Drugs online research references
Respir Physiol. 1995 Apr;100(1):45-53.
Aspects of cardioventilatory control in the adriatic sturgeon (Acipenser naccarii).
McKenzie DJ, Taylor EW, Bronzi P, Bolis CL.
School of Biological Sciences, University of Birmingham, Edgbaston, UK.
Cardioventilatory responses to hypoxia, the O2 chemoreceptor stimulant sodium cyanide (NaCN), and intra-arterial injection of atropine, noradrenaline and DL-propranolol were investigated in the adriatic sturgeon. Hypoxia elicited a bradycardia and hyperventilation. 1 mg NaCN added to water entering the buccal cavity stimulated a transient bradycardia but intra-arterial infusion of 150 micrograms NaCN did not, indicating that hypoxic bradycardia is controlled by chemoreceptors sensitive only to water O2 levels. NaCN stimulated hyperventilation both when added to the water and when infused intra-arterially, indicating that hypoxic hyperventilation is controlled by chemoreceptors sensitive to both internal and external milieux. Atropine abolished the hypoxic bradycardia and returned heart rate to normoxic values indicating that this species has no inhibitory vagal tone in normoxia. Noradrenaline stimulated ventilation, an effect abolished by DL-propranolol. Propranolol blocked ventilatory responses to intra-arterial infusion of NaCN whereas responses to NaCN added to the water remained unaffected, indicating that propranolol may inhibit internally-oriented O2-chemoreceptor activity or that ventilatory responses to intra-arterial NaCN are stimulated by a release of circulating catecholamines. Cardioventilatory control systems in sturgeon are similar to those of other actinopterygians but also show some characteristics of the system described for elasmobranchs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7604183&dopt=Abstract
Am J Cardiol. 1979 Feb;43(2):285-91.
Efficacy of a new oral agent (tocainide) in the acute treatment of refractory ventricular arrhythmias.
Ryan W, Engler R, LeWinter M, Karliner JS.
To assess the efficacy of tocainide, a new oral analog of lidocaine, 30 patients with ventricular arrhythmias refractory to quinidine, procainamide and propranolol were treated with this agent. The dose of tocainide ranged from 400 to 800 mg every 8 hours. Peak tocainide blood levels 1 to 4 hours after administration ranged from 5.0 to 15.0 microgram/ml (mean 10.3). The suppression of ventricular premature beats by 75 percent or more was arbitrarily used as a measure of drug efficacy. In 13 patients who met this criterion, ventricular premature complexes, assessed with 24 hour ambulatory tape monitoring, decreased by an average of 88 percent. In 8 of 11 patients, repeated symptomatic bouts of ventricular tachycardia were completely suppressed. Considering both the response of ventricular premature complexes and the abolition of ventricular tachycardia, 18 patients (60 percent) responded to tocainide. Twenty-one patients (70 percent) had initial gastrointestinal and central nervous system side effects; most of these were transient or responded to a reduction in dose. In two patients disorientation and a skin rash required withdrawal of tocainide. These adverse effects did not appear to be due to the interaction of tocainide with other antiarrhythmic agents. It is concluded that tocainide is an effective oral agent for the therapy of potentially lethal ventricular arrhythmias refractory to other medication.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=760482&dopt=Abstract
Pflugers Arch. 1995 Feb;429(4):555-60.
Involvement of intracellular calcium ions in the release of the fluorescent dye calcein by cholinergic and alpha-adrenergic agonists from rat parotid acinar cells.
Sugita M, Shiba Y, Furuya K, Yamagishi S, Kanno Y.
Department of Oral Physiology, Hiroshima University School of Dentistry, Japan.
Effects of cholinergic and adrenergic agonists on the secretion of the fluorescent dye calcein were examined to clarify the involvement of calcium ions in the secretion of calcein from acinar cells dispersed from the rat parotid gland. Addition of carbachol (CCh) and noradrenalin (NA), but not isoproterenol (IPR), enhanced the net release of calcein from acinar cells during the subsequent 10 min in a dose range from 10(-8) M to 10(-6) M. The net release of calcein reached a maximum 7 min after the addition of CCh. The release of calcein was suppressed by the simultaneous additions of atropine with CCh, or phenoxybenzamine with NA. Addition of CCh induced a sustained dose-dependent increase in the intracellular levels of calcium ions, ([Ca2+]i). Addition of NA at 10(-6) M increased [Ca2+]i. Phenoxybenzamine completely inhibited the NA-induced increase, but propranolol did not. The removal of extracellular calcium ions did not influence the release of calcein induced by 10(-6) M CCh, but it abolished the sustained increase in [Ca2+]i. The transient increase in [Ca2+]i induced by CCh was observed in the absence of extracellular calcium ions. A calcium ion chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) inhibited the CCh-induced release of calcein. The calcium ionophore, A23187 (2.5 x 10(-6) M), but not 10(-3) M dibutyryl cAMP, evoked the release of calcein. It also increased [Ca2+]i. Removal of extracellular calcium ions suppressed the A23187-induced release of calcein.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7617446&dopt=Abstract
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