Drugs online research references
Eur Heart J. 1983 Nov;4 Suppl G:35-40.
Hypertension in pregnancy: evaluation of two beta blockers atenolol and labetalol.
Lardoux H, Gerard J, Blazquez G, Chouty F, Flouvat B.
There is a major controversy over the relative value of anti-hypertensive drugs in hypertension in pregnancy. Our purpose was to study two different beta-adrenolytic drugs, atenolol, a cardioselective beta blocker, and labetalol, an alpha-beta blocker. Fifty-six hypertensive (BP greater than 140/90 mmHg) pregnant women were treated either with atenolol or labetalol. The patients were divided into two subgroups for which there were no statistical differences with regard to age, number of previous pregnancies, initial level of blood pressure and uricemia, proteinuric pre-eclampsia, beginning of therapeutic trial and delivery. The average daily dosage was 144.6 +/- 47.8 mg day-1 with atenolol and 614 +/- 47.8 mg day-1 with labetalol. This study shows: the same anti-hypertensive effect of the two drugs with control of blood pressure in 82% of the cases; a birth-weight significantly higher with labetalol (3280 +/- 555 g) than with atenolol (2750 +/- 630 g) (P less than 0.001); two still-births with atenolol; no adverse effects of the drugs during pregnancy and the neo-natal period; the trans-placental passage of atenolol and labetalol as shown by plasma dosages in the mothers and the new-born. It is concluded that atenolol and labetalol are safe and they are usually effective in the control of the hypertension complicating pregnancy. But labetalol appears to be better able to prevent the appearance of fetal growth retardation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6662119&dopt=Abstract
Neuroscience. 1995 Mar;65(1):241-51.
Norepinephrine modulates excitability of neonatal rat optic nerves through calcium-mediated mechanisms.
Honmou O, Young W.
Department of Neurosurgery, New York University Medical Center, NY 10016, USA.
We report that norepinephrine markedly increases excitability of neonatal rat optic nerves. To investigate the mechanisms of the norepinephrine-induced excitability increase, we studied isolated optic nerves from 42 neonatal (< three days old) and five adult (> three months old) Long-Evan's hooded rats. Norepinephrine (10(-6), 10(-5) and 10(-4) M) rapidly and reversibly increased the amplitude (mean +/- S.D.: 3.5 +/- 1.7%, 12.1 +/- 2.8% and 35.6 +/- 8.4%) of compound action potentials elicited by submaximal stimulation of neonatal optic nerves. The beta-1 adrenoceptor antagonist atenolol (10(-5) M) blocked the norepinephrine-induced increase in excitability but the alpha antagonist phentolamine (10(-5) M) did not. The beta agonist isoproterenol (10(-5) and 10(-4) M) increased response amplitudes (8.7 +/- 4.1% and 25.8 +/- 4.6%) but the alpha-1 agonist methoxamine and alpha-2 agonist clonidine did not. The beta antagonist propranolol blocked the isoproterenol effect. Replacing Ca2+ with Mg2+ or adding 0.8 mM of Cd2+ reversibly blocked the norepinephrine effects. Extracellular K+ concentrations did not change in optic nerves during norepinephrine application. Blockade of K+ channels with apamin (10(-6) M) or tetraethylammonium (10(-3) M) did not prevent the excitatory effects of norepinephrine. Adult rat optic nerves were insensitive to both norepinephrine (10(-4) M) and isoproterenol (10(-4) M). Our results indicate that norepinephrine increases neonatal optic axonal excitability through Ca(2+)-dependent mechanisms. The data suggest that the adrenoceptors are situated on the axons, that the excitability changes are not due to changes in extracellular K+ concentration or K+ channels sensitive to apamin or tetraethylammonium. The sensitivity of rat optic nerves to norepinephrine declined with age. Axonal adrenoceptors may play a role in optic axonal development and injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7753398&dopt=Abstract
J Am Coll Cardiol. 1986 May;7(5):1036-46.
Experimental exercise-induced ischemia: drug therapy can eliminate regional dysfunction and oxygen supply-demand imbalance.
Guth BD, Tajimi T, Seitelberger R, Lee JD, Matsuzaki M, Ross J Jr.
The purpose of this study was to test the hypothesis that moderately severe exercise-induced regional myocardial ischemia can be prevented by combined pharmacologic intervention. Eight chronically instrumented dogs were studied using an ameroid constrictor to produce critical stenosis of the left circumflex coronary artery. The dogs were studied during steady state treadmill exercise that induced regional myocardial dysfunction (reduced systolic wall thickening; sonomicrometers) and ischemia (reduced subendocardial blood flow; microspheres). During a control exercise run, wall thickening in the ischemic posterior wall decreased from 21.4 to 13.3% whereas subendocardial blood flow failed to increase normally (36% of that in the normal zone). In the control anterior wall, both wall thickening and subendocardial blood flow increased significantly during the control run. Wall thickness-left ventricular pressure loop areas were calculated as an index of regional work; this index increased abruptly with the onset of exercise in both regions but became significantly depressed in the ischemic region during the steady state exercise. Therapy with a combination of atenolol (0.3 mg/kg body weight orally), diltiazem (0.3 mg/kg intravenously) and isosorbide dinitrate (2.0 mg/kg orally) effectively prevented regional myocardial ischemia and regional dysfunction. After drug therapy, wall thickening in the posterior wall increased from 17.3% at rest to 18.8% during exercise, and the regional transmural blood flow pattern was markedly improved. The initial overshoot of the regional work index during exercise was blunted by the drug therapy, and at steady state no differences between the ischemic and control regions were detected. Thus, combined drug therapy can eliminate exercise-induced regional myocardial ischemic dysfunction and appears to normalize the oxygen supply-demand imbalance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2870095&dopt=Abstract
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