Drugs online research references
J Parasitol. 1996 Oct;82(5):814-9.
Effects of verapamil on acute murine Chagas' disease.
Tanowitz HB, Wittner M, Chen B, Huang H, Weiss LM, Christ GJ, Braunstein V, Bilezikian JP, Morris SA.
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Continuous administration of verapamil significantly reduced the mortality rate of acute murine Trypanosoma cruzi infection (P < 0.05). The mechanistic basis for these observations was investigated. Verapamil and other calcium-channel blockers did not inhibit the growth of epimastigotes in culture. Furthermore, verapamil did not inhibit the intracellular growth of amastigotes in endothelial cells as determined by the uptake of 3H-uracil. There were no significant differences in parasitemia between infected mice that were untreated and those treated with verapamil. Twenty days postinfection infected, untreated mice had a parasitemia of 5.8 x 10(6) trypomastigotes/ml (SD +/- 2 x 10(6)), whereas infected, verapamil-treated mice had a parasitemia of 2.2 x 10(6) trypomastigotes/ml (SD +/- 0.5 x 10(6)). There was no significant difference in mortality between mice administered verapamil only for the initial 10 days of murine infection compared to those treated continuously. A 3-day delay in the initiation of verapamil administration reduced the mortality rate, but a 10-day delay did not. Propranolol (beta-adrenergic blocker), prazosin (alpha 1-adrenergic blocker), and diltiazem (another calcium-channel blocker) reduced the mortality but not significantly (P = 0.07). In biochemical studies of the beta- adrenergic signal transduction complex, we determined that verapamil and propranolol reversed the infection-associated decrease in myocardial beta- adrenergic adenylyl cyclase activity. In contrast, complementary western blot analysis revealed no significant changes in the G-proteins of the beta- adrenergic receptor complex 45 days postinfection. Therefore, these results suggest that the basis of verapamil's influence on the early critical period of infection is multifactorial and independent of a direct trypanocidal effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8885893&dopt=Abstract
Proc Natl Sci Counc Repub China B. 1992 Apr;16(2):84-90.
Menadione-induced cardiotoxicity is associated with alteration in intracellular Ca2+ homeostasis.
Tzeng WF, Chiou TJ, Huang JY, Chen YH.
Department of Biology, Fu Jen University, Taipei, Taiwan, Republic of China.
Cardiotoxicity of menadione was elucidated in neonatal rat cardiomyocytes. When incubated with menadione, contraction of myocytes initially slowed down and eventually stopped. Later blebs appeared on the cell surface, leading to cell degeneration. During the time of diminished cellular contraction, a large portion of endogenous ATP was depleted whilst intracellular Ca2+ levels were increased. However, if menadione was washed out prior to termination of contraction, the myocytes survived and most of the cells resumed regular contraction. Preincubation of the cells with diltiazem (a Ca2+ antagonist), or fura-2 acetoxymethyl ester (a chelate for Ca2+), or antipain (a proteinase inhibitor) suppressed menadione's ability for cellular damage. These results indicate that menadione is toxic to cardiomyocytes, and that the increase of intracellular Ca2+ is related to the mechanism of cardiotoxicity of menadione.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1494605&dopt=Abstract
Arzneimittelforschung. 1986;36(1):29-34.
Antihypertensive and cardiovascular effects of the new dihydropyridine derivative methyl (E)-3-phenyl-2-propen-1-yl-1,4-dihydro-2,6-dimethyl- 4-(3-nitrophenyl)pyridine-3,5-dicarboxylate.
Yamaura T, Kase N, Kita H, Uematsu T.
The hypotensive and cardiovascular effects of a newly synthetized dihydropyridine derivative, methyl (E)-3-phenyl-2-propen-1-yl-1,4-dihydro-2,6-dimethyl-4-(3- nitrophenyl)pyridine-3,5-dicarboxylate (FRC-8411) were investigated in rats, guinea pigs, and rabbits, in comparison with nifedipine, nicardipine, and diltiazem. In conscious hypertensive rats, FRC-8411 (0.3-3 mg/kg p.o.) was found to be an orally effective antihypertensive agent and its effect lasted for more than 7 h. This effect was gradual and yet much more potent and longer than those of other reference drugs. An accompanied tachycardia was observed after oral administration of FRC-8411 and other dihydropyridine derivatives. In anesthetized rats, FRC-8411 (3-30 micrograms/kg i.v.) also showed a gradual, potent and long-lasting hypotension with a tachycardia. FRC-8411 (up to 3 mg/kg i.v.) had no effect on the PQ interval of the ECG in anesthetized rats. In isolated guinea pig atria, FRC-8411 (10(-9) - 3 X 10(-8) mol/l) showed a negative chronotropic effect, but a higher dose of the drug was needed for induction of the negative inotropic effect. In K+-depolarized rabbit aorta and guinea pig taenia coli, FRC-8411 (3 X 10(-9) - 3 X 10(-7) and 10(-7) - 3 X 10(-7) mol/l) showed a dose-dependent inhibition of the calcium-induced contraction, and its pA2 value was 8.4 and 7.1, respectively. FRC-8411 had a much higher sensitivity to the aorta than the taenia coli, though it was less potent than nifedipine and nicardipine in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3754142&dopt=Abstract
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