The putative delta opioid receptor antagonist ICI 174864 (3 mg/kg, i.v.) significantly reversed endotoxic shock hypotension at a dose which lacked significant pressor actions in normotensive, non-endotoxemic rats.
View Article and Find Full Text PDFCardiovascular effects of the high affinity, irreversible opiate antagonist, naloxazone, were investigated in conscious rats subjected to endotoxic shock. Unlike other less selective opiate antagonists such as naloxone, naloxazone failed to block or reverse the hemodynamic effects of endotoxemia. However, naloxazone pretreatment prevented the usual therapeutic effects of naloxone in endotoxic shock.
View Article and Find Full Text PDFThe effects of naloxone on endotoxic hypotension in adrenalectomized and selectively adrenal demedullated rats were evaluated. In sham-operated rats, naloxone administered intracerebroventricularly (ICV) and intravenously (IV) produced an elevation of arterial pressure in this conscious rat model of endotoxemia. By contrast, both adrenalectomy and selective adrenal demedullation (wherein cortical function remained) not only enhanced the sensitivity to endotoxin-induced hypotension at least 10- to 15-fold, but also completely prevented the pressor response to ICV or IV naloxone.
View Article and Find Full Text PDFStudies were conducted with the putative delta opiate receptor antagonist M 154,129 to evaluate its potential for reversing circulatory shock without altering nociceptive processes. M 154,129 (30 mg/kg iv) did not alter tail flick or hot plate latencies by itself, nor did it alter the antinociceptive effects of morphine (4 mg/kg iv). Following endotoxic shock hypotension in conscious rats, M 154,129 (30 or 60 mg/kg iv) produced a rapid return of arterial pressure to pretreatment levels.
View Article and Find Full Text PDFAdv Biochem Psychopharmacol
December 1982