norepinephrine/hypoxia

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Altered release and metabolism of norepinephrine in superfused canine saphenous veins in the presence of halothane and hypoxia.

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BACKGROUND Hypoxia and halothane are both known to have different effects on the release and disposition of norepinephrine at sympathetic nerve terminals during neurotransmission. In adverse clinical situations, both conditions may be present, but the effects of halothane and hypoxia together are

Norepinephrine and dihydroxyphenylglycol effluxes from sympathetic nerve endings during hypoxia and reoxygenation in the isolated rat heart.

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The present experiments were carried out in isolated rat hearts perfused according to the Langendorff method at a constant pressure of 10 kPa. The aim was to measure norepinephrine (NE) overflow and its deaminated metabolite dihydroxyphenylglycol (DOPEG) by changing the composition of the buffer

Interaction between norepinephrine and hypoxia on carotid body chemoreception in rabbits.

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The effects of both bolus injection and constant infusion of various levels of norepinephrine (NE) on the activity of single-carotid chemoreceptor nerve fibers was studied in pentobarbital-anaesthetized rabbits under normoxic and hypoxic conditions. All animals were paralyzed and artificially

Effect of hypoxia and norepinephrine on cytoplasmic free Ca2+ in pulmonary and cerebral arterial myocytes.

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The fluorescent calcium indicator, fura 2, was used to test whether contraction of primary cultured smooth muscle cells (SMC) from small pulmonary arteries in response to hypoxia and the relaxation by large pulmonary and cerebral artery SMC were mediated by changes in cytoplasmic free Ca2+ (Ca2+c).

Effects of dobutamine and norepinephrine on oxygen availability in tamponade-induced stagnant hypoxia: a prospective, randomized, controlled study.

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OBJECTIVE To explore the effects of dobutamine and norepinephrine on the global cardiovascular response and on the relationship between oxygen uptake (VO2) and oxygen delivery (DO2) during an acute reduction in blood flow associated with tamponade. METHODS Prospective, randomized, controlled acute

Norepinephrine-stimulated lipolysis in acute and chronic hypoxemia.

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The effects of acute and chronic hypoxemia on norepinephrine-stimulated lipolysis were studied in dogs. Right-to-left shunts were created in experimental dogs to render them chronically hypoxemic (PaO2 37-55 torr). Control animals received sham operations (PaO2 greater than 70 torr). During air

Effect of hypoxia on norepinephrine of various tissues in rats.

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OBJECTIVE To determine the effects of hypoxia and hypoxic exercise (HE) on the norepinephrine levels of various tissues in rats. METHODS Male Wistar rats were randomly assigned to 3 groups: an HE group (n = 6), a hypoxic-sedentary (HS) group (n = 6), and a normoxic-sedentary (NS) group (n = 6). The

Regulation of hypoxia-induced release of corticotropin-releasing factor in the rat hypothalamus by norepinephrine.

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Corticotropin-releasing factor (CRF) peptide release was activated by hypoxia in the rat hypothalamus. The mechanisms, however, of the hypoxia-induced CRF release remains unclear. In this study, we demonstrated that the norepinephrine (NE) and its receptors in the paraventricular nucleus (PVN)

Norepinephrine attenuates hypoxia-inhibited thyrotropin-releasing hormone release in median eminence and paraventricular nucleus of rat hypothalamus.

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OBJECTIVE We have previously found that chronic hypoxia inhibited thyrotropin-releasing hormone (TRH) mRNA expression in rat paraventricular nucleus (PVN). This study presented the effects of hypoxia on TRH secretion in rat hypothalamus, and the norepinephrine (NE) involvement in the modulation of

Chronic sustained hypoxia enhances both evoked EPSCs and norepinephrine inhibition of glutamatergic afferent inputs in the nucleus of the solitary tract.

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The nucleus of the solitary tract (NTS) receives inputs from both arterial chemoreceptors and central noradrenergic neural structures activated during hypoxia. We investigated norepinephrine (NE) modulation of chemoreceptor afferent integration after a chronic exposure to sustained hypoxia (CSH)

Effects of hypoxia on norepinephrine uptake by developing rabbit lung.

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Pulmonary extraction of radiolabeled norepinephrine (NE) was evaluated in newborn rabbits aged 1 to 3 days. Twenty pups were raised from birth in an hypoxic environment (FiO2 = 0.16-0.17) and 10 were raised in room air for study as controls. NE extraction was measured using an isolated, perfused

[Norepinephrine regulation of T-lymphocyte proliferation of rat during acute hypoxia].

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Interaction between the immune and neuroendocrine systems has long been noted. In the present study, the role of norepinephrine (NE) in immunoregulation of rats during simulated hypoxia in hypobaric chamber was examined. It was found that 7 km for 24 h of hypoxia inhibited T-lymphocyte proliferation

When norepinephrine becomes a driver of breathing irregularities: how intermittent hypoxia fundamentally alters the modulatory response of the respiratory network.

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Neuronal networks are endogenously modulated by aminergic and peptidergic substances. These modulatory processes are critical for maintaining normal activity and adapting networks to changes in metabolic, behavioral, and environmental conditions. However, disturbances in neuromodulation have also

Differential effects of long-term hypoxia on norepinephrine turnover in brain stem cell groups.

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The influence of long-term hypoxia on noradrenergic cell groups in the brain stem was assessed by estimating the changes in norepinephrine (NE) turnover in A1, A2 (subdivided into anterior and posterior parts), A5, and A6 groups in rats exposed to hypoxia (10% O2-90% N2) for 14 days. The NE turnover

Inositol trisphosphate is involved in norepinephrine- but not in hypoxia-induced pulmonary arterial contraction.

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The role that second messengers play in pulmonary vasoconstriction is not understood. The purpose of this study was to directly measure inositol phosphates in isolated pulmonary arterial preparations before and during norepinephrine (NE) stimulation and acute hypoxia. Rat main pulmonary arteries

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