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Biomedical subjects

T Godfraind

Publications and source records attributed to T Godfraind.

At least 181 records · Page 10Linked to original sources
PubMed1979

The cardioactive properties of SC4453, a digoxin analogue with a C17 beta-pyridazine ring.

SC4453 is a digoxin analogue with a pyridazine instead of a lactone ring in C17 beta. SC4453 was compared with digoxin with respect to effect on contractility and on activity of the sodium pump in guinea-pig isolated left atria stimulated at 3.3 Hz. The two glycosides stimulated the sodium pump at low concentrations and inhibited at high concentrations. At the time to peak inotropic effect, for a similar inhibition of the Na pump, the increase in systolic tension was higher with SC4453 than with digoxin, whereas the increase in diastolic tension was similar for both. These observations confirm that the inhibition of the Na pump is not the only mechanism responsible for the positive inotropic effect of cardiac glycosides.

Animals↗
PubMed1979

Alternative mechanisms for the potentiation of the relaxation evoked by isoprenaline in aortae from young and aged rats.

The action of cinnarizine and flunarizine on the relaxant effect of isoprenaline was studied in the isolated rat aorta and was compared with the action of papaverine. The results show that isoprenaline-induced relaxation and K+ contraction were reduced. On the contrary, in the presence of papaverine, isoprenaline relaxation and K+ contraction were reduced. On the contrary, in the presence of papaverine, isoprenaline relaxation was enhanced by cinnarizine and flunarizine at concentrations which were lower that those required for inducing an inhibition of the contraction evoked by K+ in the presence of 1.25 mM CaCl2; with concentrations higher than 10(-8) M both isoprenaline relaxation was enhanced and K+ contraction was depressed in a dose-dependent manner. In aged rats, isoprenaline-induced relaxation was tachyphylactic. The tachyphylaxis was prevented by cinnarizine and flunarizine. The present observations indicate that several processes might be responsible for potentiating isoprenaline action.

Aging↗
PubMed1979

A comparison of the inhibitory effect of cinnarizine and papaverine on the noradrenaline- and calcium-evoked contraction of isolated rabbit aorta and mesenteric arteries.

The inhibitory effects of cinnarizine and papaverine on the noradrenaline- and Ca-induced contraction of the rabbit thoracic aorta and mesenteric arteries have been compared. Papaverine was equally effective in reducing the contractile response evoked from both thoracic aorta and mesenteric arteries by the two modes of stimulation. Cinnarizine blocked the Ca-evoked contraction of the depolarized vessels but was less effective against the noradrenaline-induced contraction of the mesenteric arteries and even failed to antagonize the response of the thoracic aorta to noradrenaline. In Ca-free medium noradrenaline (10-5 M) evoked a fast non-sustained contraction. After readmission of CaCl2 a slow sustained contraction developed. In mesenteric arteries exposed to noradrenaline, cinnarizine selectively blocked the Ca0 dependent response while papaverine inhibited the initial fast response more than the Ca0 dependent one. These results suggest that cinnarizine and papaverine antagonize vascular contraction by different mechanisms. Cinnarizine seems to act by reducing membrane permeability to extracellular calcium. Papaverine inhibits the contraction by a main action on intracellular sequestration of activator calcium and to a lesser degree by an action similar to that of cinnarizine.

Animals↗
PubMed1979

Stimulation and inhibition of the sodium pump by cardioactive steroids in relation to their binding sites and their inotropic effect on guinea-pig isolated atria.

1 The actions of ouabain, ouabagenin and dihydroouabain on the contractility and on the ionic content have been investigated in left guinea-pig atria stimulated at 3.3 Hz. The specific binding of ouabain and its displacement by the other cardenolides have been determined. 2 The action of either ouabain or ouabagenin on Na and K content was qualitatively different according to the concentration employed. Low doses evoked a reduction of Nai whereas high doses produced an increase. Dihydroouabain evoked only a Nai gain. 3 The increase of KCl concentration from 2.7 to 12 mM decreased Nai in untreated atria and displaced ouabain dose-effect curves to the right. 4 ED50 values for the positive inotropic effect were lower than ED50 values for the inhibition of the pump and were not similarly affected by an increase in KCl concentration. 5 The specific binding of ouabain occurred at high and low affinity sites, related to Na pump stimulation and inhibition respectively. 6 The increase in KCl reduced the affinity of the two groups of sites for ouabain and increased the capacity of the high-affinity sites whereas the capacity of the other sites remained unchanged. 7 The results confirm the existence of two specific binding sites for ouabain in guinea-pig heart and suggest that the inhibition of the Na pump is not the only mechanism responsible for the positive inotropic effect of cardiac glycosides.

Animals↗
PubMed1979

[Beta-blockers].

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Adrenergic beta-Antagonists↗
PubMed1979

An analysis of the reduction by creatinol O-phosphate of the myocardial lesions evoked by isoprenaline in the rat.

The distribution and the size of lesions evoked in rat heart by the injection of isoprenaline 30 mg/kg have been estimated in rat pretreated or not by various dosages of N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate (creatinol O-phosphate). It has been observed that the number of lesions was inequally distributed in the various parts of the heart. Creatinol O-phosphate pretreatment reduced both the number and the size of the reactive areas. The reduction of the number of foci was dose-dependent. The action of the lowest creatinol O-phosphate doses was increased by a pretreatment during 4 days instead of the 4 h pretreatment initially used. The size of the reactive area was also reduced but in a manner indicating an action of large creatinol O-phosphate dosages on the microcirculation. It is concluded that, due to its protective action against cardionecrosis, creatinol O-phosphate has great potential value in patients with myocardial infarction in whom the extent of the infarct size may be limited by an action on the jeopardized area.

Animals↗
PubMed1979

The action of creatinol 0-phosphate on the inotropic effect of isoprenaline in isolated rat atria and in anesthetized dogs.

The action of N-methyl-N-(beta-hydroxyethyl) guanidine O-phosphate (creatinol O-phosphate) was studied on the contractility of the heart, in vitro on isolated rat atria and in vivo in anesthetized dogs. Creatinol O-phosphate was without action on the contractility of isolated rat atria stimulated by isoprenaline 10(-8) mol/l which produced the maximum inotropic effect. Creatinol O-phosphate increased the contractility evoked by isoprenaline 10(-5) mol/l and impaired the development of the negative inotropic effect evoked by prolonged treatment with this large dose. In dogs, creatinol O-phosphate pretreatment increased the positive inotropic effect of large but not low isoprenaline dosages. It is concluded that creatinol O-phosphate increased the contractile efficiency of the heart submitted to the action of an excess of catecholamines.

Animals↗
PubMed1979

Ionic changes evoked by isoprenaline in rat hearts in vivo and in vitro and their reduction by creatinol O-phosphate.

The action of large doses of catecholamines on the Ca and Mg content of rat heart has been examined both in vivo and in vitro. It was observed that the ionic changes evoked in vitro by isoprenaline 10(-5) mol/l were similar to those evoked in vivo by isoprenaline 30 mg/kg and that both were reduced by N-methyl-N-(beta-hydroxy-ethyl)guanidine O-phosphate (creatinol O-phosphate) in a dose-dependent manner. ED50 was equal to 3 x 10(-7) mol/l. These results indicate that the cardionecrotic action evoked in vivo by isoprenaline and its reduction by creatinol O-phosphate may be attributed to a direct action on the myocardial cell.

Animals↗