Cardiac performance as a function of intracellular  oxygen tension in buffer-perfused hearts

Critical intracellular myocardial oxygen tension was determined by optical spectroscopic measurement of myoglobin oxygen saturation in crystalloid-perfused guinea pig hearts. Accurate end-point determinations of the maximally oxygenated and deoxygenated myoglobin were made. Hearts were subjected to a steady decrease in perfusate oxygen tension while left ventricular developed pressure, maximal left ventricular dP/d t, myocardial oxygen consumption, lactate release, and adenosine release were measured as indices of myocardial function. Intracellular myoglobin was found to be only 72% saturated under baseline conditions with an arterial oxygen tension of >600 mmHg at 37°C. Baseline intracellular oxygen tension was 6.3 mmHg. Myocardial oxygen consumption was decreased by 10% when the oxygen tension fell to 5.7 mmHg, and cardiac contraction decreased 10% when oxygen tension was 4.1 mmHg. Adenosine release and, finally, lactate release began to increase at sequentially lower oxygen tensions. The present results indicate that the buffer-perfused guinea pig heart at 37°C has an intracellular oxygen tension just above the threshold for impaired function.

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Coronary vasomotor tonus in moderate hypothermia

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1962.203.5.825 ◽

1962 ◽

Vol 203 (5) ◽

pp. 825-828 ◽

Cited By ~ 3

Author(s):

Cecil E. Cross ◽

P. Andre Rieben ◽

Peter F. Salisbury

Keyword(s):

Oxygen Tension ◽

Coronary Vessels ◽

Arterial Oxygen Tension ◽

Left Ventricular Pressure ◽

Aortic Pressure ◽

Left Ventricular ◽

Arterial Oxygen ◽

Moderate Hypothermia ◽

Right Heart ◽

Blood Temperature

Coronary blood flow was measured in open-chest preparations with fixed cardiac output and bypassed right heart. Arterial oxygen tension (pO2), pH, and temperature were measured. The slope of regression lines between mean coronary driving pressure (aortic pressure minus left ventricular pressure) and coronary flow indicated directional changes of coronary vasomotor tonus. During periods of blood cooling in nonfailing hearts the coronary vessels dilated only when arterial oxygen tension was permitted to fall, but not when pO2 remained stable. In failing hearts moderate decreases of blood temperature and pO2 did not cause further decrements of coronary vasomotor tonus. It was concluded that blood temperature per se did not influence coronary vasomotor tonus.

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Relation between the O2 supply:demand ratio, , and adenosine formation in hearts stimulated with inotropic agents

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y90-017 ◽

1990 ◽

Vol 68 (1) ◽

pp. 110-118 ◽

Cited By ~ 5

Author(s):

John P. Headrick ◽

Roger J. Willis

Keyword(s):

Oxygen Consumption ◽

Rat Heart ◽

Myocardial Oxygen Consumption ◽

Left Ventricular ◽

Isolated Rat Heart ◽

Rate Pressure Product ◽

Inotropic Agents ◽

Flow Rates ◽

Adenosine Release ◽

Phosphorylation Potential

Mooted controllers of adenosine formation in heart are the oxygen supply:demand ratio, myocardial oxygen consumption [Formula: see text], the cytosolic phosphorylation potential (log[ATP]/[ADP][Pi]). The relationship between these parameters and purine release (adenosine + inosine) into the venous effluent was examined in isovolumic rat hearts perfused at 20 and 12 mL∙min−1∙g−1 with a glucose containing crystalloid buffer and stimulated with inotropic agents (isoproterenol, norepinephrine, 3-isobutyl-1-methylxanthine, and ouabain). The oxygen supply:demand ratio and [Formula: see text] were continuously determined using an oxygen electrode to monitor oxygen supply and consumption. The phosphorylation potential was calculated from phosphorus metabolite levels determined by 31P-NMR spectroscopy and HPLC analysis. Left ventricular function was assessed as the rate-pressure product. All inotropic agents increased the rate-pressure product, with increases in function being greater in the hearts perfused at 20 mL∙min−1∙g−1. [Formula: see text] was linearly related to the rate-pressure product at each flow rate; however, the hearts perfused at 20 mL∙min−1∙g−1 exhibited approximately twofold greater [Formula: see text] values for similar rate-pressure product values. All inotropic agents increased adenosine release into the venous effluent. While there was a significant linear relation between adenosine formation and [Formula: see text] in hearts perfused at both flow rates and stimulated with drugs, the relations differed with adenosine release being approximately fourfold greater in hearts perfused at 12 mL∙min−1∙g−1 under similar conditions of [Formula: see text]. Adenosine formation correlated exponentially with the ratio of oxygen supply:demand under all conditions (r = 0.97) and the relation did not differ significantly between hearts perfused at different rates. The phosphorylation potential was decreased from control values by all drugs at both flow rates and plotted linearly with [Formula: see text], although the relations differed between hearts perfused at different rates. Alternatively, the phosphorylation potential plotted linearly with oxygen supply:demand under all conditions (r = 0.98) and did not differ at different flow rates. These results support the idea that adenosine formation depends on the oxygen supply:demand ratio and indicate that [Formula: see text] is not a consistent index of adenosine formation in the glucose-perfused isolated rat heart. The oxygen supply:demand ratio is reflected in the cytosol by changes in the cytosolic phosphorylation potential.Key words: O2 supply:demand ratio, adenosine, crystalloid-perfused rat heart, inotropic agents, myocardial oxygen consumption.

