Raymond Gregory

Comparison of the effects of pressor and depressor agents and influences on pulmonary and systemic pressures of normotensive and hypertensive subjects.

Abstract The comparative effects on the systemic and pulmonary arterial and capillary pressures of various pressor and depressor agents, including angiotonin, and psychogenic pressor influences have been studied. These measurements have been made on eleven patients with normal blood pressures and eleven patients with essential hypertension. Epinephrine, norepinephrine, Methedrine, ephedrine and angiotonin produced an elevation of systemic, pulmonary arterial, and pulmonary capillary pressures. The PA m -PC m gradient was not significantly changed as a result of any of the agents used. We interpret this to be due to either pulmonary vascular constriction beyond the tip of the catheter, pulmonary venous constriction, or both, rather than to an increased pulmonary blood volume secondary to left ventricular failure. We particularly wish to emphasize that angiotonin elevates the pulmonary artery and capillary pressures. It is further emphasized that pulmonary artery pressure in essential hypertension is normal. Pitressin does not cause an elevation of pulmonary artery pressure in either normotensive or hypertensive patients. All the depressor agents used caused a decrease in the systemic and pulmonary arterial pressures in both normotensive and hypertensive subjects. With the exception of Pitressin, the systemic and pulmonary arterial systems reacted similarly to both pressor and depressor drugs. The data presented do not support the concept that essential hypertension is due to angiotonin or epinephrine-like substances. The possibility that a humoral substance may cause essential hypertension is supported by the effects of Pitressin which causes selective elevation of systemic arterial pressure. The selective systemic hypertension produced under hypnosis is consistent with a possible central neurogenic mechanism for producing essential hypertension.

Effects of pressor and depressor agents on pulmonary and systemic pressures of normotensives and hypertensives.

Summary and Conclusions The pulmonary and brachial artery pressures and their responses to pressor and depressor agents have been studied in normotensive and hypertensive subjects. Pulmonary artery pressure is within the same range in both groups. The response of pulmonary artery pressure to pressor and depressor agents used is also the same in both groups. It is emphasized that the elevation of pulmonary artery pressure due to angiotonin, epinephrine, and nor-epinephrine is the same in hypertensive and normotensive subjects. It is concluded that none of these or any similarly acting substances plays a part in sustaining the blood pressure elevation in patients with chronic essential hypertension.

Effect of insulin hypoglycemia on eosinophiles and lymphocytes of psychotics.

Summary Insulin hypoglycemia causes in schizophrenics a significant eosinopenia and lymphocytopenia, which is considered to be indicative of adrenocortical stimulation. Insulin does not produce such changes if hypoglycemia is prevented.

Effect of Insulin, Glucose, and Glucose and Insulin on the Rate of Metabolism of Ethyl Alcohol.

Conclusions There is no evidence from 24 experiments in 6 dogs that insulin, glucose, or insulin plus glucose increases the rate of metabolism of ethyl alcohol.

Effect of vagal stimulation on blood glucose.

There are conflicting reports in the literature concerning the influence of the vagus nerves on insulin secretion. Some reports 1 , 4 support the idea that vagal stimulation increases the pancreatic output of insulin. Other work 5 , 6 , 7 fails to substantiate this point of view. Even with the marked increase in sensitivity to insulin due to hypophysectomy, Keller 8 was unable to produce hypoglycemia in the dog by faradic stimulation of the distal end of the vagi sectioned in the upper abdomen. These conflicting reports and the studies of Portis and Zitman 9 who attempt to explain the clinical syndromes of weakness and fatigue in psychoneurotic patients on the basis of a vagal induced hyperinsulinism led us to make the following experiments. Under sodium pentobarbital anesthesia one or both vagus nerves were isolated in the neck. The right vagus was stimulated alone in some dogs; the right and left vagi were stimulated consecutively in some dogs; and the right and left vagi were stimulated simultaneously in some dogs with the tetanizing faradic current. Stimulation was of sufficient strength to cause a marked slowing of cardiac rate as a criterion of vagal effects. Stimulation was continued from 40 minutes to 5 3/4 hours. Vagal stimulation was continuous except when asystole, cyanosis, apnea, retching or restlessness necessitated either decreasing the current or stopping the stimulation for periods not exceeding 2 minutes in any dog. Insulin was given subcutaneously to 2 dogs, as indicated in Table I, to be sure that neither the anesthetic nor the vagal stimulation prevented insulin hypoglycemia. The detailed results are recorded in the table. Results. When insulin was given subcutaneously to Dog 8 during pentobarbital anesthesia, the usual hypoglycemia resulted. Similarly, when insulin was given subcutaneously to Dog 7 after 3 hours of vagal stimulation, and during continuation of the stimulation, the usual hypoglycemia resulted. This indicates that neither sodium pentobarbital nor vagal stimulation interferes with production of insulin hypoglycemia.

A Quantitative Study of the Pettenkofer Reaction for Bile Salts.

As originally described this is a qualitative test for bile salts and is performed by dissolving a small amount of bile, or, the bile containing fluid, in concentrated H2SO4 and adding a few drops of a 10 per cent solution of cane sugar. In the presence of bile salts the solution assumes a red-purple color which approaches a violet within the course of a day. As shown by a number of investigators, the reaction may be satisfactorily carried out in a 50 per cent H2SO4 solution. In attempting to use the Mylius modification of the Pettenkofer reaction quantitatively, which employs furfural instead of cane sugar, it was never possible to obtain color matches. It has been found that by performing the reaction in weaker concentrations of H2SO4 (30 to 40 per cent) a blue color is developed. This color is due to an absorption bond at 6200 A and seems suitable for quantitative colorimetric determinations. Color matches are easily obtained when the solution being tested contains twice as much bile salt as the standard. When the tested solution is within 50 per cent of the strength of the standard the error is never greater than 5 per cent. It is usually about 2 per cent. This error increases to 10 per cent when the tested solution differs from the standard by 100 per cent. Glycocoll, taurine, cholesterol, a cholesterol ester (lanodin), lecithin, kephalin, and oleic acid do not give any color reaction in the weaker H2SO4, solution mentioned. Oleic acid and the phosphatides are known to give a red color when the reaction is carried out in higher concentrations of H2SO4. Isobutyl and amyl alcohol also give a red color reaction with furfural in SO per cent H2SO4.