In 97 dogs left atrial pressure was elevated to various levels up to 50 mm. Hg by partial constriction of the aorta. The effect of these pressures for from 30 min. to 3 hours on the accumulation of lung edema was then studied. Edema was estimated by determining the ratio of the weight of the wet lung to the weight of the same lung after drying. In animals with normal plasma protein concentrations fluid began to transude into the lungs when the left atrial pressure rose above an average of 24 mm. Hg. In another series of animals the plasma protein concentrations were reduced by plasmapheresis at the beginning of each experiment until the plasma protein concentration averaged 47 per cent of the control value. In these animals fluid began to transude into the lungs when the left atrial pressure rose above a critical value of 11 mm Hg. Furthermore, the rate at which fluid accumulated in the lungs, in all series of experiments, was directly proportional to the rise in left atrial pressure above the critical pressure at which fluid began to collect in the lungs.

Effect of Elevated Left Atrial Pressure and Decreased Plasma Protein Concentration on the Development of Pulmonary Edema

Over 200 perforated plastic capsules were implanted in different tissues of the dog, and the wounds were allowed to heal. After one month, pressures measured by inserting a needle through the skin and then through a perforation of the capsule into its cavity were always negative in normal tissues, averaging-6.4 mm Hg. The pressure was always positive in edematous tissues. Evidence is presented to indicate that the pressure measured in the capsule is equal to, or nearly equal to, the interstitial fluid pressure in the tissue spaces surrounding the capsule. On the other hand, pressure measurements made by a needle technic failed except in rare instances to give negative values in normal tissues but in edematous tissues gave almost exactly the same values as those recorded by the capsules. Also, pressures measured by the capsules changed in accordance with Starling9s law of the capillaries when (a) venous pressure was raised, (b) when arterial pressure was lowered, (c) when the tissues were dehydrated by intravenous infusion of dextran, or (d) when the tissues were hydrated by intravenous infusion of saline. Pressures measured by a needle technique failed to change in accordance with this law in these same experiments. Therefore, it is concluded that needle pressure determinations in non-edematous tissue do not measure the interstitial fluid pressure.

A concept of negative interstitial pressure based on pressures in implanted perforated capsules.

Except for the electrocardiogram objective evaluation of the functional state of the coronary circulation in man is often difficult. The nature of the coronary circulation in the presence of known coronary insufficiency has not been evaluated. In this report, 17 patients were studied of whom 14 had angina pectoris. Observations were made of coronary blood flow and hemodynamics both at rest and following administration of nitroglycerin. The authors conclude that resting coronary flow is normal, but cannot increase further with dilators. They consider this phenomenon a consequence of prior exhaustion of the dilator capacity of the arterioles in compensation for the atherosclerotic obstruction of the coronary tree. The "fixed flow" concept is suggested as an objective means of detecting coronary insufficiency. Nitrites probably relieve pain in some manner other than general coronary dilatation.

Effect of Nitroglycerin on the Coronary Circulation in Patients with Coronary Artery Disease or Increased Left Ventricular Work

It is known from previous investigations (Lewis et al. 1953) that patients with coronary heart disease, previous myocardial infarction, and an enlarged heart may show the usual signs of left ventricular failure with increased pulmonary vascular pressures and a tendency to reduced cardiac output. To our knowledge, no systematic investigations of cardiac output and pressures in the lesser circulation have been made in patients with coronary heart disease and a normal-sized heart, with anginal pain as the main symptom. Nor have any observations been published from the same patients when free from pain and when complaining of pain, either spontaneous or induced by exercise. It is generally believed that the administration of nitro-glycerine leads to a dilatation of coronary vessels. An increase in coronary blood flow subsequent to nitro-glycerine has been demonstrated in animals (Gregg, 1950), and its effect on anginal pain due to coronary heart disease in man has also been attributed to its influence on the coronary blood flow (Wayne and Laplace, 1933; Russek et al., 1955). However, there are no observations by cardiac catheterization on the effect of nitro-glycerine on the left ventricular function and the lesser circulation in man. This research has been designed to fill these apparent gaps.

https://heart.bmj.com/content/heartjnl/20/3/302.full.pdf

R.J. Spiegl

Papers

Factors regulating pulmonary “capillary” pressure in mitral stenosis. IV

The effect of chronic pulmonary disease (cor pulmonale and hypoxia) on the dynamics of the circulation in man.