Drugs online research references
J Dev Physiol. 1985 Dec;7(6):387-96.
Maternal treatment with a cardioselective beta-blocking agent--consequences for the ovine fetus during intermittent asphyxia.
Dagbjartsson A, Karlsson K, Kjellmer I, Rosen KG.
To evaluate the effect of chronic beta 1-adrenoceptor blockade on physiological adaptation to asphyxia a study was done on exteriorized sheep fetuses of 127-142 days gestational age. Eleven pregnant ewes were infused with metoprolol for 5 days prior to experiment. Another 10 ewes were infused with saline and served as controls. Asphyxia was induced by intermittent complete obstruction of maternal placental blood flow. Fetal electro-cardiogram, heart rate, cardiac output, myocardial contractility and cerebral blood flow were measured together with blood pH, lactate and hypoxanthine. Neurophysiological responses were evaluated by changes in somatosensory evoked electroencephalogram. The beta 1-blocked fetuses showed less responsiveness in myocardial contractility and heart rate during reoxygenation. This curtailed reaction resulted in accelerated lactic acidosis, increased break-down of intracellular energy rich substances and impaired cerebral function. Nine of the ten controls survived the experiment and 8 of them regained their somatosensory evoked EEG potentials, whereas 7 of the 11 beta-blocked fetuses survived and only 3 regained original somatosensory evoked EEG potentials. It is concluded that beta 1-adrenoceptor blockade impairs the adaptive responses to asphyxia in the ovine fetus and decreases its ability to survive severe asphyxia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4078255&dopt=Abstract
Eur J Clin Pharmacol. 1983;25(3):287-92.
Effects of prenalterol on cardiac performance and transmural myocardial perfusion in patients with chronic renal failure.
Pedersen T, Cleemann-Rasmussen K, Brynjolf I, Ording H, Nielsen PE, Rasmussen K.
The acute haemodynamic effects of the beta-adrenoreceptor agonist, prenalterol, were studied in six patients with chronic end-stage renal failure. Prenalterol 0.8 mg, 1.6 mg, and 3.2 mg was administered i.v. as a bolus, and after the last dose the selective adrenergic beta-1-receptor antagonist metoprolol was administered i.v. in doses of 5 and 10 mg. The haemodynamic effects of the drugs were investigated using impedance cardiography and radionuclide angiocardiography. The main haemodynamic effects were a dose-related chronotropic effect, demonstrated by an increase in heart rate (26%; less than 0.05), and an inotropic effect, shown by an increase in stroke volume index (20%; p less than 0.05) and left ventricular ejection time (12%; p less than 0.05); the cardiac index was increased by 47% (p less than 0.05). Transmural myocardial perfusion (DPTI/SPTI ratio) was decreased by 22% (p less than 0.05) after prenalterol. It is concluded that prenalterol has positive inotropic and chronotropic effects in patients with chronic renal failure, that the improvement in left ventricular performance is at the expense of a decreased transmural myocardial perfusion, and that metoprolol is a specific antidote.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6628515&dopt=Abstract
Pharmacol Res. 1995 May;31(5):319-23.
Enhancement effect of carteolol on the clonidine-induced vasodilation of rat mesenteric arteries.
Ito M, Fukuda N, Izumi Y, Watanabe Y, Watanabe M, Soma M, Kanmatsuse K.
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
It has demonstrated that carteolol can increase the endothelium-dependent vasodilation induced by alpha-2 adrenergic agonist. In order to evaluate the effect of carteolol, and to clarify the mechanism, we examined the effects of 10 microM carteolol on the vasodilation induced by increasing doses (10(-7)-10(-4) M) of clonidine in perfused rat mesenteric arteries preconstricted with 100 microM phenylephrine. Clonidine elicited a dose-dependent vasodilation of the mesenteric arteries preconstricted with phenylephrine. Carteolol enhanced the vasodilation induced by higher doses (10(-5) and 10(-4) M) of clonidine, although carteolol itself exerted no direct vasodilating effect. On the other hand, 10 microM propranolol or 10 microM metoprolol did not augment the clonidine-induced vasodilation. In the presence of 100 microM NG-monomethyl L-arginine (LNMMA), an analogue of L-arginine, the enhancement of the clonidine-induced vasodilation by carteolol was abolished. This inhibition by LNMMA was restored with 300 microM L-arginine, but not with 300 microM D-arginine. These results suggest that carteolol enhances the clonidine-induced vasodilation by an endothelial-related mechanism mediated by the release of endothelium-derived nitric oxide in resistance vessels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7479530&dopt=Abstract
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