Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Practolol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,387 records · Page 77Linked to original sources
PubMed1984

Influence of long-term beta receptor stimulation with prenalterol on intrinsic heart rate in rats.

Previous studies have shown that the intrinsic heart rate (IHR) may undergo changes, e.g., decrease after long-term endurance training. The mechanism for this adaptation is not known. In this study, rats were subjected to long-term oral treatment with the beta receptor stimulating drug prenalterol. During the treatment period heart rates at rest and during submaximal exercise were measured. Heart rate after 30 min rest and also 2 min after exercise was higher in the treated animals, due to the beta stimulation. The treated rats had a significantly lower heart rate increase during exercise than untreated controls, consistent with a partial beta-blocking effect of the drug in states with a high endogenous sympathetic activity. Therefore, the animals were not trained but only exposed to the increased stimulation of cardiac beta receptors accomplished by the drug while at rest. After 25 weeks, prenalterol was withdrawn and the IHR was measured in situ after a denervation procedure. The treatment with prenalterol had not altered the IHR. Our previous results from training studies indicate that a heart rate increase above a certain level or the stimulation for a lower setting of the IHR as seen after endurance training. In this study chronic beta receptor stimulation with prenalterol did not influence the IHR, which supports that hypothesis.

Adrenergic beta-Agonists↗
PubMed1983

Effects of prenalterol on cardiac performance and transmural myocardial perfusion in patients with chronic renal failure.

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.

Aged↗
PubMed1985

Effects of beta-adrenoceptor stimulation on rectosigmoid motility in man.

Effects of selective beta-adrenoceptor agonists on rectosigmoid motility during prolonged rectal distension were studied in 12 healthy volunteers in a double-blind, randomized fashion. Continuous distension was performed with a balloon in the proximal part of the rectum. Pressure was recorded by this balloon and by a catheter in the sigmoid. Contractile activity was quantified for three consecutive periods of 25 min. On separate days prenalterol (beta-1 agonist), terbutaline (beta-2 agonist), and placebo, respectively, were administered intravenously preceded by a control period. Terbutaline, 0.5 mg intravenously, was followed by a significant decrease of sigmoid motility from 4.3 +/- 1.5 (SEM) kPa X min to 2.9 +/- 1.0 kPa X min (P less than 0.01) and of rectal motility from 4.3 +/- 1.3 to 2.4 +/- 0.7 kPa X min (P less than 0.05). After placebo a slight, but not significant, increase of contractile activity was seen compared to the initial control period. The effects of prenalterol, 1.0 and 4.0 mg intravenously, on motility did not differ from that of placebo infusion. Both drugs caused a dose-dependent increase of systolic blood pressure and of heart rate. The study shows that beta-2-adrenoceptor stimulation decreases rectosigmoid colonic pressure in man, while effects of beta-1 stimulation on motility index do not differ from that of placebo.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Arrhythmogenic dose of acetylstrophanthidin unchanged by beta-sympathomimetics in conscious dogs.

The enhanced arrhythmogenic risk of combined treatment with cardiac glycosides and beta-sympathomimetics is referred in some textbooks, but only a few detailed studies on in vivo models are available. We therefore investigated this problem in conscious dogs in an intraindividual study. We determined the dose of acetylstrophanthidin (intravenous infusion of 5 mcg/kg per min), which provoked ventricular premature beats with and without concomitant treatment with the partial beta-agonistic compounds doxaminol (3 mg/kg p.o.), prenalterol (0.4 or 1.0 mg/kg p.o.) or isoprenaline (0.31 +/- 0.100 mcg/kg per min). In some dogs a coronary artery was narrowed in order to reduce the coronary blood supply. The arrhythmogenic dose of acetylstrophanthidin was nearly the same in all the groups investigated (range from 52.1 +/- 5.66 to 59.9 +/- 3.23 mcg/kg). Whereas the arrhythmogenic dose of acetylstrophanthidin was unchanged by beta-sympathomimetics, the combination of the glycoside and each of the beta-agonistic drugs increased the contractile force more than did either single compound. We therefore conclude that the arrhythmogenic risk of the combination of glycosides and beta-sympathomimetics may be--at least in experimental models--less than has been suggested in the past.

