Ng against infarction by the lanthanide VX-222 VCH222 cation, gadolinium. We have already shown that G-d Contractile dysfunction mpft with various diseases, including normal-tron of the connected Is not normal, and Ish Mie-reperfusion cardiomyopathy. In the present study, the administration of Gd decreases in the Isch Chemistry reperfusion Infarktgr E in a dose-dependent Ngigen way by a mechanism involving the activation of two JAK / STAT and p44 MAPK and the KATP channel. The infarct-reducing effect of G-d is dose- Independent, with a maximum reduction of the apparent Infarktgr S at a dose of 20 mol / kg. Could we not observe a reduction in Infarktgr E with Gd to 40 mol / kg, the dose used to Gysembergh et al, cardioprotection induced by volume overload block, but we observed protection with D.
Gd doses of 5 to 30 mol / kg. These results illustrate the nature of the dose- Ngigen protect against heart attack with Gd and lead to stress the need for dose-response studies in determining potential cardioprotective properties of new drugs. Temporal effects of SKI-606 Gd on IR were observed in this study are important because they have a potential for broad applications for the use of Gd in various clinical scenarios suggest. Bet Similar to previous observations in Exerted myocardial Gd in this study was effective to protect the heart from infarction if, before the start of Ish Mie administered or if w Administered during Isch mie. May offer cardiovascular protection God administers if, before the Isch Chemistry in the parameters provided, where k IR occur Nnte as elective coronary bypass surgery or percutaneous intervention urgently.
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This effect may also have important clinical applications in revascularization, where recurrent ish Chemistry can occur shortly after surgery, graft occlusion or by the failure of PCI. The cardioprotective effect of Gd observed in this study, shining through multiple mechanisms, including normal, both the JAK / STAT and MAPK-mediated p42/p44 part of the road to recovery kinase reperfusion. The JAK / STAT signaling pathway plays a role Essential in the myocardium in response to various insults, including normal heart attack. In addition, it has an r The market leader in cardiovascular therapies such as isch Mix Pr Conditioning. Further studies are needed to determine whether other elements of the pre-treatment such as PKC, adenosine receptors, kinases and play Akt/PI3 r In Gdinduced cardioprotection. The JAK / STAT signaling pathway plays an R Significant zinc in development Siege Pr Conditioning. Our study shows th