The characteristic intracardiac pressure patterns of four patients with constrictive pericarditis are described. The significance of a high ratio between right ventricular end-diastolic and systolic pressure is demonstrated. Postoperative changes are described in one patient and the mechanism of the production of the pressure patterns is discussed.

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During the past five years, circulatory effects of intravenous hexamethonium have been studied in normal subjects and in patients with various cardiac diseases (1-10). With adequate doses of the drug a significant reduction of the systemic blood pressure was observed in almost all cases. In many patients, particularly those with pulmonary hypertension, a reduction of the pulmonary artery pressure was also seen. However, the pulmonary "capillary" or pulmonary artery wedge pressures were recorded in only a small number of cases and changes of resistances in the pulmonary circuit were seldom studied.The purposes of this paper are: 1) to report the hemodynamic effects of hexamethonium in a series of patients with mitral stenosis, 2) to discuss the probable mechanism of the changes of the resistances and pressures in the pulmonary circuit of these patients, and 3) to stress the therapeutic benefit of hexamethonium in patients with acute pulmonary edema secondary to mitral stenosis. CLINICAL MATERIAL AND METHODTwenty-seven patients with predominant mitral stenosis were studied. There were 10 males and 17 females. Their ages ranged from 13 to 58 years. None of the patients had a significant degree of mitral insufficiency, a demonstrable lesion of other valves, or systemic hypertension.1This study was supported in part by a grant-in-aid (H 222 C7) from the National Heart Institute of the National Institutes of Health, by a grant from the American Heart Association and New York Heart Assembly, and by the Hochstetter Fund and Ernest L. Woodward Fund.2Present address: Department of Physiology, Dartmouth Medical School, Hanover, N. H.8 Postdoctoral Research Fellow, National Heart Institute, United States Public Health Service (1956)(1957)(1958). 4 Trainee, National Heart Institute, United States Public Health Service (1956Service ( -1957.The patients were studied two to three hours after a light breakfast. In all cases 100 to 200 mg. of methyprylon (Noludar®) 5 was given by mouth as premedication.The methods of determining the cardiac output and recording blood pressures have been described in detail in several previous papers (11)(12)(13)(14). The formulae used to derive the resistances and ventricular work against pressures and mitral valve flow were adopted from the papers by Gorlin' and his co-workers (15, 16). The mean pressures were measured by planimetric integration. Pulmonary "capillary" pressure was substituted for pulmonary venous and left atrial pressures. Pulmonary vascular resistance is the resistance between pulmonary artery and pulmonary vein. Total pulmonary resistance is the resistance between pulmonary artery and a hypothetical sink at atmospheric pressure. The difference between total pulmonary resistance and pulmonary vascular resistance is termed "left heart resistance" instead of "mitral valve resistance" (17, 18). It includes the resistance at the mitral valve as well as the resistance to filling offered by the left ventricle in diastole. In patients with pure mitral stenosis, however, most of the ca...

The main thesis of this paper is the "dynamic equilibrium" between body protein and plasma protein. A steady state or balance exists between the body protein stores, protein wear and tear, and protein production. Protein production includes the plasma proteins which probably represent the largest fraction of new formed protein. Body protein reserve stores are largely intracellular. We believe the plasma proteins are the means of a fluid interchange between reserve stores and the organ cells in which protein is produced, modified, and utilized in the body economy. The term "protein pool" suggests this fluid exchange within the body.Earlier experiments in this laboratory showed that plasma protein as plasma as the sole source of protein given by vein could maintain nitrogen equilibrium for 2 to 4 weeks (3, 11, 13). The last report (3) showed evidence of some "intoxication" which developed in two of these experiments. An attempt to reproduce this "intoxication" in the experiments tabulated below was not successful, and we are inclined to explain the "intoxications" previously described. as due to contaminated plasma or vitamin deficiency or both. The experiments given below are quite satisfactory and diet deficiencies were guarded against. The plasma was handled with more complete asepsis so we conclude that "intoxication" as described (3) is not an inevitable part of the experiment when large volumes of dog plasma are givenparenterally.In several experiments in other series at various intervals the dog's circulating plasma was fractionated and various elements estimated after the parenteral injection of plasma had been started--e.g., fibrinogen, globulins, albumins using coagulation, chemical methods, and electrophoretic technique. No uniform deviation from the normal plasma protein pattern was observed. Depleted dogs have a tendency to show some increase in globulins at the expense of albumins. It seems to us that the behavior offibrinogen is a very good illustration of the fact that long continued plasma given over months does not modify significantly the level of any plasma protein in the circulation. Fibrinogen is a very special protein used in the body for the production of blood clots. Yet obviously it is used in the body economy presumably within ceils to supply special cell needs (other than coagulation) since otherwise the fibrinogen