René Wégria

An experimental study of the immediate hemodynamic adjustments to acute arteriovenous fistulae of various sizes.

In the past thirty years, numerous observations have been made on the hemodynamic effects of arteriovenous fistulae. Arteriovenous fistulae of variable size and location have been studied in patients as well as in animals. Such studies have consisted a) in observing the effect of suddenly opening and closing a fistula in acute experiments, b) in studying the effects of suddenly closing and opening a fistula in an animal or a patient who had had such a fistula for a relatively long time, and c) in recording the effect of complete surgical eradication of a long-standing fistula. While some agreement has been reached on many points, there persists some controversy about most of them (1). It is now generally agreed that an

Effect of aortic insufficiency on arterial blood pressure, coronary blood flow and cardiac oxygen consumption.

In patients with aortic insufficiency and without disease of the coronary ostia or arteries, the occurrence of chest pain having some or many of the characteristics of cardiac pain due to myocardial ischemia has been ascribed classically to a decrease in the coronary blood flow (1, 2), the aortic insufficiency presumably decreasing the coronary blood flow by lowering the mean aortic diastolic pressure. However, the data available on the effect of aortic insufficiency on the coronary blood flow are contradictory. From acute experiments on the anesthestized dog, Green (3), as well as Green and Gregg (4), concluded that when the aortic insufficiency is marked enough to lower the aortic diastolic pressure, the increase in coronary blood flow occurring during systole does not compensate for the decrease in flow during diastole and the mean coronary flow decreases. On the other hand, Foltz, Wendel, and West (5), from measurements made on anesthetized dogs in which one or two aortic cusps had been torn three or more days previously, concluded that the coronary blood flow was increased over levels usually observed in normal dogs while oxygen consumption was greatly increased over normal levels. Because of the discrepancy in the opinions about the effect of aortic insufficiency on the coronary blood flow, it was thought advisable to reinvestigate this problem.

THE EFFECT OF ACUTE ELEVATION OF THE PLASMA CHLORIDE CONCENTRATION ON THE RENAL EXCRETION OF BICARBONATE DURING ACUTE RESPIRATORY ACIDOSIS

It has been postulated recently that renal bicarbonate reabsorption is entirely dependent on the exchange of hydrogen ions, derived from the dissociation of carbonic acid within the cells of the renal tubule, for the fixed base of filtered bicarbonate in the tubular urine (1-3). According to this theory, an elevation of the CO2 tension of the extracellular fluid results in an increase in the rate of bicarbonate reabsorption because it leads to an increase in the rate of hydrogen ion

The benzol-adrenalin test as a reliable method of estimating changes in the sensitivity of the dog's ventricles to fibrillation. Application of the method to the study of quinidine sulfate

Abstract 1. 1. A new method of ascertaining repeatedly, in the same animal, the sensitivity of the dogs ventricles to fibrillation is presented. 2. 2. This method is easier to perform than the “fibrillation threshold test”, and yet it is critical. However, it does not quantitate the sensitivity to fibrillation. The procedure consists in comparing the reaction of the same dog to the combination of benzol-adrenalin before and after the intervention of some factor under study, such as a drug. This is done by ascertaining whether or not benzol-adrenalin, which induces fibrillation before the administration of the drug to be studied, still does so after the administration of the drug. Whether or not the sensitivity of the heart to the benzol-adrenalin fibrillation could be quantitated by ascertaining the amount of adrenalin required to produce fibrillation remains to be studied. 3. 3. Quinidine sulfate protects the dogs ventricles against benzol-adrenalin and prevents the benzol-adrenalin fibrillation, which confirms the results we obtained by the fibrillation threshold method. 4. 4. The protection exists whether or not the dose of quinidine sulfate administered diminishes the increase of blood pressure which normally occurs during a control benzol-adrenalin test.