Mechanism of cardiotonic steroids

To maintain anti-inflammatory effects while minimizing skin sensitization, a parthenolide-depleted (PD) extract of feverfew was developed. To ensure parthenolide was removed, over 1,200 patients were patch-tested for skin sensitization. The PD-feverfew inhibited the activity of 5-lipoxygenase, phosphodiesterase-3, and phosphodiesterase-4. It also inhibited the release of pro-inflammatory mediators, such as nitric oxide, prostaglandin E2, and tissue necrosis factor (TNF)-alpha from macrophages and TNF-alpha IL-2, IFN-gamma, and IL-4 from human peripheral blood mononuclear cells. However, it was ineffective in the inhibition of cyclooxygenase-1 or -2. 6

This report describes various old and new positive inotropic drugs with respect to their mechanisms of action. Drugs with established cardiotonic effects include cardiac glycosides, beta 1-adrenergic agents, glucagon, histamine and the methylxanthines. New agents discussed are prenalterol, beta 2- and alpha-adrenergic drugs, amrinone and sulmazole. Prenalterol is a beta 1-adrenergic agent. Beta 2-adrenergic drugs, amrinone and sulmazole, combine a positive inotropic and a vasodilator effect. The latter resemble theophylline and other methylxanthines in that they appear to act mainly as phosphodiesterase inhibitors with a subsequent increase in cyclic adenosine monophosphate (cAMP). The mechanism of the positive inotropic effect of alpha-adrenergic stimulating agents (for example, phenylephrine) is unknown. It is independent of the cAMP system and is not accompanied by changes in frequency.

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Mechanism of cardiotonic steroids

mechanism of cardiotonic steroids

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