Antiplatelet and antithrombogenic effects of suloctidil

Roba, J.; Claeys, Martine; Lambelin, G

doi:10.1016/0014-2999(76)90034-0

Cited by 34 publications

(7 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

Studies of Suloctidil in Experimental Thrombosis in Baboons

Hanson

Harker

1985

Thromb Haemost

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

Studies of Suloctidil in Experimental Thrombosis in Baboons

Hanson

Harker

1985

Thromb Haemost

View full text Add to dashboard Cite

show abstract

“…There was a perfect hepatic tolerance at all doses tested. In the rat study as well as in a 24-month study in mouse (30,60, and 120 mgkg per day in food), no carcinogenic potential of suloctidil was evident. The drug had also no mutagenic potential (Ames Salmonella test, rat micronucleus test).…”

Section: Toxicologymentioning

confidence: 86%

Suloctidil

Roba¹,

Calderon²,

Cavalier³

et al. 1986

Cardiovascular Drug Reviews

Self Cite

View full text Add to dashboard Cite

“…The relaxing effect of suloctidil on vascular smooth muscle can be ex plained by its activity as calcium antagonist [2]. The antithrombotic action of suloctidil has been demon strated in a variety of animal models of thrombosis: it decreases the incidence of occlusive thrombi in the fémoral artery of dogs, foUowing a localized removal of the endothelium, and reduces the incidence and severity of expérimental hepatic thrombophlebitis in rats [3]. This antithrombotic activity can be explained, at least partially, by an inhibitory effect on platelet aggregation, which has been demon strated in vivo in animais and man: oral suloctidil reduces the spontaneous formation of circulating platelet aggregates in aged breeder rats [4], nor malizes the reduced platelet survival time in patients bearing prosthetic heart valves [5,6] and reduces the plasma level of )Sthromboglobulin in patients with intermittent claudication [7].…”

Section: Suloctidilmentioning

confidence: 99%

Stimulation of prostacyclin production in blood vessels by the antithrombotic drug suloctidil

Boeynaems¹,

Coevorden

Demolle³

1987

Biochemical Pharmacology

View full text Add to dashboard Cite

Suloctidil is a calcium antagonist with vascular relaxing activity and an antithrombotic agent: its antiplatelet action has been demonstrated in vivo, but is difficult to reproduce in vitro and the mechanism of this effect remains unknown. We have observed that suloctidil (10 microM) stimulated the release of prostacyclin (PGI2) from the rabbit aorta, the dog vena cava and the dog portal vein, in vitro. This effect could be explained by an increased mobilization of free arachidonic acid. Neither the inactive congener CP894S, nor the two calcium channel antagonists, verapamil and flunarizine, reproduced the stimulatory effect of suloctidil. Suloctidil acted selectively on the vascular endothelium: it stimulated the release of PGI2 from bovine aortic and human umbilical vein endothelial cells, but neither from the de-endothelialized rabbit aorta nor from the bovine aortic media. The stimulatory effect of suloctidil on the release of the platelet inhibitor PGI2 from the vascular endothelium might contribute to the known antiplatelet and antithrombotic activity of this drug.

show abstract

Antiplatelet and antithrombogenic effects of suloctidil

Cited by 34 publications

References 21 publications

Studies of Suloctidil in Experimental Thrombosis in Baboons

Studies of Suloctidil in Experimental Thrombosis in Baboons

Suloctidil

Stimulation of prostacyclin production in blood vessels by the antithrombotic drug suloctidil

Contact Info

Product

Resources

About