Drugs online research references
J Pharmacol Exp Ther. 1993 Apr;265(1):346-57.
Cardiac inotropic as well as coronary and pulmonary artery actions of epinine in human isolated tissues.
Schwinger RH, Bohm M, Schulz C, Schmidt U, Schmidt U, Schmid B, Dienemann H, Reichart B, Erdmann E.
Universitat Munchen, Medizinische Klinik I, Federal Republic of Germany.
The present study was aimed to characterize the effects of epinine, the metabolite of the p.o. active dopamine derivate ibopamine in human cardiovascular tissues such as myocardium, coronary artery and pulmonary artery. Isometric force of contraction was studied in electrically driven papillary muscle strips from nonfailing (brain death), moderately failing (New York Heart Association class II-III, mitral valve replacement) and terminally failing human myocardium (New York Heart Association class IV, heart transplants) as well as in auricular trabeculae (aortocoronary bypass operation). Epinine increased force development in a concentration-dependent manner. In comparison to isoprenaline, epinine had a significantly lower potency but a similar efficacy to enhance force of contraction. Depending on the degree of myocardial failure, the effectiveness of epinine was reduced, whereas the potency was similar. Only in nonfailing myocardium, epinine increased force of contraction as effectively as Ca++. Prestimulation with forskolin or milrinone enhanced the potency of the epinine-mediated inotropic effect. In contrast, the beta-1-selective antagonist CGP 207.12A [2-hydroxy-5-(2-(hydroxy-3-(4-((1-methyl-4-trifluoromethyl)-1-H-imidazol -2-yl)-phenoxy)-propyl)-aminoethoxyl)-benzamide] and the beta-2-selective antagonist ICI 118.551 [erythro-(+-)-1-(7-methylindan-4-yloxy)-3- isopropylaminobutan-2-ol-hydrochloride] shifted the concentration-response curve of epinine significantly to the right, indicating action at both beta-2 and beta-1 adrenoceptors. Epinine exerted higher affinity at beta-2 compared to beta-1 adrenoceptors in radioligand binding experiments ([125I]iodocyanopinodolol). In human coronary artery rings and pulmonary artery rings epinine alone as well as epinine in the presence of propranolol initiated a concentration-dependent increase in tension development in precontracted (prostaglandin F2 alpha, 0.3 mumol/l) as well as in non-precontracted rings. These results suggest that epinine exerts no direct vasodilatory activity in human coronary and pulmonary arteries at concentrations which are capable to produce positive inotropic activity. The supposed beneficial effects of ibopamine in the treatment of heart failure may not be due to positive inotropic actions as the concentrations producing positive inotropy are much higher than the clinically observed plasma concentrations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8386240&dopt=Abstract
J Pharmacol Exp Ther. 1993 May;265(2):777-89.
Adrenergic, serotonergic and cholinergic components of nicotinic antinociception in rats.
Iwamoto ET, Marion L.
Department of Pharmacology, University of Kentucky College of Medicine, Lexington.
The present study was designed to determine the degree of participation of opioid, noradrenergic, serotonergic and cholinergic systems of the lumbar spinal cord in the antinociception produced by nicotinic stimulation of the pedunculopontine tegmental nucleus (PPTg) or nucleus raphe magnus (RMg). Adult, male Sprague-Dawley rats were implanted subcortically with 25-gauge cannulas into the PPTg or RMg. The animals were also implanted with intrathecal catheters terminating in the subarachnoid space just rostral to the lumbar enlargement. Seven days after surgery, animals were injected with 15 to 100 nmol of various receptor antagonists intrathecally 10 min before microinjections of 40 nmol of N-methylcarbachol (NMC) into the PPTg or RMg. Doses of antagonists were chosen which did not induce motor disturbances and did not alter hot-plate or tail-flick nociception when administered alone. NMC produced hot-plate and tail-flick antinociception for 20 to 25 min, peaking 5 to 10 min after either PPTg or RMg microinjection. Intrathecal administration of 50 nmol of idazoxan, 100 nmol of S-(-)-propranolol, 20 nmol of LY53857, 25 nmol of S-(-)-zacopride, 100 nmol of pirenzepine or 50 nmol of methoctramine each antagonized in part the antinociception produced by PPTg or RMg microinjections of 40 nmol of NMC. Intrathecal administration of 100 nmol of naloxone or 100 nmol of prazosin enhanced the antinociceptive effects of NMC. Intrathecal vehicle or 100 nmol of mecamylamine did not alter NMC-induced antinociception. Complete antagonism of PPTg-administered NMC antinociception was achieved only when animals were pretreated intrathecally with combinations of at least three of the following four antagonists, 20 nmol of S-(-)-zacopride, 15 nmol of LY53857, 25 nmol of idazoxan and 50 nmol of methoctramine. The data suggest that the antinociceptive responses produced by nicotinic stimulation of the PPTg or RMg have similar pharmacologic profiles, and are redundantly mediated via alpha-2 adrenergic, 5-HT1c/2 and 5-HT3 serotonergic, and M2 cholinergic receptor interactions in the lumbar spinal cord.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8388459&dopt=Abstract
Physiol Behav. 1993 Apr;53(4):805-11.
Noradrenergic involvement in the consolidation of maternal experience in postpartum rats.
Moffat SD, Suh EJ, Fleming AS.
Erindale College, University of Toronto, Mississauga, Ontario, Canada.
If postpartum rats are separated from pups following cesarean delivery, their maternal responsiveness declines such that in tests on day 10 they show maternal onset latencies that do not differ from those shown by virgin rats. If, however, dams are permitted a 1-h experience with pups within 36 h of cesarean delivery, rats exhibit a high level of responsiveness to foster pups on day 10 after c-section. The present research investigates the effect of the noradrenergic system in the long-term consolidation of a brief maternal experience in new mother rats. Groups of dams were cesarean delivered and were either given pups for a brief period 36 h after section (experienced) or received no experience (inexperienced). Immediately following the experience phase, dams were injected with different concentrations of the beta-adrenergic antagonist, propranolol (0, 0.5, 1.0, 5.0 mg/kg), or the adrenergic agonist, isoproterenol (0, 0.25 or 0.5 mg/kg). Ten days after cesarean delivery rats were given maternal induction tests. Rats receiving 60 min of experience and injected with propranolol exhibited significantly longer maternal onset latencies than did saline-injected rats, although their latencies were not as long as shown by the maternally inexperienced groups. In contrast, rats receiving 15 min of experience and injected with isoproterenol exhibited significantly shorter onset latencies than did saline-injected rats, whether or not they exhibited maternal behavior during the initial 15 min exposure period. These results suggest that the noradrenergic system is involved in the consolidation of a maternal experience.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8390059&dopt=Abstract
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