This report describes the clinical, angiographic, and hemodynamic findings in nine patients who manifested nonatheromatous' ischemic heart disease induced by chronic industrial exposure to nitroglycerin and subsequent withdrawal. They represent nearly 5% incidence in the group of 200 workers with similar exposure. One patient died suddenly, and the disease was commonly without premonitory symptoms. Of the eight survivors, five were studied and none showed evidence of significant organic obstructive disease. However, in one studied during the withdrawal state, coronary and digital arteriospasm was demonstrated, and was readily reversed by nitroglycerin. Survivors exhibited exercise symptomatology and hemodynamic impairment similar to other patients with myocardial dysfunction from ischemic heart disease. Complete left bundle-branch block with late sudden death occurred in one, and chronic recurrent atrial fibrillation is present in a second.An attractive hypothesis suggests that chronic vasodilatation evokes homeostatic vasoconstriction, the latter persisting during the withdrawal period with cardiac ischemia. A more detailed study of the vasodilator action of organic nitrate and the homeostatic reaction is warranted. In addition, the effect of chronic administration of potent, longacting organic nitrate-based drugs should be examined in the light of this industrial experience.Additional Indexing Words: Industrial medicine Compensatory vasoconstriction Chronic vasodilator therapy Coronary artery spasm T HE ACUTE vasodilatory effects of nitroglycerin form the basis for the symptomatic therapy of angina pectoris. Daily

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A patient with chronic fibrous mediastinitis presented with bronchial, superior vena caval, and pulmonary venous obstruction, pulmonary hypertension, and pulmonary fibrosis. Pulmonary venous obstruction was confirmed at surgery and explains the hemodynamic findings of elevated pulmonary artery and pulmonary wedge pressures despite low left atrial pressure. Pulmonary function studies showed marked alterations in ventilation-distribution, diffusion, work of breathing, and fixed airway resistance. It is concluded that the pulmonary arterial hypertension was due, in large part, to the pulmonary venous hypertension caused by pulmonary venous obstruction. Unsuccessful surgical intervention has been followed by 10 months of observation during which aldosterone inhibition together with use of chlorothiazide has prevented recurrence of heart failure and pleural effusion. The relationship between the physiological abnormalities and the patient's symptoms is discussed along with the possible relationship between pulmonary venous obstruction and pulmonary fibrosis.

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The dynamic relationship between respiratory muscle effort and the consequent changes in lung volume is investigated. A mathematical simulation based on the structures that form the connection between these two variables makes it possible to lump the contribution from all respiratory muscles into a single time-varying driving force. When this force is applied to the system model, the appropriate lung volume pattern results. The simulation results indicate the accuracy of the model and the validity of the lumped muscle force assumption. In addition, the system model adequately describes abnormal conditions such as decreased lung compliance and increased airway resistance. The results of this simulation suggest that the modeling technique is extremely useful in describing and analyzing complex respiratory system interactions.

Physiologic measurements of several circulatory parameters were made in 15 normal unanesthetized calves by cardiac catheterization. Fifty-four observations were made in the ‘resting’ state during 27 separate studies. The calves were restrained in the right lateral decubitus position in a calf chute. Oxygen consumption (Vo2) was measured by collecting expired air through a cuffed endotracheal tube. Cardiac output was determined by the direct Fick (Q·f) and/or the dye dilution (Q·d) techniques. Pulmonary artery (PAP), right heart and carotid artery (CAP) pressures were measured routinely while pulmonary artery wedge, left ventricular and central aortic pressures were obtained in a few animals. Under the conditions of the study, it is unlikely that the animals were in a truly resting state. However, absence of a statistically significant difference between two consecutive measurements of various parameters in 11 studies and good agreement between 17 paired Qf and Qd determinations suggests that the animals were in a reasonably steady state. Mean ± Sx values of the more important parameters measured were as follows: Qd 7.30 ± 0.23, Qf 7.10 ± 0.42 l/min/m2; Vo2 365 ± 29 cc/min/m2; PAP 21.6 ± 1.4, CAP 131 ± 4.5 mm Hg; pulmonary vascular resistance 2.34 ± 0.27 mm Hg/l/min/m2.

Continuous infusion of norepinephrine in man caused a rise in pulmonary arteriolar resistance as measured by pulmonary artery-pulmonary wedge pressure differences. Since no change in flow occurred during the procedures, the data suggest active constriction of the pulmonary vascular bed under these circumstances.T HE capacity of small pulmonary blood vessels for vasoconstriction remains a controversial subject.1 2 Evidence is accumulating which suggests that at least under abnormal circumstances vasoconstriction of the pulmonary vascular bed may occur.3 The following is a report on changes in pulmonary arteriolar resistance (PAR) during norepinephrine infusion based on simultaneous measurements of blood flow and pressures in the pulmonary vascular system. The pulmonary arteriolar resistance depends on the physical dimensions (geometry) of the vascular bed and on the viscosity of blood (Poiseuille-Hagen equation). If one assumes that the viscosity undergoes no measurable change during administration of norepinephrine, the decisive factor responsible for a change in resistance should be a change in radius of the small vessels. A rise in pulmonary artery pressure alone would tend to dilate vessels passively and to lower the pulmonary arteriolar resistance. An increase in this resistance in the presence of a rise in pulmonary artery pressure constitutes evidence for active vasoconstriction in the pulmonary vascular bed. METHODSTwenty-one subjects were studied. Venous catheterization of the heart was performed in the usual manner. Cardiac output (Q) was deterFrom the Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah. Supported in part by a grant from the Utah Heart Association, the U. S. Public Health Service (National Heart Institute), and the Wyeth Laboratories.This work was carried out during Dr. Patel 's tenure of an American Heart Association Fellowship. mined by the Fick principle by means of gas analysis. Pressure measurements were made during the Fick determination with a Statham resistance wire transducer, the output of which was fed directly to a D'Arsonval type galvanometer and recorded photographically.' Pulmonary artery (PA) and "pulmonary artery wedge" (PA-wedge) positions were selected as 2 points between which the fall in pressure (AP) was noted. These pressures were determined in rapid succession or simultaneously by means of no.-6 catheters. The pressures measured at these points were taken to be those proximal and distal to the anatomic or physiologic locus of resistance to flow. Since simultaneous measurements of pressure from the pulmonary artery-wedge and from the left atrium have yielded identical values under many varying conditions, one may assume that the pulmonary artery-wedge pressure affords a reasonably satistory measurement of the postarteriolar pressure. A wedge position was assumed to be present when (a) the catheter could not be advanced farther, and the tip did not move with the cardiac cycle, (b) the pressure contour changed abruptly in the face ...