Drugs online research references
Neurosci Lett. 1994 Oct 24;180(2):167-70.
Beta 1-adrenergic mechanism is involved in stress-induced increase in arousal.
Shibasaki T, Yamada K, Yamauchi N, Imaki T, Hotta M, Demura H.
Department of Medicine, Tokyo Women's Medical College, Japan.
It has been shown that 1 h restraint shortens pentobarbital (PbNa)-induced sleeping time and that brain corticotropin-releasing hormone (CRH) is involved in the mechanism by which restraint shortens. PbNa-induced sleeping time. The present study was designed to further examine the mechanism of the antagonistic effect of 1 h restraint on PbNa in rats. Intracerebroventricular (i.c.v.) administration of propranolol and metoprolol, but not butoxamine reversed the shortening of PbNa-induced sleeping time by 1 h restraint. The i.c.v. administration of phentolamine blocked the shortening of PbNa-induced sleeping time by restraint, while the same dose of phentolamine prolonged the sleeping time in unrestrained rats. Atropine did not affect the PbNa-induced sleeping time in restrained rats. These results suggest that in addition to CRH, the brain beta 1-adrenergic system is involved in the restraint stress-induced increase in arousal.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7700573&dopt=Abstract
Agents Actions. 1984 Oct;15(3-4):119-24.
Effects of the H2-receptor agonist dimaprit on lymphocyte responsiveness in vitro.
Binderup L.
The histamine H2-agonist dimaprit was found to increase the response of rat spleen cells to the T-cell mitogen Concanavalin A, when present at concentrations of 10(-5) and 10(-4)M. Higher concentrations of dimaprit were cytotoxic. The enhanced response seemed to be associated with an inhibitory effect of dimaprit on T-suppressor cell activity rather than with a direct mitogen-like stimulation of lymphocyte proliferation or with an interference with monocyte/macrophage functions. The stimulatory effects of dimaprit were not reversed by the H2-receptor antagonist, cimetidine, nor by the beta-receptor antagonists metoprolol and H 35/25. Addition of the H1-receptor antagonist, mepyramine, further increased the stimulatory effect of dimaprit on lymphocyte responsiveness.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6240928&dopt=Abstract
tip.gazi.edu.tr
Myocardial ischemia and reperfusion result in endothelial and ventricular dysfunction. Beta-blockers protect the myocytes from injury by acting as anti-ischemia agents. These anti-ischemic effects of the beta-blockers are due not only to their negative inotropic/chronotropic effects but also to a lipid peroxidation reducing mechanism. Thus, beta-blockers enhance myocardial recovery. In the present study 20 isolated guinea-pig hearts were perfused with Krebs-Henseleit buffer (KHB) using a Langendorff apparatus. The animals were allocated into 2 groups. In the study group (Group I), metoprolol, as the beta-blocker agent, was added into the KHB and in the control group (Group II) perfusion was performed without metoprolol. The percentage change (%change) of heart rate, developed pressure and dP/dtmax; malondialdehyde (MDA) and glutathione (GSH) levels of the perfusate and heart tissue were obtained as data. The %change of heart rate was 70.5+/-9.2 in the study group and 87.3+/-8.2 in the control (p = 0.003). The %change of developed pressure was 68.7+/-14.4 and 55.9+/-8.6 in the study group and control group, respectively (p = 0.04). The % change of dP/dt was 63.3+/-10.0 in the study group and 54.4+/-5.3 in the control group (p = 0.01). The tissue MDA level was 31.0+/-5.5 nmol/g tissue in the study group and 53.5+/-4.2 nmol/g tissue in the control group (p = 0.0002). The tissue GSH levels were 1.08+/-0.20 and 0.80+/-0.07 (mol/g tissue) in Groups I and II, respectively (p = 0.001). The levels of the perfusate MDA decreased and the levels of the perfusate GSH increased significantly in the metoprolol group in the postreperfusion period in comparison with the preischemia term (p = 0.003 and p = 0.03, respectively). Metoprolol reduces ischemic injury via prevention of lipid peroxidation and reduces the myocardial energy demand by decreasing the heart rate.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10496488&dopt=Abstract
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