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Fetal cerebral oxygen consumption at different levels of oxygenation

Journal of Applied Physiology ◽

10.1152/jappl.1977.43.6.1080 ◽

1977 ◽

Vol 43 (6) ◽

pp. 1080-1084 ◽

Cited By ~ 41

Author(s):

M. Jones ◽

R. E. Sheldon ◽

L. L. Peeters ◽

G. Meschia ◽

F. C. Battaglia ◽

...

Keyword(s):

Oxygen Consumption ◽

Oxygen Tension ◽

Venous Blood ◽

Arterial Oxygen Tension ◽

Arterial Oxygen ◽

Cerebral Oxygen ◽

Fetal Sheep ◽

Sagittal Sinus ◽

Cerebral Oxygen Consumption ◽

Highly Correlated

Cerebral oxygen consumption (VCO2) was measured in 10 unanesthetized, chronically catheterized fetal sheep at 130–140 days of gestation. The VCO2 was calculated using cerebral blood flow (QC) measured with radioactive microspheres and the cerebral arteriovenous difference of O2 content (C(a-V)O2) calculated from preductal arterial and sagittal sinus venous blood. The ewe was exposed to varying concentrations of oxygen, resulting in fetal arterial oxygen contents (CaO2) of 0.89–5.58 mM, arterial oxygen tension (PaO2) values of 14–36 Torr, and cerebral venous oxygen tension (PVO2) values of 9–25 Torr. Although there was a clear relationship between the fetal CaO2 and C(a-V)O2, this was shown to be the result of changes in Qc rather than changes in VCO2. There was not a statistically significant correlation between either CaO2 or PVO2 and VCO2 over this range of oxygenation. On the other hand, C(a-V)O2 was highly correlated with Qc. There is no evidence that VCO2 is a function of oxygen tension (PO2) in the unanesthetized fetal sheep as long as the sagittal sinus PO2 is greater than or equal to 9 Torr.

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The Effects of Hypoxia on Myocardial Blood Flow and Oxygen Consumption: Negative Role of Beta Adrenoreceptors

Clinical Science ◽

10.1042/cs0410257 ◽

1971 ◽

Vol 41 (3) ◽

pp. 257-273 ◽

Cited By ~ 10

Author(s):

J. P. Vance ◽

J. R. Parratt ◽

I. McA. Ledingham

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Oxygen Consumption ◽

Myocardial Blood Flow ◽

Oxygen Tension ◽

Coronary Sinus ◽

Perfusion Pressure ◽

Arterial Oxygen Tension ◽

Arterial Oxygen ◽

Inspired Oxygen

1. Myocardial blood flow was measured by using a 133xenon clearance technique in closed-chest dogs anaesthetized with trichlorethylene. A gradual decrease in the inspired oxygen tension resulted in an increase in myocardial blood flow only when the Pa,o2 fell to between 30 and 35 mmHg. 2. When hypoxia was rapidly induced and sustained for a mean period of 18.3 min, myocardial blood flow markedly increased (from a mean of 118 ± 5 to 162±6 ml 100 g−1 min−1). There was a critical mean arterial oxygen tension (35 mmHg) above which increases in myocardial blood flow did not occur. This corresponded to a mean coronary sinus Po2 of 18 mmHg or an oxygen content of 50 ml/100 ml. These flow increases were not dependent on changes in arterial or coronary sinus pH or carbon dioxide tension, nor were they dependent on changes in perfusion pressure or heart rate. 3. Despite the fact that oxygen availability was substantially decreased, myocardial oxygen consumption was maintained throughout the period of hypoxia by means of increased oxygen extraction. 4. Towards the end of the hypoxic period, Pa,co2 rose significantly from 40 ± 1 to 48 ± 1.5 mmHg. There was no significant change in the non-respiratory component of acid-base balance. 5. During prolonged hypoxia (more than 30 min) myocardial blood flow remained consistently elevated, but oxygen consumption tended to fall progressively and this was associated with an increasingly severe metabolic acidosis. The haemodynamic and oxygen consumption changes returned to normal within a short time (15 min) after the resumption of a normal inspired oxygen concentration, as did the frequently observed electrocardiographic disturbances. 6. The responses to hypoxia were unaffected by a combination of atropine and propranolol. There was no evidence either that hypoxia-induced coronary vasodilatation was mediated through vascular β-adrenoreceptors or that propranolol interfered with the self-regulating control of myocardial blood flow. It has been recognized for some time that hypoxia is capable of producing considerable increases in blood flow in the myocardium (Hilton & Eichholtz, 1925; Eckenhoff, Haf kenschiel, Landmesser & Harmel, 1947; Berne, Blackmon & Gardner, 1957; Feinberg, Gerola & Katz, 1958; Aukland, Kiil, Kjekshus & Semb, 1967). Little is known, however, about the exact relationship between arterial oxygen tension and myocardial blood flow. Further, although several factors associated with hypoxia are known to influence myocardial blood flow, the relative importance of each is uncertain; such factors include a direct effect of hypoxia on coronary vascular smooth muscle and indirect effects relating to changes in perfusion pressure, heart rate, extravascular support and associated metabolic disturbances. Likewise, the influence of neurogenic factors on myocardial vascular tone during hypoxia has not been systematically examined.

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Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

Nuklearmedizin ◽

10.1055/s-0037-1620682 ◽

1978 ◽

Vol 17 (04) ◽

pp. 142-148

Author(s):

U. Büll ◽

S. Bürger ◽

B. E. Strauer

Keyword(s):

Oxygen Consumption ◽

Left Ventricle ◽

Muscle Mass ◽

Myocardial Oxygen Consumption ◽

Animal Experiments ◽

Left Ventricular ◽

Left Ventricular Wall ◽

Ventricular Wall ◽

Flow Measurements ◽

Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

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