Respiratory and cardiovascular effects of met-enkephalin applied to the ventral surface of the brain stem

Flórez, Jesús; Mediavilla, A.

doi:10.1016/0006-8993(77)90699-0

Cited by 209 publications

(31 citation statements)

References 18 publications

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“…50 The same brain stem nuclei and the same neurotransmitters, monoamines and endorphins, are associated with both functions. [51][52][53][54][55][56] Therefore, blood pressure changes can be viewed as a related evaluation of pain. On the other hand, pulse remained the same after PRP treatment in all our patients.…”

Section: Discussionmentioning

confidence: 99%

Interventions for relieving pain associated with panretinal photocoagulation: a prospective randomized trial

Hsu

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Interventions for relieving pain associated with panretinal photocoagulation: a prospective randomized trial

Hsu

et al. 2005

Eye

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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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“…The administration ofopiates and opioid peptides provokes profound cardiovascular changes including marked hypotension in animals and man (Fennessy & Rattray, 1971;Laubie et al, 1977;Florez & Mediavilla, 1977;Lemaire et al, 1978). Moreover areas in the brain known to play a role in the autonomic control of cardiovascular function are rich in opioid receptors and opioid peptides (Atweh & Kumar, 1977;Wamsley et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Circulating [Met]enkephalin and catecholamine responses to acute hypotension and hypertension in anaesthetized greyhounds

Mason

Medbak

Rees

1987

British J Pharmacology

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4 Intravenous hexamethonium (2.5 mg kg-') provoked a fall in blood pressure which was not associated with any changes in plasma MLI. However, it produced a fall in plasma noradrenaline and a rise in plasma adrenaline. Thus it appears that neural mechanisms are required, at least in part, for the release of MLI. 5 Angiotensin 11 (1.25 jig kg-' min ') and noradrenaline (8 pg kg-' min ') infusions produced an elevation in blood pressure without altering the circulating MLI levels. 6 Study of the molecular forms of circulating MLI, before and during hypotension, revealed that the large molecular weight enkephalin-containing peptides with approximate molecular sizes of 1 8kD and 8kD were the predominant forms both in the basal and stimulated states. 7 It is concluded that circulating [Metlenkephalin is not involved in the tonic control of blood pressure but it may modulate catecholamine release following hypotension as part of the stress response.

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Respiratory and cardiovascular effects of met-enkephalin applied to the ventral surface of the brain stem

Cited by 209 publications

References 18 publications

Interventions for relieving pain associated with panretinal photocoagulation: a prospective randomized trial

Interventions for relieving pain associated with panretinal photocoagulation: a prospective randomized trial

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

Circulating [Met]enkephalin and catecholamine responses to acute hypotension and hypertension in anaesthetized greyhounds

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