Adrenergic blockade blunts adenosine concentration and coronary vasodilation during hypoxia.

Herrmann, Steven C.; Feigl, Eric O.

doi:10.1161/01.res.70.6.1203

Cited by 59 publications

(41 citation statements)

References 37 publications

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“…Blockade of cardiac -adrenoceptors attenuated the incidence of arrhythmia in the second hypoxic period, demonstrating the possible role of catecholamines in the course of HPC. Myocardial ischemia, as well as non-ischemic hypoxia, stimulate efferent adrenergic nervous endings (Daly & Scott, 1963, 1964Herrmann & Feigl, 1992), the assumption being that the ventricular arrhythmias induced by systemic hypoxia depend on intact adrenergic innervation (O'Connor & Merrill, 1993), which was also shown in our experiments. These interventions deliver possible protection by PC against electrogenic and mechanical effects of the prolonged ischemic period of the myocardium (Lasely et al, 1993).…”

Section: Ventricular Arrhythmia Threshold -A Measure Of the Electricasupporting

confidence: 77%

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Švorc¹,

Marossy²,

Grešová³

et al. 2012

Cardiac Arrhythmias - New Considerations

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Section: Ventricular Arrhythmia Threshold -A Measure Of the Electricasupporting

confidence: 77%

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Švorc¹,

Marossy²,

Grešová³

et al. 2012

Cardiac Arrhythmias - New Considerations

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“…Actually, a correlation has been found repeatedly between venous adenosine concentration and physiological effects attributed to endogenous adenosine (Berne 1980;Dobson et al 1986;Herrmann and Feigl 1992;Rubio et al 1974). It is therefore not surprising that much attention has been paid to the production of adenosine by endothelial cells.…”

Section: Functional Implications Of Ecto-5'-nucteotidase In Interstitmentioning

confidence: 98%

Ecto-5?-nucleotidase is expressed by pericytes and fibroblasts in the rat heart

Mlodzik

Loffing

Hir

et al. 1995

Histochem Cell Biol

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Ecto-5'-nucleotidase is anchored at the outer surface of cell membranes and thus its reaction product adenosine is released into the extracellular space. Extracellular adenosine displays via specific receptors a wide range of physiological effects in heart. There are discrepancies in the literature concerning the distribution of ecto-5'-nucleotidase in heart. Since we suspected that these may be due to technical problems, in the present study on ecto-5'-nucleotidase in rat heart we attempted to circumvent some technical pitfalls. Good preservation of the tissue with open capillary lumina, providing a clear identification of endothelium, was obtained by perfusion fixation. At the light microscopic level, the distribution of ecto-5'-nucleotidase studied by enzyme histochemistry and immunohistochemistry using a monoclonal and a polyclonal antibody yielded congruent results. The enzyme was rather homogeneously distributed throughout the myocardium, with a slightly higher incidence of stained cells in the outer thirds than in the inner third of the wall. Consistently high levels of ecto-5'-nucleotidase were seen only in interstitial cells. The walls of large vessels and heart muscle cells were constantly negative for ecto-5'-nucleotidase. The endothelia of capillaries were mostly negative but a few profiles occasionally displayed a weak immunoreaction. The interstitial cells staining positive for ecto-5'-nucleotidase could be identified as pericytes and as fibroblasts according to their shapes and localizations. The immunoreactivity of fibroblasts was confirmed by electron microscopy. These data indicate that adenosine may be formed extracellularly in the interstitium of the myocardium, where it would have direct access to important targets such as myocytes, arterioles and nerve endings.

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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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Adrenergic blockade blunts adenosine concentration and coronary vasodilation during hypoxia.

Cited by 59 publications

References 37 publications

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Ecto-5?-nucleotidase is expressed by pericytes and fibroblasts in the rat heart

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

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