Methylthioninium chloride: pharmacology and clinical applications with special emphasis on nitric oxide mediated vasodilatory shock during cardiopulmonary bypass

Abstract

Vasodilatory shock after cardiopulmonary bypass is a common complication requiring treatment with high doses of inotropes and prolonged stays in the intensive care unit. The vasodilatory shock is initiated by an inflammatory response to the extracorporeal circuit. The inflammatory response results in endothelial synthesis and release of nitric oxide resembling the clinical features observed in vasodilatory shock caused by septicaemia. During vasodilatory shock, the inhibition of nitric oxide synthase and the nitric oxide/cyclic guanylyl monophosphate pathway is an attractive adjunct to therapy with traditional inotropes. Methylthioninium chloride inhibits nitric oxide/cyclic guanylyl monophosphate mediated vasodilation and can successfully be used as a supplement in the treatment of vasodilatory shock associated with cardiopulmonary bypass. The application of methylthioninium chloride in septicaemia has not produced comparable positive clinical results.