(2) The hyperglycemic effect of morphine could be blocked by prior injection of the opiate receptor blocker naloxone similarly administered into cerebral ventricles.
Acute experiments were performed on rabbits anesthetized with pentobarbi-tal and arterial blood pressure(BP)was recorded. 1.Intracerebroventricular(ivt)injection of 50μg of β-endorphin causedlowering of BP by 12.2±2.0 mmHg,which could be reversed by ivt injection ofnaloxone,an antagonist of opiate receptors.
the excitement action of morphine and leu-enkephalin on the sphincter of oddi might not be mediated by norepinephrine; the endogenous opiate-like substances and their receptors may play an important role in the regulation of the motility of the sphincter of oddi.
After injecting naloxone(1.8μg)into bilateral nucleus accumbens, the discharging from LHPE was no longer inhibited by electro-acupuncture (P<0.05) ; and the discharging from LHPI induced did not appear (P<0.05) at all. Cerebrospinal fluid was injected into bilateral nucleus accumbens for control, and this did not cause significant change of discharging from lateral habenular pain-units.
Preliminary intravenous injection of δ-opiate receptor (OR) agonists DSLET (0.1 mg/kg) or DTLET (0.1 mg/kg) increased tolerance of isolated perfused myocardium to damage by oxidative stress simulated in vivo with FeSO4 + ascorbic acid.
Microinjection of opiate receptor antagonist naloxone 3 nmol into CNTS did not itself affect the level of blood pressure and heart rate, but could markedly attenuate the cardiovascular effects of NE in CNTS.