Drugs online research references
Thromb Res. 1984 Aug 15;35(4):421-30.
Vasoactive agonists prevent erythrocyte extravasation in thrombocytopenic hamsters.
Shepro D, Welles SL, Hechtman HB.
The mediating action of selected vasoactive amines and their respective antagonists on vascular fragility, visible as cutaneous petechiae, was assayed with thrombocytopenic (TCP) hamsters. Serotonin (5-HT), norepinephrine (NE), epinephrine, dopamine and isoproterenol administered IP reduced petechiae significantly within 10 min; phenylephrine had no effect. Of the natural amines, 5-HT and NE were most effective in reducing petechial sensitivity to values obtained with untreated, normal animals; hence these two amines only were tested pharmacologically. Pretreatment of TCP animals with Ketanserin or propranolol, administered IP or IV, abolished any petechial inhibitory action of 5-HT and NE respectively; pretreatment with phenoxybenzamine reduced significantly the NE inhibition of petechiae, but to a lesser degree than propranolol. In contrast, atenolol, prazosin and yohimbine had no significant effect. Ketanserin abolished the action of NE, but adrenoceptor blockers had no effect on 5-HT-treated TCP hamsters. The results suggest that 5-HT and NE inhibition of petechiae may be receptor-mediated and that there may be receptor interaction. This was supported by the observation that non-additive subthreshold doses of 5-HT and NE, which individually did not prevent petechial formation in TCP hamsters, when combined totally inhibited petechiae. The theorized importance of endogenous 5-HT and NE to maintain postcapillary venule junctional integrity (site of petechial hemorrhaging) was also demonstrated by treating normal hamsters with drugs known to block or antagonize either 5-HT or NE uptake. In every instance petechial sensitivity rapidly occurred, and the loss of microvascular integrity in Ketanserin-treated hamsters mimicked quantitatively the petechial sensitivity observed with TCP animals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6484891&dopt=Abstract
Arch Inst Cardiol Mex. 1983 Jan-Feb;53(1):49-56.
[Acute electrocardiographic effects of minoxidil in hypertensive subjects]
[Article in Spanish]
Sanchez Torres G, Panzzi ME, Kuri J, Trevethan S, Castillo LR.
Unexplained ST-T segment (ST-TD) or T wave depressions (TWD) in the electrocardiogram (EKG) are seen during minoxidil therapy. To study the possible cause of this phenomenon 69 essential systemic hypertensive patients were evaluated. At the 5th day of a double therapy (DT) period consisting in the administration of atenolol 100 mg/day and chlorthalidone 50 mg/day systolic blood pressure (SBP), Sokoloff Index (SI) (EKG: Svl + Rv5-v6), EST-T (sum of ST-TD and TWD areas in 9 derivations of EKG) and potassium (K) serum levels were determined. Minoxidil (10 mg/day) was added and 3 to 6 days after, all parameters were repeated. Patients were classified in group A: (GA, n25 =) or B: (GB, n = 44) at the end of the study according to the absence or presence of ST-TD or TWD, respectively. During DT, SBP and SI were lower in GA (145.3 +/- 20.9 mm of Hg and 23.8 +/- 7.5 mm, respectively): (all values in X and S) than GB (173.5 +/- 24.4 and 34.0 +/- 8.3 respectively) (p less than 0.001 for both values) delta SBP (X and S of changes at the end of the study) diminished more in GB (-40.7 +/- 22.2 mm of Hg, p less than 0001) than in GA (-20.1 +/- 15.0, p less than 0.001) (GB-GA p less than 0.001). Correlation coefficient of SBP -delta SBP in both groups and delta SBP-delta EST-T in GB was 0.75 and 0.66 (p less than 0.001 for both values) respectively. delta K was not significant. Twenty five out of 27 patients of GB didn't have stenotic lesions by coronariography. Minoxidil induced ST-TD or TWD may be due to a fall in coronary perfusion pressure in patients with left ventricular hypertrophy and poor coronary circulatory reserve. This hipothesis implies that coronary autoregulation is lost in this stage of disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6870384&dopt=Abstract
Eur J Pharmacol. 1990 May 31;181(1-2):83-8.
Reversal of alpha-adrenoceptor blockade by propranolol in isolated rat pulmonary artery.
Abdelrahman A, Nguyen H, Pang CC.
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Pulmonary artery rings were prepared from rats (group I to VI, n = 5-7 per group) in order to investigate if a beta-adrenoceptor antagonist interferes with the effect of alpha-adrenoceptor blockade. In I, four cumulative noradrenaline (NA) dose-response curves (10(-9) to 10(-3) M) were constructed. In II, NA curves were constructed first, without blockers, then in the presence of phentolamine (10(-6) M), then propranolol (10(-8) M), then phentolamine plus propranolol (10(-8) M). III, IV and V were treated similar to II, except that atenolol (10(-8) M), ICI 118,551 (10(-8) M) and propranolol (10(-6) M), respectively, were added instead of propranolol (10(-8) M). In VI, NA (10(-6) M) was added followed by phentolamine and then propranolol (10(-9) to 10(-6) M). Phentolamine shifted the NA curve to the right with an increase in the EC50 value. Propranolol but not atenolol or ICI 118,551, reduced the elevated EC50 values caused by phentolamine. In group VI, the increase in force by NA was reduced by phentolamine; the effect of phentolamine was completely abolished by propranolol. Thus, propranolol interferes with the effect of phentolamine in the rat pulmonary artery.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1974860&dopt=Abstract
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