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T Godfraind

Publications and source records attributed to T Godfraind.

260 records · Page 15Linked to original sources
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Calcium channels and cation transport ATPases in cardiac hypertrophy induced by aortic constriction in newborn rats.

Cardiac enlargement due to gradual pressure overload was induced by abdominal aortic constriction in 2-day-old rats. On day 90, the functional performance of the left ventricle was assessed by acute load test (ligation of ascending aorta) in open-chest anaesthetized animals. Two subgroups, designated compensated and decompensated hypertrophy (CH and DH), were distinguished on the basis of the functional reserve of left ventricle, which was significantly impaired in DH but not in CH, and of right ventricle weight, which was markedly increased in DH but not significantly modified in CH. In total particulate fractions prepared from hypertrophied left ventricles, the levels (per g tissue) of sarcoplasmic reticulum Ca(2+)-transport systems were decreased, either slightly (by 13-16%: [3H]ryanodine binding) or moderately (by 28%: thapsigargin-sensitive Ca(2+)-ATPase activity). The number of sarcolemmal L-type Ca2+ channels ([3H]PN200-110 binding) was not modified significantly, while that of beta 1-adrenoceptors ([3H]CGP-12177 binding) was reduced, especially in the DH group (by 39%). Na+,K(+)-ATPase activity was reduced by 28% in CH and 41% in DH. [3H]Ouabain binding experiments (saturation and dissociation) indicated the existence of two high-affinity binding sites, attributable to the Na+, K(+)-ATPase alpha 3 and alpha 2 subunit isoforms; while the relatively minor alpha 3 component did not change significantly in hypertrophied ventricles, the alpha 2 component was markedly down-regulated, decreasing by 57% in CH and 82% in DH.

Animals↗
PubMedDate not supplied

Effect of a flavonoid preparation (S 5682) on experimental capillary permeability increase in rat paw and rabbit skin.

S 5682 is constituted by a flavonoid mixture of 90% diosmin and 10% hesperidin. Its action has been studied in vivo on microcirculation by measuring experimental alterations of capillary permeability and of venous pressure. Rats were pretreated by IV injection of 25 mg S 5682/kg, one hour before being submitted to a transitory compression of the posterior paw, resulting in reversible oedema that was estimated by plethysmography. The swelling of the paw in pretreated rats was lower than in controls (p less than 0.02), indicating a smaller increase of capillary permeability in rats treated with S 5682. A direct action on capillary permeability has been examined by measuring accumulation of IV injected Evans blue at the site of injection of zymosan, this accumulation was lower in pretreated rats than in controls (p less than 0.05). Similarly, in CFY rats, the pressure required to evoke capillary fragilisation was higher in S 5682 pretreated rats. Evans blue extravasation was also studied in the rabbit in which skin was irritated by topical application of chloroform of by gamma rays. Subcutaneous accumulation of Evans blue was lower in animals pretreated either IV or by oral route than in controls (p less than 0.05). S 5682 has a complex effect on microcirculation as indicated by a smaller increase in femoral venous pressure after ligation of homolateral iliac vein. The above experimental results indicate that S 5682 is acting at the venous side of the microcirculation.

Animals↗
PubMedDate not supplied

[Mechanism of action of positive inotropic substances].

The understanding of the mechanisms of action of positive inotropic substances requires an understanding of the cellular processes of cardiac contraction. The authors then examine the pharmacology of beta-adrenergic receptors and the intracellular functions of cAMP and discuss the action of dopamine, ibopamine, dobutamine, Corwin, amrinone and Vardax. They also summarize the state of the research into the digitalis receptors which revealed the existence of inotropic receptors with high affinity, different from the receptors responsible for inhibition of the Na-K pump. Finally, they discuss the possible role of cardioginine, an endogenous digitalis factor.

Calcium↗
PubMedDate not supplied

[Experimental pharmacology of calcium antagonists].

Calcium antagonists (calcium channel blockers) constitute a chemically heterogeneous group of drugs which block voltage-operated calcium channels of L-type. They specifically interact with the alpha 1 subunit of the calcium channel. Their mechanism of action has been demonstrated using pharmacological, electrophysiological and radiochemical techniques. Their therapeutic effects are not only related to their hemodynamic action but also to their remodeling effect in hypertrophic heart and arteries, to their anti-ischaemic action and to the preservation of vascular integrity during several pathologies. Drugs belonging to the second generation of calcium antagonists show various pharmacological profiles responsible for their tissue selectivity. The latter is a rational basis for novel therapeutic indications including atherosclerosis and cardiac failure.

Animals↗