Adrenergic beta-Agonists↗
PubMed1979

Modification by levo-propranolol of tremors induced by harmine in mice.

It has been recently reported that the levo isomer of propranolol possesses anti-serotonin properties in animals. Since harmine-induced behavioural changes in mice are reported to be mediated through central serotonergic receptors, an attempt was made to test whether 1-propranolol would also modify harmine-induced responses by virtue of its anti-serotonergic or anti-adrenergic property. The results indicated that l- and dl-propranolol inhibited central serotonin receptor mediated responses to harmine in mice, a finding that is analogous to other recent observations.

Animals↗
PubMed1984

Apparent superiority of H2-receptor stimulation and simultaneous beta-blockade over conventional treatment with beta-sympathomimetic drugs in post-acute myocardial infarction: cardiac effects of impromidine--a new specific H2-receptor agonist-in the surviving catecholamine-insensitive myocardium.

Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to beta-adrenergic and H2-histaminergic stimulation by isoproterenol and impromidine tested in the isolated perfused heart preparation. Adenylate cyclase activity as well as binding characteristics of [3H]-dihydroalprenolol ([3H]-DHA), [3H]-methyl-tiotidine ([3H]-TIOT) and [3H]-quinuclidinyl benzilate ([3H]-QNB) to cardiac beta 1-, H2- and cholinergic muscarinic receptors were determined in sarcolemmal membrane preparations of the right ventricle of the same hearts. In addition, an attempt was made to elucidate the therapeutic value of post-AMI treatment with impromidine in the presence and absence of beta-blockade, in contrast to administration of prenalterol and the conventional therapy with beta-sympathomimetic drugs, e.g. dobutamine. Three days post-AMI the dose-response curve for isoproterenol of right ventricular dP/dtmax was significantly depressed, while the inotropic effect of impromidine was not impaired. Stimulation of adenylate cyclase activity by isoproterenol was reduced by 80% whereas impromidine and NaF stimulation rates were unaltered. Receptor-binding studies indicated a 90% loss and 10-times lowered affinity (KD) of the remaining beta-receptors while specific [3H]-TIOT- and [3H]-QNB-binding was unchanged. Administration of dobutamine increased mortality rates and extension of infarct size, led to a further decrease in contractile response to isoproterenol, induced complete insensitivity of adenylate cyclase to isoproterenol stimulation and caused pronounced additional reduction of number and affinity of [3H]-DHA-binding sites. In contrast, all above alterations were prevented by treatment with either prenalterol or combined administration of impromidine plus metoprolol. It is concluded, that these alterations in the non-ischemic, uninvolved myocardium post-AMI are the result of catecholamine-induced specific damage of sarcolemmal beta-receptors. Furthermore, treatment with H2-agonists in combination with beta-blocking agents may have beneficial effects, whereas conventional therapy with beta-sympathomimetic drugs tends to worsen the already depressed function of the beta-adrenergic stimulation mechanism.

Adenylyl Cyclases↗
PubMed1981

Short- and long-term effects of hydralazine and combined hydralazine-prenalterol therapy in severe chronic congestive heart failure.

The hemodynamic benefits of combined administration of prenalterol (P) with hydralazine (H) were evaluated in ten patients with severe chronic heart failure. Single administration of 100 mg H increased cardiac index (CI) from 2.3 to 3.0 l/min/m2, whereas pulmonary capillary wedge pressure (PWC) remained unchanged. After 3--4 weeks of treatment with 200 mg H hemodynamic improvementt was maintained (CI: 2.9 l/min/m2). Additional administration of P caused further augmentation of CI (3.3 l/min/m2). After long-term treatment with the combination of H and P sustained augmentation of CI (3.2 l/min/m2), and, furthermore, a slight but significant decrease of PCW were observed (p less than 0.05 vs. chronic single H-therapy). Five patients were able to perform exercise testing; H improved maximal exercise capacity and exercise hemodynamics in three patients. Further improvemen was observed after combined treatment (H + P) in three of five patients. It is concluded, the prenalterol may enhance the effectiveness of hydralazine therapy in congestive heart failure by providing concomitantly the principal actions of the vasodilator and positive inotropic agent used separately. Furthermore, the results indicate that oral long-term administration of hydralazine and prenalterol can produce sustained beneficial improvement.

Adult↗