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Stran 1 iz 62 rezultatov
The effects of reserpine and hypoxia on the amine-storing granules of the hamster carotid body.
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The carotid bodies from control, reserpine-treated, and hypoxia-treated hamsters were fixed with phosphate-buffered glutaraldehyde and osmium tetroxide, s-Collidine-buffered osmium tetroxide, or phosphate-buffered glutaraldehyde followed by potassium dichromate incubation. Following
Intrapulmonary neuro-epithelial bodies in newborn rabbits. Influence of hypoxia, hyperoxia, hypercapnia, nicotine, reserpine, L-DOPA and 5-HTP.
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Neonatal rabbit neuro-epithelial bodies (NEB) were investigated under various experimental conditions with light microscopy, microspectrography, morphometry and electron microscopy. (1) Hypoxia causes a decreased amine fluorescence intensity and an increased secretory exocytosis of dense core
Effects of reserpine and propranolol on anoxia-induced enzyme release from the isolated perfused guinea-pig-heart.
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The possibility of a protective effect by reserpine or propranolol on anoxia-induced released of malate and lactate dehydrogenase was investigated in isolated perfused hearts of guinea-pigs. After allowing 30 min of aerobic perfusion for the development of a steady state, the hearts from the
Influence of reserpine and of adrenolytic agents on the pulmonary arterial pressor response to hypoxia and catecholamines.
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Antagonism to the actions of hydrallazine, reserpine, potassium cyanide, sodium azide and anoxia on arterial smooth muscle.
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Effect of hypoxia on the development of gastric ulcers in pylorus-ligated, reserpine-treated and immobilized rats.
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[Effect of reserpine on the process of mobilization of a glycogen depot in the myocardium during hypoxia].
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[Effects of reserpine on respiratory functions, with special reference to the increase of anoxemia in cardiac and pulmonary diseases].
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Effect of reserpine treatment on cardiovascular response to hypoxia in dog.
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Pulmonary vascular dynamics during acute hypoxia: modification by reserpine pretreatment or adrenalectomy.
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Nonexocytotic noradrenaline release induced by pharmacological agents or anoxia in human cardiac tissue.
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In acute myocardial ischemia, noradrenaline is released locally from sympathetic varicosities by a Ca(2+)-independent nonexocytotic release mechanism that is effectively suppressed by inhibitors of the neuronal noradrenaline carrier (uptake1). The purpose of the present study was to elucidate the
Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular response to hypoxia.
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The highly reactive pulmonary vascular bed of the neonatal calf was utilized to determine whether the hypoxic pulmonary pressor response is modified by alpha-adrenergic blockade with phenoxybenzamine (Group A) or by tissue catecholamine depletion with reserpine (Group B). In addition, in Group A,
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
Alpha 2-adrenoceptor-mediated antisecretory effect of hypoxia in conscious rats.
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Gastric acid secretion is suppressed, resulting in a significant rise in gastric pH, when conscious rats are exposed to hypoxia (Yamaji et al., 1996). When adrenal medullectomized rats were exposed to moderate (10.5% O2) hypoxia for 3 h, gastric acid secretion was restored to nearly the level in
[Creatine phosphokinase release from perfused cardiac muscle under hypoxic conditions. Effect of propranolol, verapamil, reserpine and deslanoside].
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Experiments were undertaken to determine if some drugs (propranolol, reserpine, verapamil and deslanoside) have an effect on CPK release from hypoxic heart muscle. Hypoxia was induced in isolated Langerdorff perfused rabbit hearts by gassing the perfusate with 95% N2 + 5% CO2. Hypoxic induced damage
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