Antagonism by suloctidil of arterial thrombus formation in rats

Roba, J.; Bourgain, R.H.; Andries, R.; Claeys, Martine; Opstal, W. Van; Lambelin, G

doi:10.1016/0049-3848(76)90106-7

Cited by 12 publications

(5 citation statements)

References 8 publications

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“…Previous reports show that suloctidil has marked antispasmodic effects (4), inhibits some in vitro measurements of platelet function and is an effective antithrombotic agent in a number of experimental models and some clinical conditions (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). These effects have been attributed to membrane changes (25,26), cellular metabolic alterations (26,27) or competitive inhibition of stimuli (3).…”

Section: Studies With Suloctidilmentioning

confidence: 99%

“…Suloctidil, used originally as an antispasmodic agent for the treatment of cerebral and peripheral artery insufficiencies (3,4), has been reported to decrease arterial thrombosis in dogs and rats (5,6), rabbits (7) and bats (8). In man, suloctidil (200 mg tid) has been reported to normalize shortened platelet survival in patients with artificial heart valves (9, 10) suggesting that the drug altered platelet function in vivo, as implied by ex vivo studies (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

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Studies of Suloctidil in Experimental Thrombosis in Baboons

Hanson

Harker

1985

Thromb Haemost

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SummarySuloctidil has been evaluated in the baboon for its antithrombotic efficacy using models of both acute and chronic arterial thrombogenesis. Acute thrombus formation was initiated by Dacron vascular grafts inserted as extension segments into chronic arteriovenous shunts. 111In-platelet deposition was measured by scintillation camera imaging for one hour. The results after oral administration of suloctidil (100 mg/kg/d in two divided doses) were not different from control studies. Moreover, concurrent heparin anticoagulation did not affect 111In-platelet deposition compared with control data. In contrast, ticlopidine (20 mg/ kg/d) significantly decreased platelet deposition that was reduced further by the addition of heparin.Chronic arterial-thromboembolism was initiated by segments of polyurethane (Biomer) cannula introduced into chronic arteriovenous shunts. Thrombus formation by the polyurethane cannula was measured as 111In-platelet turnover (corrected for removal of senescent platelets). Cannula platelet consumption was unaffected by suloctidil (20 mg/kg/d given in two divided doses for two days preceding and throughout the period of platelet survival measurement). In contrast, dipyridamole (10 mg/ kg/d) and sulfinpyrazone (100 mg/kg/d) completely interrupted cannula platelet consumption.We conclude that suloctidil probably has little or no effect on platelet-dependent thrombus formation.

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Section: Studies With Suloctidilmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Studies of Suloctidil in Experimental Thrombosis in Baboons

Hanson

Harker

1985

Thromb Haemost

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“…Aggregation induced by ADP in extracorporeal circuitry connected to the circulation of anesthetized rats was effectively prevented by suloctidil at 0.1 mg/kg, i.v. or higher doses (57). By oral administration, the drug at doses from 50 mglkg protected mice dose-dependently against lethality caused by ADP, an effect that is believed to be caused by embolization of platelet aggregates.…”

Section: Effect On Platelet Functionmentioning

confidence: 99%

Suloctidil

Roba¹,

Calderon²,

Cavalier³

et al. 1986

Cardiovascular Drug Reviews

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“…Our study is there fore designed to evaluate the effectiveness of a new drug, suloctidil, on the coagulation and platelet parameters in patients with cardiac valve prosthesis and abnormal platelet functions. suloctidil exhibits a marked antithrombotic effect in various experimental animal models (15) and an inhibitory action in vitro and in vivo on platelet aggregation (16,17).…”

Section: Introductionmentioning

confidence: 99%

Effects of Suloctidil on Platelet Survival Time Following Cardiac Valve Replacement

Beys¹,

Ferrant²,

Moriau³

1981

Thromb Haemost

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SummaryPlatelet functions and blood clotting parameters were examined in 23 patients with a shortened platelet survival time after cardiac valve replacement.Treatment was given at random: for a first group antivitamins K with suloctidil and for the second group antivitamin K alone.Six weeks of treatment with antivitamin K alone did not induce any significant change in the platelet survival time, platelet retention or platelet factor 4 in plasma.In contrast, the shortened platelet survival time increased significantly after 6 weeks of treatment with suloctidil. Moreover the platelet retention and the amount of platelet factor 4 in plasma were significantly reduced, indicating that normalization of platelet survival is the result of decreased destruction, presumably at the level of the prosthetic surface. The clinical benefits expected from these results remain to be validated by a longer follow up period.

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Antagonism by suloctidil of arterial thrombus formation in rats

Cited by 12 publications

References 8 publications

Studies of Suloctidil in Experimental Thrombosis in Baboons

Studies of Suloctidil in Experimental Thrombosis in Baboons

Suloctidil

Effects of Suloctidil on Platelet Survival Time Following Cardiac Valve Replacement

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