Drugs online research references
Jpn Circ J. 1996 Mar;60(3):157-65.
Caffeine induces ventricular tachyarrhythmias possibly due to triggered activity in rabbits in vivo.
Ishida S, Ito M, Takahashi N, Fujino T, Akimitsu T, Saikawa T.
Department of Laboratory Medicine, School of Medicine, Oita Medical University, Japan.
Caffeine induces delayed afterdepolarizations (DADs) and triggered activity in isolated cardiac tissue. We investigated the ability of caffeine to induce triggered ventricular arrhythmias in rabbits in vivo. During continuous infusion of caffeine at doses of 0.3 or 1.0 mg/kg per min, ventricular pacing was performed with 50 stimuli with a cycle length of 220 msec (basic pacing train) every 5 min until ventricular tachycardia (VT) was induced. The effects of programmed stimulation and pharmacologic agents on the induction of ventricular ectopic beats (VEBs) were examined. Pacing protocols were carried out in the presence of vagal-induced slowing of sinus rhythm. VT was induced by a basic pacing train during the infusion of caffeine at 1.0 mg/kg per min, but not at 0.3 mg/kg per min. An increase in the pacing rate or the number of stimuli resulted in 1) a decrease in the first postpacing interval, and 2) an increase in the number of postpacing VEBs. Induction of VT was suppressed by intravenous bolus injections of verapamil, propranolol and adenosine. At the time of the initial induction of VT, the plasma concentration of caffeine was 87 +/- 2 micrograms/ml and the plasma level of norepinephrine increased from 666 +/- 166 pg/ml at baseline to 1121 +/- 245 pg/ml. These results suggest that catecholamine-associated triggered activity may be responsible for caffeine-induced VT.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8741241&dopt=Abstract
J Am Geriatr Soc. 1977 Aug;25(8):349-53.
Aging and insulin resistance in a group of nonobese male volunteers.
Kimmerling G, Javorski WC, Reaven GM.
The relationship of age to insulin resistance was determined in 100 nonobese men whose ages ranged from 22 to 69 years. Seventy of the 100 subjects had normal glucose tolerance, and 30 had chemical diabetes. Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. This approach permitted inhibition of endogenous insulin release, achievement of a comparable steady-state plasma level of exogenous insulin, and use of the height of the steady-state plasma glucose response as a direct estimate of insulin resistance. With this experimental method, no correlation was found between age and insulin resistance over the age span of the experimental population. Furthermore, there was no correlation between age and the height of the plasma glucose response to an oral glucose challenge in this population of nonobese, healthy ambulatory men.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=874246&dopt=Abstract
Res Commun Mol Pathol Pharmacol. 1995 Nov;90(2):221-33.
Biological effects of diesel exhaust particles (DEP) on tissues and cells isolated from respiratory tracts of guinea pigs.
Hirafuji M, Sakakibara M, Endo T, Murakami S, Mori Y, Sagai M, Minami M.
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Japan.
Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) instilled intratracheally into mouse caused lung edema accompanying endothelial cell damage. In order to clarify further the biological effects of DEP on the respiratory system, the primary target of DEP instillation, we examined the direct action of DEP on isolated tissues and the cytotoxicity of DEP on cultured cells of respiratory tracts in guinea pigs. DEP were collected on glass fiber filters from a light-duty (2730 cc), four cylinder diesel engine. DEP induced a dose-dependent relaxation in tracheal smooth muscle and lung parenchymal preparations from guinea pigs. Neither propranolol nor ranitidine inhibited the relaxing effect of DEP on tracheal preparations. DEP also exhibited concentration- and time-dependent cytotoxicity on cultured tracheal smooth muscle cells and lung fibroblasts from guinea pigs, as assessed by specific [51Cr] release. These cytotoxicities induced by DEP were significantly inhibited by catalase, deferoxamine and MK-447, whereas SOD and mannitol had little effect. These inhibitory effects were blunted by the higher concentration of DEP. These results suggest that the cytotoxicity of DEP may cause dysfunction of respiratory tissues, which are mediated via oxygen radicals, probably hydroxyl radicals or hydrogen peroxides.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8747791&dopt=Abstract
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