Hypoxemia and Coronary Blood Flow

Berne, Robert M.; Blackman, Jane; Gardner, Thomas H.; Hoff, Hebbel E.

doi:10.1097/00132586-195812000-00004

Cited by 27 publications

(34 citation statements)

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“…Myocardial respiration wanes despite increasing ADP and intracellular phosphate (Pi),' which both stimulate mitochondrial ATP production under aerobic conditions. The intact animal generally maintains or increases myocardial oxygen consumption during early or moderate hypoxia (7)(8)(9). Small decreases in myocardial phosphocreatine content with no depletion of the cytosolic ATP pool have been documented during moderate hypoxic conditions (10,11).…”

Section: Introductionmentioning

confidence: 99%

Relation of myocardial oxygen consumption and function to high energy phosphate utilization during graded hypoxia and reoxygenation in sheep in vivo.

Portman¹,

Standaert²,

Ning³

1995

J. Clin. Invest.

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IntroductionThis study investigates the relation between myocardial oxygen consumption (MV 02), function, and high energy phos- Severe hypoxia ultimately leads to contractile failure, which is attributed to an imbalance between myocardial oxygen supply and demand (1)(2)(3)(4). Sudden extreme oxygen deprivation causes rapid depletion of energy stores in the form of the high energy phosphates, phosphocreatine, and ATP, as well as accumulation of ATP hydrolysis products. In isolated myocytes (5) and buffer-perfused hearts (5, 6) anoxia or hypoxia results in a reduced oxidative phosphorylation rate. Myocardial respiration wanes despite increasing ADP and intracellular phosphate (Pi),' which both stimulate mitochondrial ATP production under aerobic conditions. The intact animal generally maintains or increases myocardial oxygen consumption during early or moderate hypoxia (7-9). Small decreases in myocardial phosphocreatine content with no depletion of the cytosolic ATP pool have been documented during moderate hypoxic conditions (10, 11). However, myocardial oxygen consumption rates have not been directly measured during periods of rapid high energy phosphate depletion and repletion in the intact animal. The purpose of this study was to examine the relation between myocardial oxygen consumption, function, and high energy phosphates during severe hypoxia and reoxygenation in vivo. Additionally, rephosphorylation parameters were measured to determine if evidence of respiratory uncoupling or mitochondrial damage occurs during reoxygenation in vivo. Graded hypoxia was performed in an effort to gradually reduce arterial oxygen tension to attain the P02 at which high energy phosphate stores rapidly decreased. Highly time-resolved 31P nuclear magnetic resonance (NMR) spectroscopy enabled monitoring of myocardial phosphates throughout hypoxia and recovery with simultaneous measurement of oxygen consumption. Consequently, these measurements enhanced analysis of mitochondrial function in vivo during reoxygenation. MethodsAnimal preparation. Animals used in this study were handled in accordance with institutional and National Institutes of Health animal care and use guideline. Sheep between 30 and 70 d old (mean 47 d±6.8) were sedated with an intramuscular injection of 10 mg/kg ketamine, and 0.2-0.4 mg/kg xylazine, intubated, and then ventilated (C-900 pediatric ventilator; Siemens Corp., Schaumberg, IL) with room air and oxygen, followed by an intravenous dose of alpha-chloralose (40 mg/ kg). Femoral arterial cannulation was performed for monitoring systemic blood pressure and sampling blood. Arterial pH was maintained between 7.35 and 7.45 by adjustment of ventilatory tidal volume and 1. Abbreviations used in this paper: FIo2, fractional inspiratory oxygen

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Section: Introductionmentioning

confidence: 99%

Relation of myocardial oxygen consumption and function to high energy phosphate utilization during graded hypoxia and reoxygenation in sheep in vivo.

Portman¹,

Standaert²,

Ning³

1995

J. Clin. Invest.

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“…A number of putative controlling variables have been postulated for both of these phenomena, for references see Belloni (1979). In recent times oxygen tension in the tissue or vessel walls has been considered an inadequate controller because of the apparent insensitivity of resistance to coronary venous oxygen over the higher part of this variable's physiological range (Berne, Blackman & Gardner, 1957). Re-examination of the data suggested to us that this conclusion might have been premature since the 'oxygen hypothesis' is only presented in the literature in a vague form.…”

Section: Introductionmentioning

confidence: 99%

Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.

