The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

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.

The effect of blood transfusion or hemorrhage on the venous return curve has been studied in 10 dogs with normal circulatory reflexes and in 10 additional areflex dogs. At all right atrial pressures transfusion increased the venous return and hemorrhage decreased it. Following transfusion the venous return remained elevated only transiently, returning progressively toward the control value during the ensuing 10–20 minutes. Following hemorrhage, however, the venous return remained depressed for prolonged periods of time. The same effects were observed after infusion of Tyrode's solution as after transfusion of blood.

The circulation of dogs was stopped by fibrillation of the heart, and needle pH electrodes were placed in various tissues of dogs. The pH electrodes were connected to a continuous recording pH meter and the pH of the tissues was measured for a period of 1 hour following circulatory arrest. A few incidental studies on metabolic inhibitors, hypothermia and alkalinizing agents were made in addition to studies on the normal animals. It was found that the initial pH in the normal animals was 7.2–7.3, but within a short period of time decreased to values lethal to an animal with a normal circulation. The cerebral cortex showed the most rapid decrease in pH following circulatory arrest. The injection of sodium bicarbonate before circulatory arrest was of little value in preventing the development of acidity. Oxythiamine was effective in preventing the development of severe acidity but appears of little practical use. Hypothermia to 25°C proved effective in retarding the development of severe acidity in the two animals studied.