Relation of coronary flow to oxygen supply

1960 ◽  
Vol 199 (1) ◽  
pp. 179-182 ◽  
Author(s):  
Abraham Guz ◽  
George S. Kurland ◽  
A. Stone Freedberg

Coronary flow, heart rate, myocardial oxygen consumption and Walton strain gauge tension were determined in the isolated rabbit heart perfused with hemoglobin solutions of varying oxygen content. Perfusion was carried out under constant pressure and with the hemoglobin solution in equilibrium with 3% CO2 and 97% air under atmospheric tension. Oxygen content was varied from 2 to 18 vol. % by diluting hemoglobin with Ringer-Locke solution. Change from a higher to lower oxyhemoglobin concentration resulted in increased coronary flow; the reserve led to decreased flow. Heart rate, myocardial tension and oxygen consumption were constant at oxygen capacity above 2 vol. %.

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.


1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.


1986 ◽  
Vol 250 (6) ◽  
pp. H998-H1007 ◽  
Author(s):  
C. L. Gibbs ◽  
G. Kotsanas

Basal metabolism has been measured in isolated whole hearts from rabbits and compared with myothermic and polarographic measurements on isolated papillary muscles. Hearts were perfused at constant pressure (Langendorff method) using a modified Krebs-Henseleit solution (KH) with glucose as substrate. Higher levels of basal O2 consumption (MVO2) and coronary flow (CF) were observed when arrest was induced by calcium depletion (low Ca; 0.1 mM CaCl2, 10.0 mM KCl) rather than by potassium excess (high K; 30.0 mM KCl). The metabolic rate of high K arrested hearts was close to earlier myothermic estimates (J. Mol. Cell. Cardiol. 16: 953-962, 1984); polarographic values, however, were about twofold higher, and somewhat higher than the value obtained in low Ca arrested hearts. The addition of erythrocytes, albumin, or dextran significantly reduced CF but did not substantially alter basal MVO2. Basal metabolic rate was substrate- and O2 tension-dependent, and under all experimental conditions there was linear relationship between MVO2 and CF. Extrapolations to zero flow showed that the basal MVO2 values so obtained were similar in low Ca or high K and were not altered by the presence of erythrocytes. Our results show that there are several factors regulating basal metabolism.


1983 ◽  
Vol 244 (6) ◽  
pp. H799-H806 ◽  
Author(s):  
K. A. Fox ◽  
H. Nomura ◽  
B. E. Sobel ◽  
S. R. Bergmann

Assessments of myocardial metabolism based on external detection of accumulation of radiolabeled substrates may be influenced, as a result of alterations in flow, by altered substrate delivery as well as altered work (with concomitant changes in metabolic requirements). To determine whether reduced delivery limits substrate utilization under defined conditions of reduced perfusion, an isolated rabbit heart preparation was employed in which flow was reduced but myocardial oxygen consumption (MVo2) and work were kept constant by adjustment of left ventricular end-diastolic pressure and heart rate. Flow was reduced from 1.5 to 0.5 ml . g-1 . min-1, while work was maintained constant in hearts functioning at either low or high levels of MVo2. Consumption of palmitate remained constant (48.8 +/- 11.6 and 68.8 +/- 23.3 nmol . g-1 . min-1), because the proportion of palmitate extracted increased (8.8 +/- 4 to 29.1 +/- 7.2% and 10.3 +/- 3.4 to 21.0 +/- 6.1%). The results indicate that, despite reduction of flow, hearts at constant work loads can extract increasing proportions of delivered substrates such that net utilization remains constant until flow is reduced below the level required to maintain cellular function. They suggest that, under conditions of low flow, impaired extraction of substrates reflects either primarily or secondarily depressed myocardial metabolism rather than simply decreased delivery of substrate.


1961 ◽  
Vol 16 (5) ◽  
pp. 819-826 ◽  
Author(s):  
E. F. Adolph ◽  
A. Naberschnig ◽  
D. P. Orchard

Ventilation (Vi), oxygen consumption (Vo2) and heart rate (H) were measured at esophageal temperatures (T) of 8—24 C. The trachea was cannulated; a body plethysmograph and pressure transducer registered breath volumes. Vo2 was computed from oxygen content of effluent air. Vi, Vo2, and H were each related to T by a regression of low slope from 8 to 18 C, and a high nearly-linear slope above 18∘ But the proportions among the three parameters changed; Vi was relatively less below 18∘. Breaths were increasingly irregular as T decreased below 24∘. Hypoxia induced greater Vi at 16—21∘, but not at 13∘, nor after excision of the carotid bodies. Vo2 in hypoxia was greatly reduced; at 12—17∘ a Vo2 as low as one-fifth of that in air continued for an hour. H also decreased sharply at Po2 below 50 mm Hg. Carbon dioxide induced faster Vi even at 12∘; its effects were not modified by carotidectomy. Gasps were regularly induced by hypoxia, and usually by hypercapnia; they occurred just as frequently after carotidectomy. Submitted on October 26, 1960


