morphine/hypoxia

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Effects of naloxone, morphine and kappa-opioid receptor agonists on hypoxia/hypoglycemia-induced reduction of 2-deoxyglucose uptake in hippocampal slices from U-50,488H-tolerant rats.

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The aim of the present study was to determine whether U-50,488H and U-62,066E, kappa-opioid receptor agonists cause a neuroprotective action against hypoxia/hypoglycemia-induced reduction in 2-deoxyglucose (2-DG) uptake of hippocampal slices from U-50,488H-tolerant rats. Both U-50,488H and U-62,066E

Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man.

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Although morphine depresses respiration the mechanism of this depression remains unknown. Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects. This procedure produced

A prospective study of post-cesarean delivery hypoxia after spinal anesthesia with intrathecal morphine 150μg.

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BACKGROUND Delayed respiratory depression is a feared complication of intrathecal morphine in patients undergoing cesarean delivery. The incidence, timing and risk factors for hypoxia in this population are not known. METHODS Patients undergoing cesarean delivery under spinal anesthesia at a

Effects of opioid antagonists and morphine in a hippocampal hypoxia/hypoglycemia model.

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The influence of opioid antagonists and of morphine on rat hippocampal slices in a model of reversible hypoxia/hypoglycemia was investigated by assessment of evoked field potentials (population spike amplitude). In control slices, a brief hypoxia/hypoglycemia led to a loss of field potentials

Influences of morphine on the ventilatory response to isocapnic hypoxia.

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BACKGROUND The ventilatory response to hypoxia is composed of the stimulatory activity from peripheral chemoreceptors and a depressant effect from within the central nervous system. Morphine induces respiratory depression by affecting the peripheral and central carbon dioxide chemoreflex loops.

Effects of intrathecal morphine on the ventilatory response to hypoxia.

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BACKGROUND Intrathecal administration of morphine produces intense analgesia, but it depresses respiration, an effect that can be life-threatening. Whether intrathecal morphine affects the ventilatory response to hypoxia, however, is not known. METHODS We randomly assigned 30 men to receive one of

Endomorphins and morphine limit anoxia-reoxygenation-induced brain mitochondrial dysfunction in the mouse.

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The protection of brain mitochondria from oxidative stress is an important therapeutic strategy against ischemia-reperfusion injury and neurodegenerative disorders. Isolated brain mitochondria subjected to a 5 min period of anoxia followed by 5 min reoxygenation mirrored the effect of oxidative

The effect of chronic intermittent hypoxia on respiratory sensitivity to morphine in rats.

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OBJECTIVE Chronic intermittent hypoxia (CIH) is a characteristic of obstructive sleep apnea syndromes (OSAs). Recurrent hypoxia during the developmental period increases respiratory sensitivity to subsequent administration of opioids. However, it is unknown whether CIH affects respiratory

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure.

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OBJECTIVE Ischemia reperfusion (I/R) injury is an inevitable event arising during the cardiovascular diseases development and the process of potent surgical treatments. microRNAs (miRNAs) are critical regulators of multiple cell processes including I/R injury. The present study aims to quantify

Morphine-induced delayed pre-conditioning against anoxia/reoxygenation injury in pulmonary artery endothelial cells: The role of mitochondrial KATP channels.

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Opioids produce delayed pre-conditioning (PC) in vivo and in vitro. Our previous research revealed that opioid‑induced delayed PC has an antiapoptotic effect on pulmonary artery endothelial cells (PAECs) suffering from anoxia/reoxygenation (A/R) injury. The present study hypothesized that activation

Anti-apoptotic effect of morphine-induced delayed preconditioning on pulmonary artery endothelial cells with anoxia/reoxygenation injury.

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BACKGROUND Opioid preconditioning (PC) reduces anoxia/reoxygenation (A/R) injury to various cells. However, it remains unclear whether opioid-induced delayed PC would show anti-apoptotic effects on pulmonary artery endothelial cells (PAECs) suffering from A/R injury. The present study was conducted

The effects of morphine on gas exchange, ventilation pattern and ventilatory responses to hypercapnia and hypoxia in dwarf caiman (Paleosuchus palpebrosus).

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Morphine and other opioids cause respiratory depression in high doses and lower the ventilatory responses to hypoxia and hypercapnia in mammals. Recent studies indicate that turtles respond similarly, but although they are used routinely for post-surgical analgesia, little is known about the

Morphine sulfate inhibits hypoxia-induced vascular endothelial growth factor expression in endothelial cells and cardiac myocytes.

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Vascular endothelial growth factor (VEGF) is an angiogenic mitogen, specific for endothelial cells. Hypoxia-induced VEGF in endothelial cells and cardiomyocytes leads to autocrine and paracrine stimulation, respectively. During myocardial ischemia, VEGF is upregulated in the endothelium and

Behavioral and neurochemical correlates of morphine and hypoxia interactions.

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Decreased oxygen availability (hypoxia) impairs the synthesis of dopamine and serotonin in parallel with a decline in open-field behavior. If hypoxic-induced deficits in dopamine and serotonin metabolism are physiologically important, then stimulation of their synthesis may help reverse

Morphine consumption during pregnancy exacerbates neonatal Hypoxia-Ischemia injury in rats.

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Hypoxia-Ischemia (HI) is the most common cause of death and disability in human infants. The use of opiate in pregnant women affects their children. The aim of this study was to evaluate the effect of morphine consumption during pregnancy and lactation on vulnerability to neonatal HI

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