1. In peptone shock there is a marked, precipitate fall in arterial pressure. At the same time there is a fall in venous pressure.
2. In experimental fat embolism, (a) the fall in blood pressure is always gradual; (b) approximately 1 cc. of oil for each pound of body weight must be injected before a lasting fall in arterial pressure is produced; (c) it makes only a slight difference whether this amount is injected in small doses at a time or in relatively large quantities; and (d) when the arterial pressure falls, but not till then, the venous pressure rises.
3. In peptone shock, dyspnea, by its suction and force-pump action upon the reservoir of stagnating blood in the liver, brings more blood to the heart and causes a rise in arterial pressure. By repeatedly inducing short periods of dyspnea at frequent intervals, permanently beneficial results are obtained and the life of the animal can be saved.
4. In experimental fat embolism, dyspnea will cause a rise in blood pressure. But permanently beneficial results have not been obtained by this method. If dyspnea is found to bring permanent improvement in surgical shock, it is indirect evidence that this condition is not due to fat embolism. Respiratory suction is probably not responsible for the rise in blood pressure in experimental fat embolism. It seems more likely that the dyspnea in some way facilitates the passage of blood through the embarrassed pulmonary circulation. Artificial respiration with a bellows will also frequently cause a rise in blood pressure in experimental fat embolism.
5. In peptone shock the respiration is usually not affected, although there is some evidence that the respiratory center may be in a state of increased irritability. In experimental fat embolism, in some animals a violent dyspnea develops spontaneously. This is usually accompanied by edema of the lungs. In other instances, an apnea occurs, even before the blood pressure has begun to decline.