1961 ◽  
Vol 200 (2) ◽  
pp. 238-242 ◽  
Author(s):  
H. Feinberg ◽  
Sister Mary Alma

Ammonia production, oxygen consumption, heart rate and blood pressure were observed in the isolated working rabbit heart perfused with Krebs-Ringer solution and with Krebs-Ringer solution containing dog hemoglobin. Oxygen consumption and an index to cardiac effort (heart rate x blood pressure) were shown to be correlated. There was a lesser correlation between ammonia production and cardiac effort. The ratio, ammonia production/oxygen consumption, when both are expressed as micromoles/minute/ gram of heart weight, averaged 0.064 ± .006. Perfusate pH was altered by alternately exposing the perfusate to 95%O2– 5%CO2 and 90%O2–10%CO2. No effect on the ratio ammonia production/oxygen consumption was noted. l-Epinephrine, 0.1–1.0 µg/ml, was continuously infused and resulted in an increase in cardiac effort, oxygen consumption, ammonia production and the ratio of ammonia production/ oxygen consumption.


1959 ◽  
Vol 196 (4) ◽  
pp. 719-725 ◽  
Author(s):  
A. Gerola ◽  
H. Feinberg ◽  
L. N. Katz

Effects of hypothermia (at 32° and 27°C) were determined in the open-chest anesthetized dog prepared for measurement of total coronary flow and myocardial oxygen consumption. When hypothermia was induced at any fixed cardiac output, cardiac oxygen consumption and heart rate declined while blood pressure remained constant. Cardiac external mechanical efficiency increased at the same time. Hypothermia did not alter the relationship between the myocardial oxygen requirement and the total cardiac effort as indicated by the product of blood pressure times heart rate. Without regard to the large individual variability, the coronary venous O2 rose; thus the general trend during the induction of hypothermia was a decline in the coronary A-V oxygen difference, the percentage O2 extracted by the heart and the ratio: cardiac O2 consumption/O2 availability. The coronary venous O2 content and the coronary A-V O2 difference remained fairly constant as the cardiac effort and its oxygen requirement varied during hypothermia, just as in the control period. Thus coronary flow was the only means of adjusting to the altered cardiac oxygen need in both periods.


1958 ◽  
Vol 193 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Harold Feinberg ◽  
Louis N. Katz

The effect of continuously infused intravenous l-epinephrine and l-norepinephrine (0.1–2.5 gamma/kg/min.) was determined in the open-chest, anesthetized dog prepared for measurement of total coronary flow. Coronary blood flow, myocardial oxygen availability and coronary venous oxygen content consistently increased after catecholamine administration despite wide fluctuations, above and below control values, in heart rate and mean aortic pressure at constant cardiac output. Thus, there was a significant decrease in the coronary arteriovenous oxygen difference after catecholamine administration. The increase in coronary flow and decrease in the coronary A-V oxygen difference were seen even when blood pressure and heart rate were lowered. It is concluded that the departure from the usual relationship between coronary flow and myocardial oxygen consumption is attributable to coronary vasodilatation. However, myocardial oxygen consumption is still the primary factor controlling coronary flow during catecholamine action.


1964 ◽  
Vol 207 (3) ◽  
pp. 683-690 ◽  
Author(s):  
N. M. Buckley ◽  
E. P. Porter ◽  
L. A. Jedeikin

The effects of coronary perfusion on ventricular function have been studied in isolated ventricle preparations working under different conditions. Coronary flow, oxygen consumption, ventricular stroke work, rate of ventricular pressure change during isovolumetric contraction (dPC), and diastolic ventricular pressure (DVPm) and pressure/inflow ratio were determined. Maintenance of coronary flow and oxygen consumption in 5 experiments did not prevent irreversible changes in DVPm, stroke work, and dPC when the right ventricle was acutely overloaded. These ventricles did not accumulate water. Decreasing coronary perfusion pressure at constant arterial oxygen content in 11 experiments led to inconsistent changes in DVPm, stroke work and dPC. Decreasing arterial oxygen content at constant coronary perfusion pressure in 10 experiments led to increased DVPm but inconsistent changes in stroke work and dPC. There was an inverse relationship between DVPm and oxygen consumption in the variable perfusion experiments, but not in the overloading experiments. Ventricular function did not change significantly with time in 6 experiments in which the conditions of workload and coronary perfusion were kept constant. It was concluded that irreversible changes in performance of acutely overloaded ventricles could be independent of coronary flow, myocardial water content, or duration of experiment.


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