Nor-epinephrine is a sympathomimetic drug similar in structure to epinephrine, but lacking a methyl group on the nitrogen atom contained in the latter compound (1). Its levo-isomer is twice as active as the optically inactive preparation. Some investigators believe that 1-nor-epinephrine is identical with sympathin E (1); others feel that it is more likely that nor-epinephrine is the precursor of epinephrine at adrenergic nerve endings (2, 3). Goldenberg and associates (1) found that in man l-nor-epinephrine increases total peripheral resistance, and in further contrast to epinephrine, does not increase the cardiac output. Goldenberg also (1) found a consistent elevation in pulmonary artery pressure during the infusion of l-nor-epinephrine in man. However, since he did not measure pulmonary venous pressure, one cannot determine from his study the primary site of action of l-nor-epinephrine in producing transient pulmonary hypertension. For these reasons it seemed desirable to investigate further the action of l-nor-epinephrine upon the pulmonary circulation.The purpose of the study reported here is to determine how l-nor-epinephrine produces pulmonary arterial hypertension in man. In man the pulmonary venous pressure may not ordinarily be measured directly. However, Hellems and coworkers (4) have described a method of obtaining pulmonary "capillary" pressure, and have shown that in animals the pulmonary "capillary" pressure varies with the pulmonary venous pressure. If pulmonary artery pressure, pulmonary "capillary" pressure and cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (5 terial constriction, then a rise in pulmonary arteriolar resistance is to be expected during the pulmonary hypertension resulting from its exhibition.
MATERIALThirteen subjects were studied. Eleven had normal hearts as shown by physical examination, X-ray, and the electrocardiogram. One (E. B.) was convalescing from beriberi heart disease, with only residual tachycardia. One (C. F.) had a systolic murmur at the cardiac apex and a pulmonary "capillary" pressure tracing suggestive of incompetency of the mitral valve (6). C. F. had also moderate elevation of the mean pulmonary arterial pressure while in the resting state. As controls, six subjects with various types of cardio-pulmonary disease were studied.
METHODAll subjects except E. B. were studied in the fasting condition, sedated by 0.1 or 0.2 gm. of seconal given two to two and a half hours prior to study. Cardiac catheterization was performed as described previously (7). A double lumen catheter was used, so that pulmonary "capillary" pressure and pulmonary arterial pressure could be measured simultaneously. Pulmonary "capillary" pressure was obtained by the method of Hellems and co-workers (4). The criteria of satisfactory pulmonary "capillary" pressures were (1) the nature of the pressure curve, showing "a" and "c" waves; (2) the peripheral location of the catheter tip in the lung; and (3) the securing of a specimen of blood satur...