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antiadrenergic/hypoxia
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Pharmacological manipulations of anoxia-induced free fatty acid accumulation in the mouse brain.
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The accumulation of free fatty acid (FFA) in the brain occurs within minutes of anoxia, induced by exposing mice to a 100% N2 atmosphere. The rate of FFA release is high within the first minute and continues to increase moderately hereafter. FFA is apparently accumulated at the highest concentration
On the mechanism by which antiadrenergic drugs increase survival of critical skin flaps.
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In order to asses the possibility that degeneration release of noradrenaline influences the survival of critical skin flaps, we studied the effect of various antiadrenergic drugs on skin-flap levels of noradrenaline, ATP, and cyclic AMP. Reserpine treatment depleted the skin flaps of noradrenaline
Metabolic determinants of defibrillation. Role of adenosine.
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BACKGROUND
The single most important determinant of cardiac arrest outcome is the duration of ventricular fibrillation (VF) preceding delivery of a high-energy shock, because of the adverse effect of VF duration on defibrillation threshold (DFT). Although a metabolic mechanism has been proposed,
Increased myocardial adenosine production and reduction of beta-adrenergic contractile response in aged hearts.
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The contractile response of the aged adult heart to beta-adrenergic stimulation is known to be reduced compared with the young adult heart. Since endogenous adenosine exerts an antiadrenergic action in the heart, this study was undertaken to determine if the basal endogenous level of myocardial
Endogenous adenosine does not activate ATP-sensitive potassium channels in the hypoxic guinea pig ventricle in vivo.
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BACKGROUND
The activation of ATP-sensitive K+ (K+ ATP) channels by K+ ATP openers, eg, pinacidil, hypoxia, and ischemia, is known to shorten the ventricular action potential. Since adenosine is released in increased amounts during cardiac hypoxia and ischemia, the hypothesis that endogenous
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