2011
DOI: 10.1016/j.thromres.2011.02.009
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Investigation into the mechanism(s) of antithrombotic effects of carbon monoxide releasing molecule-3 (CORM-3)

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Cited by 25 publications
(23 citation statements)
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“…In other in vitro and in vivo investigations involving either mice or rats [24][25][26][27], COHb concentrations varied following CORM exposure, with little increase seen with CORMs that release CO quickly (e.g., CORM-3, tricarbonyldichloro(glycinato)ruthenium (II)), contrasted with COHb values between 8% to 17% after exposure to slow releasing CORMs (e.g., CORM-A1, sodium boranocarbonate, Na 2 [H 3 BCO 2 ]). In sum, when exposed to CO at low or high concentrations (based on COHb), platelet function and measures of intravascular thrombus formation were decreased in mice and rats [18][19][20][21][22][23].…”
Section: Clinical Preclinical and In Vitro Evidence That Co Is An Anmentioning
confidence: 92%
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“…In other in vitro and in vivo investigations involving either mice or rats [24][25][26][27], COHb concentrations varied following CORM exposure, with little increase seen with CORMs that release CO quickly (e.g., CORM-3, tricarbonyldichloro(glycinato)ruthenium (II)), contrasted with COHb values between 8% to 17% after exposure to slow releasing CORMs (e.g., CORM-A1, sodium boranocarbonate, Na 2 [H 3 BCO 2 ]). In sum, when exposed to CO at low or high concentrations (based on COHb), platelet function and measures of intravascular thrombus formation were decreased in mice and rats [18][19][20][21][22][23].…”
Section: Clinical Preclinical and In Vitro Evidence That Co Is An Anmentioning
confidence: 92%
“…Similarly, administration of different CORMs Nielsen et al 5 5 [21,22] or upregulation of HO-1 [23] in rats, decreased intravascular thrombus formation following vascular injury [21,22], increased tail tip amputation bleeding time [21], and improved hepatic reperfusion following ischemia [23]. The proposed mechanism in most of these works involved platelet inhibition [20][21][22][23], and unlike in humans [12,16], rats exhibited a soluble guanylate cyclase dependent mechanism by which CO decreased platelet aggregation [21]. Critically, the investigations that evaluated plasmatic coagulation function did not demonstrate any important CO mediated hemostatic changes in vitro (e.g., prothrombin time, activated partial thromboplastin time) [21,22].…”
Section: Clinical Preclinical and In Vitro Evidence That Co Is An Anmentioning
confidence: 97%
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