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Myocardial Ischemic Preconditioning- Isoflurane-induced myocardial preconditioning is dependent on p
- Umar Sadat (20 November 2005)
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Umar Sadat, Clinical Fellow.Vascular Surgery. Addenbrooke's Hospital,Cambridge University Hospitals NHS Foundation Trust. Cambridge, UK.
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I read with great interest the article by Raphael .J et al. No doubt that authors have contributed greatly to this interesting and challenging reality of Myocardial preconditioning. However I would like to comment more about the ongoing advancements about Ischemic pre conditioning and myocardial preconditioning. Ischemic preconditioning is the strongest form of in vivo protection against myocardial ischemic injury other than early reperfusion; the possibility of using this phenomenon in clinical practice would be very desirable. Despite state-of-the-art reperfusion strategies, 30-day mortality of myocardial infarction is still quite high and the prevalence of cardiac failure is rapidly increasing and is often caused by (ischemic) death of cardiomyocytes. Thus, there is a need for additional therapeutic strategies that increase tolerance to ischemia and reperfusion. Exploitation of ischemic preconditioning may offer such a strategy. Fortunately, the accumulating knowledge about the molecular mechanisms mediating preconditioning has provided us with the possibility to modulate ischemia and limiting infarct size in myocardium in the same way as ischemic preconditioning. Several studies have shown that indeed the presence of preinfarction angina, especially within 24 hours before infarction, is associated with improved clinical outcome after acute myocardial infarction, including death and the incidence of heart failure, with reduced CK release and with a smaller area of necrosis as assessed by nuclear imaging1. Moreover, Andreotti et al. showed that preinfarction angina is associated with a more rapid reperfusion of the infarct-related artery following thrombolysis, which is an attractive alternative explanation for the beneficial effect of angina2. Besides above-mentioned mechanism of cardio protection by Isoflurane, protection against ischemia-reperfusion injury is partly by attenuating cytochrome c release from subsarcolemmal mitochondria in isolated rat hearts (Qian et al). Myocardioprotective effects of isoflurane preconditioning have been associated with attenuation of cytochrome c loss from the inner membrane of subsarcolemmal mitochondria. Different volatile anesthetics have been compared. Desflurane and sevoflurane has been found to reduce myocardial infarct size when administered during the first 15 min of reperfusion in rabbits3. In contrast, results have demonstrated that 1.0 MAC isoflurane reduces infarct size when administered 3 min before and 2 min after the onset of reperfusion. These results are supported by the findings of another previous study indicating that isoflurane enhances the functional recovery of isolated rat hearts when administered solely during reperfusion4. The beneficial effects of sevoflurane during reperfusion have also been shown to be dose-dependent5. These previous observations with sevoflurane have als been supported by the current results with Isoflurane. Opioid induced Cardio protection (OIC) has been investigated (Eric et al). The data indicates that OIC occurs via the phosphorylation of GSKß (Glycogen synthase kinase) at Ser9 during reperfusion. (GSK inhibition produced by ischemic preconditioning has been previously shown to be regulated through phosphatidylinositol-3 kinase (PI3K). Therefore, it was determined that Opioid-induced cardio protection (OIC) occurs during reperfusion by altering GSK phosphorylation through PI3K. Regarding development of pharmaceutical preparations that could help in myocardial preconditioning, the research continues. 1 Yamagishi H, Akioka K, Hirata K, et al. Effects of preinfarction angina on myocardial injury in patients with acute myocardial infarction: a study with resting 123I-BMIPP and 201T1 myocardial SPECT. J Nucl Med 2000;41:830-6. 2 Andreotti F, Pasceri V, Hackett DR, Davies GJ, Haider AW, Maseri A. Preinfarction angina as a predictor of more rapid coronary thrombolysis in patients with acute myocardial infarction. N Engl J Med 1996;334:7-12. 3 Preckel B, Schlack W, Comfere T, Obal D, Barthel H, Thamer V: Effects of enflurane, isoflurane, sevoflurane and desflurane on reperfusion injury after regional myocardial ischaemia in the rabbit heart in vivo. Br J Anaesth 1998; 81:905-12 4 Schlack W, Preckel B, Stunneck D, Thamer V: Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart. Br J Anaesth 1998; 81:913-9 5 Obal D, Preckel B, Scharbatke H, Mullenheim J, Hoterkes F, Thamer V, Schlack W: One MAC of sevoflurane provides protection against reperfusion injury in the rat heart in vivo. Br J Anaesth 2001; 87:905-11 Conflict of Interest:None declared |
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