge of the pulmonary venous or "capillary" pressure, it cannot be determined whether changes in pulmonary arterial pressure, themselves, are due primarily to changes in cardiac output or to variations in pulmonary arteriolar resistance.In 1948 Hellems and co-workers (7) described a method for determining pulmonary "capillary" pressure in man and have since given adequate proof that this pressure varies with the pulmonary venous pressure (8). When the pulmonary artery pressure, the pulmonary "capillary" pressure, and the cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (9).It should be emphasized, as is mentioned by Dexter and his co-workers (10), that the term "arteriolar" resistance is used in the physiological sense, since no vessels having the anatomical characteristics of systemic arterioles are found in ...

It has been generally believed that the autonomic nervous system plays an insignificant role in the regulation of pressure within the pulmonary or lesser circulation. In 1939, Hamilton (1) studied the effect of various drugs upon the pulmonary arterial and venous pressures in unanesthetized dogs. He concluded that there was no evidence of autonomic control of the pulmonary circulation. Dirken and Heemstra (2), however, in 1948 found that resection of part of the sympathetic trunk increased pulmonary blood flow in rabbits. They found that vagotomy had no effect upon pulmonary flow.Without knowledge of the pulmonary venous or "capillary" pressure, one cannot ascertain whether changes in pulmonary arterial pressure are due primarily to a change in cardiac output or to a variation in pulmonary arteriolar resistance. Until recently, the study of autonomic regulation of pulmonary blood flow in man could not be undertaken because of the lack of a satisfactory method of measuring pulmonary venous pressure, except in an occasional case of atrial septal defect. In 1948, Hellems and co-workers (3) described a method for determining pulmonary "capillary" pressure and have since given adequate proof that this pressure varies with the pulmonary venous pressure (4). When the pulmonary artery pressure, pulmonary "capillary" pressure, and cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (5).With the foregoing in mind, it was decided to determine the effect of the autonomic blocking agent, tetraethylammonium chloride (TEAC), upon the pulmonary arteriolar resistance in man; this report describes the results of such studies. MATERIALIt was thought that patients having pulmonary hypertension would be more likely to show a lowering of pulmonary pressure following autonomic blockade by tetraethylammonium because the effect of such blockade is much more pronounced in the systemic circulation when hypertension is present (6). A total of 15 patients were studied. Five were normal; two had pulmonary emphysema; two, congestive heart failure; one, active pneumonia; three, hypertensive vascular disease; one, bronchiectasis; one, diaphragmatic hernia with cor pulmonale. METHODThe majority of the patients were studied in the fasting condition. Cardiac catheterization was performed by the method of Cournand and Ranges (7). A double lumen catheter was used in order that pulmonary "capillary" pressure and pulmonary arterial pressure could be measured simultaneously. Pulmonary "capillary" pressure was obtained by the method of Hellems and his associates (3). The catheter was advanced into a branch of the pulmonary artery as far as possible, so that the branch was occluded and the pressure distal to the point of occlusion was obtained. Resting cardiac outputs were obtained usually after the catheter had been in place 15 to 30 minutes or more.

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