Neurologic findings characteristic of the impending hepatic coma syndrome occur in some cirrhotic patients treated with diuretic agents that may induce potassium losses (1-5). Even when diuretic agents are not employed, hypokalemia may be associated with this syndrome (6-8). Patients demonstrating these signs often improve after treatment with potassium salts. This result of therapy might indicate that potassium deficiency per se is a pathogenetic factor in the impending hepatic coma syndrome (9). Because of the extensive evidence relating abnormalities in nitrogen metabolism to hepatic coma (10), however, it seemed possible that some derangement of nitrogen metabolism might be associated with potassium deficiency.This hypothesis, relating potassium deficiency indirectly to the hepatic coma syndrome by an influence this cation has on ammonium metabolism, provided the rationale for undertaking this investigation. The relation of potassium to ammonium metabolism was studied in patients with cirrhosis of the liver and ascites rendered acutely potassium deficient by a diuretic regimen. The results of these studies demonstrate that metabolism of ammonium by the kidney is altered in potassium-deficient patients and that significant quantities of ammonium may be delivered to the cir-* A preliminary report of this investigation was included in the proceedings of the American Association for Study of Liver Disease, Chicago, 1959 (Gastroenterology 1960, 38, 803).

Although many published studies relevant to the effects of exercise on the gross pulmonary hemodynamics of patients with heart disease are available in the literature, few data are to be found which deal with normal man (1-6). There have been conflicting claims that there is no increase, no significant increase, a consistent increase, or an occasional decrease in the pulmonary artery pressure of normal man as the result of exercise loads eventuating in oxygen uptakes up to 400 ml. per M.2 per min. (2) and pulmonary blood flows two to three times the resting basal levels (1, 5). Moreover, comparison among the published data is difficult because of variations in the exercise posture, the duration of exercise, the work loads employed, and the timing of blood and pressure sampling, which often are varied in different subjects within the same body of data.Slonim, Ravin, Balchum, and Dressler (6) alone have systematically studied the continuous pulmonary artery pressure variations in 5 normal subjects in the recumbent position over a 7-minute period of exercise, employing an almost uniform work rate between 784 and 840 foot-pounds per minute. These authors noted immediate increases in pulmonary systolic, diastolic and mean pressures, which usually reached a peak between the first and third minutes of exercise with an overall tendency to a slight secondary decline by the sixth minute. A steady state was not achieved.The present report is intended to extend these findings employing a mild and uniform external work load of 850 foot-pounds per minute sustained over a period of 39 minutes. This mild amount of work was selected in order that steady state be attained in a reasonably uniform period of time, 1 Supported by a grant from United Appeal, Lorain County, Ohio. that it be maintained as long as possible, and that some lower limit of valid, measurable change be established for comparison in subjects with heart disease physically unable to exercise at higher work loads and achieve the steady state (7). MATERIALS AND METHODSStudies were conducted on 12 subj ects with normal cardio-respiratory systems who had convalesced from various illnesses (bronchopneumonia, active peptic ulcer, eczematoid dermatitis), or had been admitted for investigation of minor complaints. None were anemic or febrile. All had been ambulatory for several days before the studies were conducted. On the day prior to the experiment the subjects were exercised in the supine position at a standard work rate of 850-foot pounds per minute for a period of 39 minutes. In all but three instances the steady state, as determined by repetitive determinations of the oxygen consumption (8), was attained within 10 to 12 minutes of exercise; in the remaining three, it was attained at the 12 to 14-minute period. The following morning, at an ambient temperature of 23 degrees C., cardiac catheterization was performed in the post-absorptive state with mild sedation (Pentobarbital Sodium, 0.1 Gm.), employing standard No. 7F Cournand catheters. The supine position was...

Purified natural decapeptide angiotensin was infused intravenously at a constant rate for 32 minutes in 5 normotensive subjects. There was no significant change in the cardiac output. There were significant increases in the pulmonary artery, the pulmonary wedge, and the brachial artery pressures. There were significant increases in the systemic vascular and the total pulmonary resistances. There was no significant change in the pulmonary arteriolar resistance. The data indicate that angiotensin I produces peripheral arteriolar constriction and fail to demonstrate a concomitant pulmonary arteriolar constriction. Thus, they are consistent with an hypothesis implicating angiotensin as a causative agent in human essential hypertension.

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After a lapse of some years, surgeons and anesthesiologists alike are re-exploring the use of high spinal anesthesia, which is designed to produce a "useful" hypotension coupled with maximal relaxation. In the present study the hemodynamic changes induced by low and high spinal anesthesia, the latter arbitrarily defined as ablation of sympathetic, sensory and somatic nerves fibers above the fourth dermatomic segment, have been investigated in a series of waking patients not undergoing surgery.