Adenosine, Cardioprotection and Its Clinical Application by Robert M. Mentzer Jr., Masafumi Kitakaze, James M. Downey,
By Robert M. Mentzer Jr., Masafumi Kitakaze, James M. Downey, Masatsugu Hori
It's been virtually 15 years because the fIrst studies seemed indicating that adenosine exerted a .protective influence in ischemic and reperfused myocardium. quite a few experimental experiences have proven that adenosine (both exogenous and endogenous adenosine) delays the onset of ischemic contracture, modulates myocardial metabolism in the course of ischemia, attenuates reversible postischemic ventricular disorder (myocardial stunning), and decreases myocardial infarct measurement. preliminary experiences on adenosine's cardioprotective influence have been in line with its skill to stimulate postischemic ATP resynthesis, raise coronary blood stream, and decrease center price. even supposing those activities of adenosine are absolutely necessary to the ischemic/reperfused center, it now seems that adenosine's cardioprotective influence should be particular of those houses. The large progress within the variety of articles on adenosine cardioprotection within the final numerous years has been similar largely to the speculation that adenosine performs a task in ischemic preconditioning. Ischemic preconditioning is the phenomenon during which a short interval of ischemia (and reperfusion) ahead of a extra lengthy occlusion reduces myocardial infarct measurement. this kind of myocardial security has got a lot curiosity simply because ischemic preconditioning has been proven to be the main powerful technique of lowering infarct measurement in all animal versions so far validated. actually sooner than experiences implicating adenosine's position in ischemic preconditioning, adenosine's infarct decreasing influence was once now not good well-known.
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Extra resources for Adenosine, Cardioprotection and Its Clinical Application (Developments in Cardiovascular Medicine)
The occurrence of apoptosis in ischemic myocytes only when they are subjected to reperfusion suggests a reperfusionspecific process that could lead to delayed cell death. , myocardial stunning which often persists for several days. It is 21 II. CARDIOPROTECfION AND MECHANISMS OF ISCHEMIC AND REPERFUSION INJURY reported that intracoronary infusion of the cell-permeable antioxidant MPG (N-[2mercaptopropionyl]glycine) 1 min before reperfusion significantly attenuated the stunning in a canine model subjected to 15 min-ischemia and reperfusion.
In the preliminary study, adenosine-induced coronary vasodilation was strongly enhanced when we additionally administered nicorandil and cromakalim, K+ channels openers. This potentiation of adenosine-induced coronary vasodilation may be also beneficial for the ischemic myocardium, however, how this linkage is related to coronary flow autoregulation is unknown. As the mechanical factors which may regulate autoregulation, tissue pressure and myogenic mechanism have been proposed. 16 The tissue pressure hypothesis indicates that a rise in arterial pressure transiently increases fluid exudation at the capillaries and the perivascular fluid pressure increases vascular resistance by mechanical compression.
Acknowledgments Supported in part by NIH ROI Grants HL-43151 and HL-55757. References \. 2. 3. 4. 5. Bolli R. The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase: an overview. Basic Res Cardiol 1996;91 :57-63. Sun J-Z, Tang X-L, Knowlton AA et al. Late preconditioning against myocardial stunning: An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 hours after brief ischemia in conscious pigs.