Drake-Holland¹,

Laird²,

Noble³

et al. 1984

The Journal of Physiology

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SUMMARY1. The hypothesis that tissue oxygen tension controls coronary vascular resistance during changes in perfusion pressure and oxygen consumption was expressed in a simplified mathematical form capable of making quantitative predictions.2. The predictive value of this formulation of the hypothesis was tested in experiments on anaesthetized mongrel dogs subjected to constant-pressure perfusion of the left main coronary artery, with measurements of coronary blood flow and arterio-venous oxygen content differences. Coronary venous oxygen content was used as an index of tissue oxygenation. t 3. The responses of coronary blood flow and arterio-venous oxygen content difference, made over a range of perfusion pressures (which caused autoregulation) and heart rates (which caused metabolic regulation) were predicted qualitatively by the model. 4. Coronary vascular conductance was positively related to metabolic rate only during metabolic regulation (heart rate changes); during autoregulation the relationship between these two variables was inverse.5. Coronary vascular conductance and resistance values taken from both interventions (both perfusion pressure and heart rate variations) were closely related to coronary venous oxygen content and calculated Po2.6. These findings suggest that further examination of oxygen tension, as the controller of the coronary vascular bed under physiological conditions should be considered.

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“…24 -26 Hyperperfusion permits the heart to meet its requirements by greater oxygen extraction from the coronary perfusate instead of increasing flow. 25 ^ The isolated heart has no neurohumoral control and myocardial metabolites are diluted by the high volume of perfusate; thus, there is less regulation of coronary flow in the perfused heart compared with hearts in situ in this range of perfusion pressures. As workload is increased during hyperperfusion, maximum oxygen extraction occurs at high workloads.…”

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confidence: 99%

Effects of perfusion pressure on energy and work of isolated rat hearts.

Watters

Wikman‐Coffelt

et al. 1989

Hypertension

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A chemomechanical study of hypertrophied hearts of 6-month-old spontaneously hypertensive rats (SHR) and that of age-matched Wistar-Kyoto (WKY) rats was carried out, analyzing the response of the heart to steady-state changes in coronary perfusion pressure. The ratio of heart (dry)-to-body (wet) weight of WKY rats was 0.37±0.02 (10 3 ) and for SHR was 0.58±0.03 (1(T 3 ) (/7<0.01). In the apex-ejecting, isolated, pyruvate-perfused working hearts of WKY rats and SHR, coronary flow was constant when coronary perfusion pressure was set between 140 and 190 cm H 2 O (range of autoregulation). Coronary flow was perfusion pressure dependent when the coronary perfusion pressure was set below 110 cm H 2 O for both WKY rats and SHR. Cardiac output, developed pressure, rate of pressure development (dP/dt), and oxygen consumption were constant in the range of autoregulation but decreased in the direction of coronary flow when coronary flow was reduced by a drop in perfusion pressure. Similarly, the phosphorylation potential, phosphocreatine, adenosine triphosphate, and cyclic adenosine monophosphate were constant in the range of autoregulation but decreased directionally with coronary perfusion pressure below 110 cm H 2 O for both SHR and WKY rats. There was a significantly lower phosphorylation potential in SHR as compared with WKY rats when coronary perfusion pressure was reduced to 80 cm H 2 O. In the region of autoregulation, coronary flow and oxygen consumption were significantly less in SHR, although developed pressure was significantly greater at both high and low workloads. The importance of coronary perfusion pressure in SHR using the apex-ejecting working heart model was confirmed using other isolated perfused heart models (i.e., the Langendorff apex-vented heart model to simulate low workloads and the Langendorff isovolumic heart model to simulate high workloads). Furthermore, findings were not changed if FC-43 was added to the perfusate to facilitate delivery of oxygen to the myocardium and increase the viscosity of the perfusate. (Hypertension 1989;13:480-488) C oronary flow depends on perfusion pressure and vascular resistance.'-7 Vascular resistance depends on neurohormonal factors, myocardial contraction, myocardial metabolites, partial gas pressure, and alterations in the vascular endothelium. '-10 Both in situ 7 and in the isolated perfused heart 8 there is a range of coronary perfusion pressures from about 100 to 180 cm H 2 O 7 -8 where coronary perfusion pressure does not influence coronary flow; however, with values lower than 100 cm H 2 O, alterations in perfusion pressure result in a direct correlation between coronary flow

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Hypoxemia and Coronary Blood Flow

Cited by 27 publications

References 0 publications

Relation of myocardial oxygen consumption and function to high energy phosphate utilization during graded hypoxia and reoxygenation in sheep in vivo.

Relation of myocardial oxygen consumption and function to high energy phosphate utilization during graded hypoxia and reoxygenation in sheep in vivo.

Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.

Effects of perfusion pressure on energy and work of isolated rat hearts.

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