The effects of changes in heart rate must be understood before ventricular performance can be evaluated in studies of the response to drugs, injury, or abnormal circulatory states. This report describes the effects of sudden changes in heart rate on the stroke, end-systolic, and enddiastolic volume of the canine left ventricle. The ventricular volumes were measured by thermodilution, an indicator dilution method in which injected cold blood serves as the indicator (1). METHODSThere were 160 experimental periods in 11 mongrel dogs that were anesthetized with a chloralose-urethane mixture. Aortic thermodilution curves were obtained after rapid injection of cooled autologous blood into the left ventricle. A 4F catheter with an ultrasmall bead thermistor secured to its end 1 was used to record blood temperature. It was introduced into a carotid artery and advanced so that its tip was just above the aortic valve. The time constant of this assembly was 0.12 second when tested in slowly flowing water. A 7F catheter with multiple side holes and a closed end was manipulated into the left ventricle from a femoral artery for injection purposes and to record left ventricular pressure with a strain gauge. A bead thermistor was secured within its lumen near the tip to monitor the temperature of the injected blood immediately before it entered the left ventricle. This assembly had a time constant of 0.05 second in flowing water. Inj ections were made with a metal syringe driven by compressed air that introduced a known amount, usually 3 to 5 ml, of cooled, heparinized, autologous blood into the left ventricle in less than 0.5 second. The mean temperature of the inj ected blood was determined by planimetry of the recorded temperature curve during injection. Stroke volume (SV), end-systolic volume (ESV), and end-diastolic volume (ED V) were calculated from the resultant aortic thermodilution curve sensed by the aortic thermistor catheter. The formulas used to calculate these volumes were:where Vi = volume of injected cooled blood in ml, Tb = left ventricular blood temperature before injection, T1 = mean temperature of injected blood, just before it entered the left ventricle, and 2;(ATb) = the sum of the differences between base-line aortic temperature and that resulting in the aorta from each systole, as measured at end-diastole;2) ES V/ED V = AT,+, ATn' where AT,, and AT,,+, are differences between base-line aortic temperature and that at beats n and n + 1, respectively, measured at end-diastole from the exponential step-function of the aortic thermodilution curve;3) SV ED V(ml) = ES V; EDV ESV(ml) = EDV -SV; 4) and 5) Cardiac output (L/min) = (heart rate) (S V)The details of this method have been published previously (1) -One to five determinations of left ventricular volumes, left ventricular pressure, and heart rate were made during each control and experimental period. Various heart rates faster than control were produced with a 6F electrode catheter passed up a femoral vein and placed fluoroscopically against the right...

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The effects of intravenous isoproterenol on left ventricular stroke and on end-systolic and end-diastolic volumes were studied in anesthetized dogs before and after bleeding. Volumes were measured by a thermodilution technique. In this indicator-dilution method a small amount of cooled blood is rapidly injected into the ventricle, and the washout of cold from the ventricle is sensed by a thermistor catheter at the root of the aorta. Control values showed that approximately two-thirds of the end-diastolic volume remained in the ventricle at the end of systole. Bleeding decreased all three volumes. Isoproterenol consistently increased ventricular emptying, as shown by the fall in the proportion of the end-diastolic volume which remained at end systole. This effect did not depend on an increase or decrease in the end-diastolic volume itself. End-systolic force-circumference relationships were derived from a consideration of idealized ventricular dimensions. A linear relationship between these calculated values was not altered by isoproterenol. Submitted on July 5, 1962

To study the hemodynamic effects of stimulation of the aortic and carotid body chemoreceptors, we injected 2.5– 20 µg/kg nicotine into the ascending aorta of anesthetized, artificially ventilated open-chest dogs. Pressures in the pulmonary artery, left atrium, and systemic arteries, and the stroke output of the right ventricle were measured simultaneously. Pulmonary and systemic vascular resistances (PVR, SVR) were calculated. Changes began 1.5–3.0 sec after the injection; the following two 5-sec periods were compared to a 5-sec control period immediately preceding injection. The injection of nicotine was followed by a significant reflex rise in PVR; the sensory receptors for the reflex were aortic chemoreceptors and the efferent paths were sympathetic fibers. Similar effects were not elicited by stimulation of the carotid body. Bronchoconstriction, changes in bronchial flow, shifts of blood volume between the vascular beds, and liberation of catecholamine were excluded as factors in the PVR increase. Bradycardia, increased SVR, and decreased flow also occurred after combined stimulation of the aortic and carotid chemoreceptors; however, when bradycardia was prevented by atropinization, no significant change in flow occurred.