Hemodynamic changes following corticosteroid and naloxone infusion in dogs subjected to hypovolemic shock without resuscitation

Vargish, T; Gurll, Nelson J.; Reynolds, David G.; Lutz, Stephen A.; Ganes, Eric

doi:10.1016/0024-3205(83)90799-3

Cited by 4 publications

(2 citation statements)

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“…These effects of ACTH were not abolished by adrenalectomy.4 Exogenous corticosteroids also have been shown to block the effect of naloxone in hemorrhagic shock. 45 The results indicate that the "antishock" action of ACTH is a result of neither intact adrenal glands nor adrenal release of corticosteroids. Instead, the beneficial ef- In conclusion, ,B-endorphin is elevated in chronic CHF, and the endogenous opioids probably contribute significantly to the circulatory dysfunction observed in CHF.…”

Section: Discussionmentioning

confidence: 95%

The role of endogenous opioids in congestive heart failure: effects of nalmefene on systemic and regional hemodynamics in dogs.

Liang¹,

Imai²,

Stone³

et al. 1987

Circulation

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We studied the role of endogenous opiates and their interrelationships with the sympathetic nervous system in an experimental preparation of right-sided congestive heart failure (CHF) produced by surgical tricuspid avulsion and progressive pulmonary arterial constriction. Three groups of dogs with CHF and one group of sham-operated dogs were studied. One group of dogs with CHF was given normal saline as pretreatment, while the other two groups were pretreated with either propranolol alone ((3-blockade) or propranolol plus prazosin (a-plus /3-blockade). CHF was characterized by weight gain, ascites, elevated right atrial pressure, tachycardia, and reduced cardiac output. Compared with sham-operated animals, animals with CHF exhibited significantly higher baseline levels of plasma /3-endorphin and cortisol. Furthermore, only the animals with CHF responded to the opiate receptorantagonist nalmefene with significant increases in plasma /3-endorphin, cortisol, and adrenocorticotropic hormone. Administration of nalmefene increased aortic blood pressure, cardiac output, left ventricular dP/dt and dP/dtIP, and blood flow to the myocardium, skeletal muscle, and kidneys in dogs with CHF, but had no appreciable effects in sham-operated dogs. 13-Receptor blockade abolished the increase in cardiac output, left ventricular performance, and blood flow produced by nalmefene, but had no effect on the pressor response to nalmefene. The increase in mean aortic pressure in the ,3-blockade group was accompanied by an increase in skeletal muscle vascular resistance. Addition of prazosin in the a-plus 13-blockade group abolished the increases in mean aortic pressure and skeletal muscle vascular resistance, suggesting that the changes after propranolol probably resulted from unmasking of a-receptor-mediated vasoconstriction. Our present study indicates that the heightened opiate system accompanying CHF limits sympathetic activation, and that the beneficial effects of opiate-receptor inhibition are mediated, at least in part, via stimulation of the sympathetic nervous system.

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