Pharmacodynamically induced changes in left ventricular work, using an intravenous infusion of Hypertensin, were studied in intact anesthetized dogs. Coronary and systemic hemodynamics and cardiac metabolism under a combined morphine- "Dial" -urethane-pentobarbital-sodium (MDUP) anesthesia were measured during the action of the drug. The significant hemodynamic changes induced were increased mean arterial pressure and increased left ventricular work. A greater cardiac lactate utilization during the Hypertensin infusion was the only change in cardiac metabolism. The oxygen tension in left ventricular venous blood was not reduced during the action of the drug.
Q UANTITATIVE measurement of coronary blood flow by indicator-dilution methods has been attempted by various groups within the past five years. The theory upon which these studies have been based is that after injection into either the pulmonary artery or left ventricle, the first activated blood to reach the right ventricle on recirculation returns by way of the coronary vessels. 1Henly and eo-workers rapidly injected a bolus of I 131 human serum albumin into the distal pulmonary artery and monitored the curves in the right side of the heart.2 The resulting calculations gave coronary-flow values averaging less than 5 per cent of the cardiac output. No standard was used for comparison. Precordial counting to approximate coronary blood flow has been investigated by Love and Burch and compared with a direct method of measuring the blood emptying from the coronary sinus, using an infusion of the radioactive tracer. Supported in part by a research grant (H1817) from the National Heart Institute, U.S. Public Health Service, and in part by grants from the Tobacco Industry Research Committee (QH17), the Committee on Problems of Alcohol of the National Academy of Sciences-National Research Council (UV25), Ciba Pharmaceutical Products Inc., and the Heart Association of Southeastern Pennsylvania.A preliminary report of this investigation was made by Ivan E. Forte on April 12, 1960, before the American Physiological Society at Chicago, Illinois (Fed. Proc. 19: 90, 1960).Dr. Schmitthenner was a Postdoctoral Research Fellow of the National Heart Institute (HF6498) at Lankenau Hospital, Philadelphia, Pennsylvania, 1956-1958 Received for publication November 14, 1960. possible, by injecting a radioactive bolus into the left side of the heart, to record an isotopedilution curve in the blood of the coronary sinus draining the left ventricle, and if so, is this dilution reflected in the proximal pulmonary arterial circulation curve or in a precordial curve? (b) If such curves following bolus injection into the left side of the heart are meaningful, how does the quantitative estimate of the myocardial blood now and of its ratio to the cardiac output, similarly derived, compare with a blood-flow value recorded almost simultaneously by the nitrousoxide desaturation method, and what fraction of the Fick cardiac output is this value ? Injections were made into the distal pulmonary artery, aortic root, left ventricle, or coronary artery. As to question (b), our familiarity with the application and use of the formulas for the nitrous-oxide technique and Fick cardiac output during the past few years afforded the opportunity to compare calculated isotope-dilution formula values. It was in this way that the indirect nitrous-oxide method was calibrated against direct measurement of coronary blood flow by moans of a bubble flowmeter. 4 However, no formulas have been found which, when applied to our data, have yielded acceptable fractions of the cardiac output. Therefore, the present report deals with our interpretation of question (a) ab...
The authors of the second edition of The Pharmacological Basis of Therapeulics state: "There is no proof that the use of tobacco causes arteriosclerosis or results in angina pectoris. However in a rare individual, who already has coronary sclerosis and angina pectoris, over-indulgence in tobacco may occasionally be a factor in precipitating anginal attacks. It is probable that the nicotine-inducedincrease in blood pressure and in heart rate is the basis for the occasional precipitation of an anginal seizure by smoking."' In so far as we are aware the mechanism of anginal seizures has not been precisely defined in terms of the physiological derangements.In order to obtain more information on this problem, a study of cardiac metabolism was designed, using intravenous infusions of nicotine in intact but anesthetized animals, each dog serving as its own control and returning several times for retesting. Our objective was to simulate in this preparation, under morphine-Dial-urethane-pentobarbital anesthesia (MDUP), a type of investigation that might later be pursued in patients. Specifically, we measured coronary blood flow, using the nitrous oxide desaturation method, cardiac oxygen, glucose, lactate, and pyruvate utilization and left ventricular pressure work in young, healthy dogs with normal coronary arteries. Measurements were made before and during infusions of nicotine that were anticipated to increase heart rate and left ventricular work. The results are compared with data obtained in if study of a newly syiithesised pressor substance Hypertensin I1 peptiden,$ the same animals and the same experimental design being used in the latter series of experiments under MDUP anesthesia. Hypertensin did increase left ventricular work significantly in this preparation.We asked this question: When the work load of the left ventricle is increased acutely by an infusion of nicotine or Hypertensin, is the myocardial oxygen extraction coefficient [(A-VIA) x 1001 increased, unchanged or reduced? Put another way, the question asks whether, during the action of nicotine or Hypertensin, the heart muscle is able to increase its oxygen uptake without reducing the cardiac capillary mean oxygen tension as this might be reflected in cardiac venous blood.
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