The normal venous return curve has been determined in 12 open-chest dogs with intact circulatory reflexes and in 14 open-chest areflex dogs. These curves show that venous return reaches a maximum value when the right atrial pressure falls to –2 to –4 mm Hg and remains at this maximum value down to infinitely low negative pressures. As the right atrial pressure rises to positive values venous return falls and reaches zero when the right atrial pressure has risen to equal the mean circulatory pressure. A venous return curve for the normal, intact dog has been tentatively formulated on the basis of these studies and previous studies in which individual points on the venous return curves of intact dogs have been measured.

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. Despite this recent emphasis on pulmonary capillary pressure in relation to pulmonary edema, precise studies describing the dynamics of fluid exchange at the capillary membrane of the lungs have not been reported. For this reason we undertook the present project, in which the left atrial pressures of dogs were held at elevated but constant levels for long periods of time. In each dog the degree of fluid accumulation in the pulmonary tissues was assessed as accurately as possible. In an additional group of dogs the plasma protein concentration was decreased to approximately one half normal at the beginning of each experiment and the same studies with elevated left atrial pressure were repeated. Thus, in these two groups of experiments the effects of both pressure and plasma protein concentration on the dynamics of fluid exchange have been studied.

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The ability of the right ventricle to compensate as the pulmonary artery is constricted appears to be determined by four major factors: (I) there occurs the well-known increased force of contraction as the right heart becomes distended; (2) the adequacy of the coronary circulation determines to a great extent the degree of pulmonary arterial constriction which can occur before failure occurs;(3) the circulatory reflexes apparently aid the compensation to a moderate extent; and (4) the greater the blood volume, the greater is the limit of compensation before right ventricular failure occurs.T H E effects on the dynamics of circulation of progressive pulmonary embolism and progressive constriction of the pulmonary artery have been investigated numerous times. 1 " 4 These previous investigations have demonstrated clearly the following basic principles of right ventricular compensation when pulmonary resistance is increased: First, even the slightest pulmonary embolism or slightest constriction of the pulmonary artery causes an increase in the pulmonary arterial pressure proximal to the constriction but little change in the pulmonary arterial pressure distal to the constriction. Second, for the first few ensuing heart beats following acute increase in pulmonary circulatory resistance, the right ventricle progressively dilates, and there occurs a concurrent increase in the right ventricular systolic pressure associated at first with only minor changes in enddiastolic pressure but followed later, as the right ventricle fails, by a pronounced rise in the end-diastolic pressure. Third, it has been pointed out in several studies that the pulmonary artery must be occluded approximately 60 per cent of its total cross-sectional area before the right ventricular end-diastolic pres-

The effect of epinephrine on venous return has been measured in 11 dogs under total spinal anesthesia. The mechanism by which epinephrine increases venous return seems to be to increase the tone of the vascular walls thereby increasing the mean circulatory pressure. This in turn increases the pressure gradient forcing blood from the systemic vessels toward the right atrium. By equating the recorded venous return curves with curves that depict the effect of epinephrine on the heart's ability to pump blood, it is shown that under normal operating conditions cardiac output is determined far more by the tendency for blood to return to the heart than by the heart's ability to pump blood.