Central cardiovascular effects of morphinomimetic peptides in dogs

Laubie, Michel; Schmitt, Henri; Vincent, M; Rémond, Georges

doi:10.1016/0014-2999(77)90146-7

Cited by 241 publications

(58 citation statements)

References 9 publications

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“…This possibility is consistent with the frequently biphasic responses observed after i.c.v. or cisterna magna administration of opiates (Laubie, Schmitt, Vincent & Remond, 1977;Bolme et al, 1978). Moreover, recent studies from our laboratory indicate that the injection site is a major factor determining the cardiovascular response to centrally administered opiates (Feuerstein & Faden, 1982;Hassen, Feuerstein & Faden, 1982a,b).…”

Section: Introductionmentioning

confidence: 93%

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Faden

Feuerstein

1983

British J Pharmacology

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Section: Introductionmentioning

confidence: 93%

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Faden

Feuerstein

1983

British J Pharmacology

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“…Cardiovascular depression can be produced in experimental animals by central or intravenous administration of endogenous opioid peptides (Laubie et al, 1977;Florez & Mediavilla, 1977;Lemaire et al, 1978). In addition, the specific opiate receptor antagonist, naloxone, has been shown to produce cardiovascular improvement in animal models of haemorrhagic shock Gurll et al, 1982a), spinal shock and endotoxin shock (Holaday & Faden, 1978;Reynolds et al, 1980;Gahos et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Effects of intravascular volume expansion on the cardiovascular response to naloxone in a canine model of severe endotoxin shock

Evans

Hinds

Varley

1984

British J Pharmacology

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1 The specific opiate receptor antagonist, naloxone, can produce haemodynamic improvement and increased survival in experimental shock. The efficacy of naloxone therapy in a canine model of endotoxin shock has been evaluated both with and without intravascular volume replacement. 2 Animals were anaesthetized with cx-chloralose and allowed to breathe spontaneously. A large bolus dose of endotoxin was followed by a continuous infusion, and treatment was instituted one hour after the endotoxin bolus. 3 In the absence of volume replacement, naloxone caused only limited and transient increases in mean arterial pressure (MAP) and left ventricular (LV) dp/dt max, with little effect on cardiac index (CI). Total peripheral resistance index (TPRI) tended to rise in both control and naloxone-treated dogs. 4 In volume-replaced animals, naloxone produced substantial and sustained increases in the MAP and LV dp/dt max with an associated rise in the CI. TPRI rose initially in this series and then fell progressively. Further analysis of the improvements in the CI showed an increase in stroke index with a tendency for heart rate to fall. 5 These findings suggest a myocardial action of naloxone in endotoxin shock, which is augmented by volume replacement. An initial, transient vasoconstrictor effect cannot, however, be excluded. Further work is required to determine the mechanism of the effects described.

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“…It has been reported that the acute administration of opioids suppresses the electrical activity of sympathetic nerves in animals (Laubie et al, 1977;Willette et al, 1982;Jurna & Rummel, 1984 injected morphine because this dose of the opiate, 16mgkg-1, produces significant analgesia in rats (Figure 2). Chronic treatment with morphine has been reported not only to lead to the development of opiate tolerance and dependence in experimental animals but also to produce other functional changes which may not be seen after acute morphine administration (Schulz & Goldstein, 1973;Llorens et al, 1978;Collier, 1980;Kromer & Steigemann, 1982;Rae & De Moraes, 1983).…”

Section: Discussionmentioning

confidence: 99%

Arterial catecholamine levels in morphine‐treated rats subjected to sympathetic nerve stimulation

Leung

Dai

Ogle

1989

British J Pharmacology

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The effect of acute or chronic morphine treatment on the changes in arterial noradrenaline and adrenaline levels in response to sympathetic nerve stimulation was studied in rats. Rats which had been chronically treated with morphine in their drinking fluid for 21 days were shown to be morphine‐tolerant, as revealed by the tail‐immersion test for analgesia. It was found that animals given either acute or chronic morphine treatment had similar basal concentrations of arterial catecholamines to their controls. Sympathetic nerve stimulation produced significant increases in arterial noradrenaline and adrenaline levels in both the control and morphine‐treated animals. However, the degree of arterial noradrenaline elevation was significantly less in morphine‐tolerant animals. This phenomenon was not observed in acutely morphine‐treated rats or at 2 weeks following opiate withdrawal in animals which had been treated previously with morphine for 3 weeks. The findings suggest that chronic morphine treatment in rats not only leads to opiate tolerance but also reduces catecholamine release in response to sympathetic nerve stimulation.

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Central cardiovascular effects of morphinomimetic peptides in dogs

Cited by 241 publications

References 9 publications

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Effects of intravascular volume expansion on the cardiovascular response to naloxone in a canine model of severe endotoxin shock

Arterial catecholamine levels in morphine‐treated rats subjected to sympathetic nerve stimulation

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