Differential hemodynamic, metabolic and hormonal effects of morphine and morphine-6-glucuronide

Molina, Patricia E.; Hashiguchi, Yojiro; Ajmal, Mohammed; Mazza, Michael; Abumrad, Naji N.

doi:10.1016/0006-8993(94)91962-3

Cited by 27 publications

(22 citation statements)

References 25 publications

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“…In addition, a marked hypotensive response can be induced following systemic administration of morphine in rats (22). Indeed, rats with heat stroke displayed a marked hypotensive response accompanied by a marked elevation of serum b-endorphin in the present study.…”

Section: Discussionsupporting

confidence: 51%

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

et al. 2005

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Abstract. Heat stroke is characterized by hyperthermia, arterial hypotension, decreased baroreflex sensitivity, and increased serum levels of b-endorphin. Whereas naltrexone may have therapeutic potential in heat stroke, the underlying mechanism remains unclear. We tested the hypothesis that naltrexone may attenuate heat stroke by reducing hyperthermia, hypotension, decreased baroreceptor sensitivity, and / or increased serum levels of b-endorphin. Heat stroke was induced by exposing the anesthetized adult Sprague-Dawley rats in an incubator at 43°C. The moment in which the mean arterial pressure dropped irreversibly from the peak level was taken as the onset of heat stroke. Control rats were exposed to 24°C. Mean arterial pressure, baroreceptor sensitivity, and maximal reflex bradycardia, after the onset of heat stroke, were all significantly lower than in control rats. However, rectal temperature and serum levels of bendorphin were all greater after the onset of heat stroke. Intravenous delivery of naltrexone (10 mg / kg) 20 min before the initiation of heat stress, but not immediately at the onset of heat stroke, significantly attenuated the above-mentioned reactions. Accordingly, naltrexone improved survival during heat stroke. These results suggest that naltrexone protects against hypotension and decrement of both baroreceptor sensitivity and maximal reflex bradycardia during heat stroke by reducing both hyperthermia and increment of serum b-endorphin and thus improves survival.

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Section: Discussionsupporting

confidence: 51%

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

et al. 2005

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“…This altered glucose metabolism was attributed to an increase in endogenous morphine levels in the brain associated with an increase in ACTH, corticosterone, and catecholamine levels in the plasma [15]. Similar to the ICV injection of TNF-␣, Molina et al [10] reported that ICV injection of morphine caused an increase in the stress hormone levels in the plasma, resulting in an elevation of glucose production. Taken together, these studies suggest that morphine is involved in changes in the hormonal milieu initiated by cytokine as a second messenger.…”

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confidence: 77%

Effect of surgical stress on endogenous morphine and cytokine levels in the plasma after laparoscopoic or open cholecystectomy

et al. 2000

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“…Previous studies from our laboratory demonstrated the catabolic effects of central morphine administration, characterized by hyperglycemia, glycogenolysis, and an elevation in the circulating levels of catecholamines and corticosterone, which are hallmarks of the stress response. 5,6 Moreover, we have also demonstrated the greater potency of morphine-6-glucuronide (M6G) in eliciting these effects. 5,6 M6G is the second major metabolite of morphine in humans which has potent opioid effects, and it has been hypothesized that the biological effects of morphine may be partially enhanced by this metabolite.…”

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confidence: 93%

“…5,6 Moreover, we have also demonstrated the greater potency of morphine-6-glucuronide (M6G) in eliciting these effects. 5,6 M6G is the second major metabolite of morphine in humans which has potent opioid effects, and it has been hypothesized that the biological effects of morphine may be partially enhanced by this metabolite. Despite the profound influence of opiates on brain activity, the effects of opiates on brain glycogen metabolism have not been well investigated.…”

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confidence: 93%

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Differential responses of brain, liver, and muscle glycogen to opiates and surgical stress

et al. 1998

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We examined the effects of intracerebroventricular (ICV) cannula implantation followed by the administration of morphine sulfate (MOR) and its metabolite, morphine-6-glucuronide (M6G), on the glycogen content of the brain, liver, and muscle. ICV cannulation resulted in nearly a 30% reduction in brain glycogen, and ICV MOR resulted in a 36% reduction in liver glycogen content compared to time-matched controls, but it had no additional effect on either the brain or muscle glycogen content. ICV M6G showed a more significant reduction, to 50% of liver glycogen, but it had no effect on either brain or muscle glycogen. Neither IV MOR nor M6G produced any significant alteration in tissue glycogen content. These results indicate that the stress response associated with neurosurgery, especially the placement of the ICV cannula, is associated with a decrement in brain glycogen. The activation of opioid receptors in the brain results in enhanced hepatic glycogenolysis but has no additional effect on the brain glycogen content.

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Differential hemodynamic, metabolic and hormonal effects of morphine and morphine-6-glucuronide

Cited by 27 publications

References 25 publications

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

Effect of surgical stress on endogenous morphine and cytokine levels in the plasma after laparoscopoic or open cholecystectomy

Differential responses of brain, liver, and muscle glycogen to opiates and surgical stress

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