Centrally mediated bradycardia and hypotension induced by narcotic analgesics: Dextromoramide and fentanyl

Laubie, Michel; Schmitt, Henri; Canellas, J; Roquebert, J; Demichel, P

doi:10.1016/0014-2999(74)90113-7

Cited by 130 publications

(37 citation statements)

References 24 publications

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“…These results demonstrate clearly that the hypotension in the rat is associated with respiratory depression. It seems therefore that the effects of morphine-like drugs may depend on species differences, since in artificially ventilated dogs the hypotensive effect is predominant (Laubie, Schmitt, Canellas, Roquebert & Demichel, 1974;Laubie et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Central Cardiovascular Effects of Narcotic Analgesics and Enkephalins in Rats

Bellet

Meyer

et al. 1980

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

Central Cardiovascular Effects of Narcotic Analgesics and Enkephalins in Rats

Bellet

Meyer

et al. 1980

British J Pharmacology

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“…There are close similarities between a 2 -and opioid receptors with respect to their distribution in the central nervous system (Pazos 1988), transduction system coupled to the agonist-receptor complexes (North et al 1987), and their actions such as analgesia (Filos et al 1992) and decreasing the sympathetic tone (Laubie et al 1974;Feldberg & Wei 1977). Some overlaps also exist between these two systems.…”

mentioning

confidence: 99%

Lithium Inhibits the Development of Physical Dependence to Clonidine in Mice

Dehpour¹,

Sadr

Roohi-Azizi

et al. 2002

Pharmacology & Toxicology

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Based on our previous finding that chronic lithium treatment reduced naloxone-precipitated withdrawal syndrome in morphine-treated mice, the effect of chronic lithium treatment was evaluated on the development of dependence to clonidine. Dependence was induced by injection of either morphine (50, 50 and 75 mg/kg, intraperitoneally with 3 hr interval for 3 consecutive days), or clonidine (2 mg/kg/day, intraperitoneally for 10 days). Naloxone (4 mg/kg, intraperitoneally) precipitated withdrawal signs in both morphine-and clonidine-treated mice. Yohimbine (5 mg/kg, intraperitoneally) precipitated withdrawal signs in the clonidine-treated mice, similar to morphine withdrawal signs; but failed to precipitate any significant sign in the morphine-treated mice. Coadministration of lithium was carried out by adding lithium chloride to drinking water (600 mg/l for 20 days; 10 days before the beginning of clonidine administration and 17 days before the administration of morphine to allow the lithium concentration to reach steady-state). The results indicated that chronic lithium administration significantly attenuated the withdrawal signs, precipitated either by yohimbine or naloxone, in clonidine-treated mice. As a conclusion, clonidine withdrawal signs are very similar to opioid withdrawal signs, and lithium is able to prevent the development of physical dependence to clonidine.

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“…1,2 Acute administration of -opioid receptor agonists provides little insight in this respect, because any effects are blurred by respiratory depression, an altered state of consciousness, or even anesthesia. [3][4][5][6][7][8][9][10][11] Furthermore, under resting conditions, -opioid receptor blockade by naloxone, which attenuates the effects of endogenous opioids, does not change muscle sympathetic activity (MSA), arterial baroreflex gain, or catecholamine plasma concentrations in healthy volunteers. [12][13][14][15][16] Conversely, naloxone potentiates the increase in MSA during exercise and in response to lower-body negative pressure, indicating inhibition of MSA by endogenous opioids when the sympathetic nervous system is activated.…”

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confidence: 99%

Chronic μ-Opioid Receptor Stimulation in Humans Decreases Muscle Sympathetic Nerve Activity

et al. 2001

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Background-Opioid-addicted patients undergoing detoxification provide a unique opportunity to assess the effects of chronic opioid receptor stimulation on the sympathetic nervous system. We tested the hypothesis that chronic oral methadone intake decreases resting efferent sympathetic nerve activity to muscle (MSA). Furthermore, we assessed whether this effect is reversed by -opioid receptor blockade during antagonist-supported detoxification under general anesthesia. Methods and Results-Fifteen young patients (30Ϯ1 years old, meanϮSEM) with a long history of mono-opioid addiction and under oral methadone substitution therapy (65Ϯ10 mg/d for 21Ϯ6 months) were selected. Peroneal MSA (microneurography) and catecholamine plasma concentrations (high-performance liquid chromatography) were assessed in the awake state and compared with those of age-matched healthy control subjects. The effects of -opioid receptor blockade by naloxone (12.4 mg IV) were determined during propofol anesthesia. Compared with healthy volunteers, resting MSA (4Ϯ2 versus 22Ϯ2 bursts/min, PϽ0.0001) and antecubital venous norepinephrine plasma concentration (100Ϯ64 versus 256Ϯ48 pg/mL, Pϭ0.01) were markedly decreased in addicted patients despite similar arterial blood pressure and heart rate. Opioid receptor blockade markedly increased MSA (5Ϯ2 to 24Ϯ3 bursts/min) and norepinephrine (49Ϯ12 to 305Ϯ48 pg/mL) and epinephrine (13Ϯ2 to 482Ϯ67 pg/mL) arterial plasma concentrations as well as mean arterial pressure (82Ϯ4 to 108Ϯ3 mm Hg) and heart rate (70Ϯ3 to 86Ϯ4 beats/min). Conclusions-Chronic

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Centrally mediated bradycardia and hypotension induced by narcotic analgesics: Dextromoramide and fentanyl

Cited by 130 publications

References 24 publications

Central Cardiovascular Effects of Narcotic Analgesics and Enkephalins in Rats

Central Cardiovascular Effects of Narcotic Analgesics and Enkephalins in Rats

Lithium Inhibits the Development of Physical Dependence to Clonidine in Mice

Chronic μ-Opioid Receptor Stimulation in Humans Decreases Muscle Sympathetic Nerve Activity

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