Biomedical subjects

B Y Qin

Publications and source records attributed to B Y Qin.

31 records · Page 2Linked to original sources

PubMed1996

[Binding of [3H] dihydroetorphine to opioid receptors in rat brain membrane].

AIM: To study the binding characteristics of dihydroetorphine (DHE) to opioid receptors. METHODS: The binding of [3H] DHE to rat brain membrane opioid receptors was observed by radioligand binding study. RESULTS: Saturation study showed the binding of [3H] DHE to rat brain membrane presented a single high-affinity class of binding sites with Kd = 0.19 nmol.L-1 and Bmax = 115 pmol/g protein. Kinetics study showed the association rate of [3H] DHE to opioid receptor was very rapid and dissociation very slow. NaCl 100 mmol.L-1 + guanosine triphosphate (GTP) 50 mumol.L-1 inhibited the binding of [3H] DHE and made Kd increase to 7.87 nmol.L-1, without effect on Bmax. Competitive inhibition of agonists and antagonists indicated that the affinity of [3H]DHE to mu opioid receptor was higher than to delta and kappa opioid receptors. CONCLUSION: DHE is a selective agonist of mu opioid receptors.

Analgesics, Opioid↗

PubMed1995

Dihydroetorphine is a mu-receptor-selective ligand.

The selectivity to opioid receptors of dihydroetorphine, a potent analgesic with only mild physical dependence, was investigated using radioligand binding assay and its analgesic activity in mice determined. The relative affinity ratio of dihydroetorphine to mu-, delta- and kappa- opioid receptors was 333:1:1. The analgesic effect of intracerebro-ventricular injection in mice could be antagonized by the mu-antagonist beta-funaltrexamine but could not be antagonized by delta- and kappa-selective antagonists naltrindole and norbinaltorphimine. We conclude that dihydroetorphine is a selective ligand for the mu-opioid receptor.

Analgesics, Opioid↗

PubMed1995

Influences of locus coeruleus lesions and reserpine treatment on opioid physical dependence in rats.

AIM: To study the role of locus coeruleus (LC) noradrenergic neurons in the opioid dependence. METHODS: Chemical lesion of LC was produced by 6-hydroxydopamine (4 micrograms in 1 microL). Reserpine (Res) was used to deplete central noradrenaline. Composite scores of naloxone (4 mg.kg-1, ip) precipitated abstinence syndromes were calculated and the magnitude of weight loss was determined in chronic morphine (Mor)- or dihydroetorphine (DHE)-treated rats. RESULTS: Lesions of LC made Mor, but not DHE, abstinence syndrome more serious. Multiple doses of Res (0.5 mg.kg-1.d-1 x 3 d) increased scores of Mor and DHE abstinence syndrome, made worse the loss of body weight in chronic Mor-, but not DHE-, treated rats. A single dose of Res (0.5 mg.kg-1) speeded up the development of physical dependence on Mor. CONCLUSION: The LC noradrenergic neurons play a role in suppression of some withdrawal symptoms.

Animals↗

PubMed1991

[Effect of dihydroetorphine on contraction response of guinea pig ileum, mouse, and rabbit vas deferens induced by electric field stimulation in vitro].

Dihydroetorphine (DHE) inhibited contraction response of isolated guinea pig ileum and mouse vas deferens induced by electric field stimulation with IC50 values of (4.4 +/- 4.3) x 10(-16) mol.L-1 and (1.1 +/- 1.4) x 10(-18) mol.L-1 respectively. These effects of DHE were antagonized by naloxone (Nal). On guinea pig ileum, the antagonistic effect of Nal against DHE was similar to those against morphine and etorphine. However, on mouse vas deferens, the antagonistic effect of Nal against DHE was more potent than those against morphine and etorphine. Besides, DHE showed antagonistic effect on k-receptors in isolated rabbit vas deferens.

Analgesics, Opioid↗

PubMed1990

[Effects of 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone (MHDF) on hemodynamics and aorta in rats].

MHDF is a synthetic isoflavone derivative with anti-ischemic effect. In this paper, the effects of MHDF on in vivo hemodynamics and in vitro contraction of rat aorta were reported. MHDF (3-12.8 mg/kg) was found to decrease +/- dP/dtmax, Vmax, Vpm and LVSP, prolong T-dP/dtmax of left ventricle and slow the HR in rats. It was also shown to inhibit the changes of heart performance induced by CaCl2 in rats. In isolated rat aorta, MHDF caused a noncompetitive antagonism of noradrenaline-and CaCl2-induced contraction with the pD2' of 3.11 +/- 0.21 and 3.73 +/- 0.07. The high K(+)-evoked contraction with IC50 of 17.6 mu mol/L was also found to be inhibited. The results suggest that the effect of MHDF on vascular muscle is different from that of an alpha-blocker and may be attributable to inhibition of extracellular calcium influx or intracellular calcium release.

Animals↗

PubMed1990

[Effects of 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone on heart atrium and ventricular papillary muscles of guinea pig].

In isolated guinea pig right atria, 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone (MHDF), a new synthetic isoflavone produced noncompetitive antagonisms to isoproterenol- and histamine-induced positive chronotropic actions with pD'2 values of 5.04 +/- 0.10 and 4.90 +/- 0.18, respectively. MHDF inhibited the positive chronotropic response to CaCl2. In isolated left atria, the negative inotropic action of MHDF increased as the frequency increased. In papillary muscles, MHDF 3 mumol/L reduced the contractile force, while Vmax was decreased and APD and ERP were prolonged. These results indicated that the mechanism of MHDF on myocardium is related to inhibition of Ca2+ influx, Na+ influx and K+ efflux, not by blocking beta or H2 receptors.

Action Potentials↗

PubMed1990

[Inhibitory properties of cycloguanide phenylsulfone on acetylcholinesterase].

Mouse brain homogenates, mouse RBC, immobilized enzyme of pig brain, and human RBC were chosen as source of AChE, AChE activities were determined by colorimetric and gasometric methods. Cycloguanide phenylsulfone (CGP) exerted a moderate inhibitory effect on AChE. The pI50 (negative logarithm of molar concentration causing 50% inhibition of AChE) towards AChE in mouse RBC and brain were 5.75 and 5.50, respectively. The binding potency to AChE was very loose. The AChE inhibition was easily reversed by washing. It showed that CGP belonged to the contra-competitive AChE inhibitor.

Acetylcholinesterase↗

PubMed1988