Oxygen extraction rate of the myocardium at rest and on exercise in various conditions.

Binak, K; Harmanci, N; Sirmaci, Necati; Ataman, N; Ogan, H

doi:10.1136/hrt.29.3.422

Cited by 34 publications

(12 citation statements)

References 9 publications

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“…5,[7][8][9] In contrast, in humans, minimal changes in O 2 extraction occur at mild to moderate levels of exercise, [15][16][17][18][19][20] although an increase in O 2 extraction and a decrease in cvO 2 content have been reported in humans during heavy exercise (Ͼ85% of maximum heart rate). 18,[23][24][25] The present study indicates that at mild to moderate levels of exercise, swine resemble humans more closely than dogs.…”

Section: Myocardial O 2 Extraction During Treadmill Exercisementioning

confidence: 99%

“…1,2 In humans, myocardial O 2 extraction, [15][16][17][18][19][20] cvSO 2 , 16,18 -20 cvO 2 content, 15,16,19 -21 or cvPO 2 19,22 are, in contrast to dogs, minimally affected during mild to moderate exercise (Ͻ80% of maximum heart rate), but an increase in fractional O 2 extraction and a decrease in cvO 2 content occur during heavy exercise (Ͼ85% of maximum heart rate). 18,[23][24][25] In humans, the minimal changes in cvPO 2 at low to moderate levels of exercise could be due to an increased importance of ␤-adrenergic coronary vasodilation 26,27 or decreased importance of ␣-adrenergic vasoconstriction, but this has not been studied in humans.…”

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confidence: 99%

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Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Duncker

Stubenitsky

Verdouw

1998

Circulation Research

110

159

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Abstract-To date, no studies have investigated coronary vasomotor control of myocardial O 2 delivery (MDO 2 ) and its modulation by the autonomic nervous system in the porcine heart during treadmill exercise. We studied 8 chronically instrumented swine under resting conditions and during graded treadmill exercise. Exercise up to 85% to 90% of maximum heart rate produced an increase in myocardial O 2 consumption (MV O 2 ) from 163Ϯ16 mol/min (meanϮSE) at rest to 423Ϯ75 mol/min (PՅ0.05), which was paralleled by an increase in MDO 2 , so that myocardial O 2 extraction (79Ϯ1% at rest) and coronary venous O 2 tension (cvPO 2 , 23.7Ϯ1.0 mm Hg at rest) were maintained. ␤-Adrenoceptor blockade blunted the exercise-induced increase of MDO 2 out of proportion compared with the attenuation of the exercise-induced increase in MV O 2 , so that O 2 extraction rose from 78Ϯ1% at rest to 83Ϯ1% during exercise and cvPO 2 fell from 23.5Ϯ0.9 to 19.6Ϯ1.1 mm Hg (both PՅ0.05). In contrast, ␣-adrenoceptor blockade, either in the absence or presence of ␤-adrenoceptor blockade, had no effect on myocardial O 2 extraction or cvPO 2 at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O 2 extraction and an increase in cvPO 2 at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was likely due to an increased ␤-adrenoceptor activity, since combined muscarinic and ␤-adrenoceptor blockade produced similar changes in O 2 extraction and cvPO 2 , as did ␤-adrenoceptor blockade alone. In conclusion, in swine myocardium, MV O 2 and MDO 2 are matched during exercise, which is the result of feed-forward ␤-adrenergic vasodilation in conjunction with minimal ␣-adrenergic vasoconstriction. ␤-Adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor-mediated inhibition of ␤-adrenergic coronary vasodilation. The observation that cvPO 2 levels are maintained even during heavy exercise suggests that a decrease in cvPO 2 is not essential for coronary vasodilation during exercise. (Circ Res. 1998;82:1312-1322.)

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Section: Myocardial O 2 Extraction During Treadmill Exercisementioning

confidence: 99%

mentioning

confidence: 99%

Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Duncker

Stubenitsky

Verdouw

1998

Circulation Research

110

159

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show abstract

“…The working heart is a highly metabolic organ that under normal resting conditions extracts nearly 70% of the oxygen supplied by the coronary circulation 34,35 representing close to 10% of the total body oxygen consumption. However, the heart has minimal capability for extracting additional oxygen such that increases in metabolic demands can only be met by autoregulatory increases in coronary blood flow through vasodilation of the coronary circuit.…”

Section: Myocardial Abnormalities During Cardiac Resuscitationmentioning

confidence: 99%

Protecting Mitochondrial Bioenergetic Function During Resuscitation from Cardiac Arrest

Gazmuri

Radhakrishnan

2012

Critical Care Clinics

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Synopsis Successful resuscitation from cardiac arrest requires reestablishment of aerobic metabolism by reperfusion with oxygenated blood of tissues that have been deprived of oxygen for variables periods of time. However, reperfusion concomitantly activates pathogenic mechanisms known as “reperfusion injury.” At the core of reperfusion injury are mitochondria, playing a critical role as effectors and targets of such injury. Mitochondrial injury compromises oxidative phosphorylation and also prompts release of cytochrome c to the cytosol and bloodstream where it correlates with severity of injury. Main drivers of such injury include Ca2+ overload and oxidative stress. Preclinical work shows that limiting myocardial cytosolic Na+ overload at the time of reperfusion attenuates mitochondrial Ca2+ overload and maintains oxidative phosphorylation yielding functional myocardial benefits that include preservation of left ventricular distensibility. Preservation of left ventricular distensibility enables hemodynamically more effective chest compression. Similar myocardial effect have been reported using erythropoietin hypothesized to protect mitochondrial bioenergetic function presumably through activation of pathways similar to those activated during preconditioning. Incorporation of novel and clinical relevant strategies to protect mitochondrial bioenergetic function are expected to attenuate injury at the time of reperfusion and enhance organ viability ultimately improving resuscitation and survival from cardiac arrest.

show abstract

“…The working heart is a highly metabolic organ that under normal resting conditions extracts nearly 70% of the oxygen supplied by the coronary circulation (1,2) representing close to 10% of the total body oxygen consumption. However, the heart has minimal capability for extracting additional oxygen, such that increases in metabolic demands can only be met by autoregulatory increases in coronary blood flow through vasodilatation of the coronary circuit.…”

Section: Myocardial Ischemic Injury During Cardiac Resuscitationmentioning

confidence: 99%

NHE-1 Inhibitors and Erythropoietin for Maintaining Myocardial Function during Cardiopulmonary Resuscitation

Gazmuri

Ayoub

Radhakrishnan

2010

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Oxygen extraction rate of the myocardium at rest and on exercise in various conditions.

Cited by 34 publications

References 9 publications

Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Protecting Mitochondrial Bioenergetic Function During Resuscitation from Cardiac Arrest

NHE-1 Inhibitors and Erythropoietin for Maintaining Myocardial Function during Cardiopulmonary Resuscitation

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