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.

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 Starling's 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.

In dogs with cardiovascular reflexes completely blocked by total spinal anesthesia, the total peripheral resistance was increased five- or more fold in two ways: first, by injecting small plastic microspheres into the arteries, thereby increasing the arterial resistance, and, second, by inflating pneumatic cuffs around the major veins, thereby increasing venous resistance. A small increase in venous resistance decreased cardiac output eight times as much as an increase in arterial resistance of similar magnitude. This difference was caused principally by a) a marked rise in systemic arterial pressure when arterial resistance was increased; this maintained the cardiac output at almost normal levels and b) a fall in systemic arterial pressure when venous resistance was increased; this promoted even more fall in cardiac output than increased total peripheral resistance alone would have caused.