By Marcel E. Zughaib, Paul B. McCay, Mohamed O. Jeroudi, Craig Hartley, Jian-Zhong Sun (auth.), Hans Michael Piper, Claus J. Preusse (eds.)
In open middle surgical procedure, defense of the myocardium opposed to harm via ischemia-reperfusion is an argument of maximum scientific curiosity. the data at the causal mechanisms of myocardial damage in ischemia-reperfusion has enormously advanced in recent times, either to medical and experimental study. This booklet offers a serious and finished evaluate at the present dialogue of myocardial defense in cardiac experimental examine and surgical procedure. prime teams from Europe, the U.S. and Japan have contributed stories in their distinct fields.
at the uncomplicated technology facet, significant themes mentioned are the mechanisms of lovely and deadly reperfusion damage, the function of the endothelium and leukocyte activation in postischemic myocardial disorder, and the diversities among the grownup and neonatal myocardium. at the medical aspect, the main recommendations and methods for cardioplegic myocardial safety, their rationales, program and respective advantages are mentioned. In a 3rd a part of the e-book, attainable techniques for the tracking of myocardial harm in the course of ischemia and reperfusion are evaluated, with specific awareness to their intraoperative use.
This e-book brings jointly the medical discussions on ischemia-reperfusion in experimental cardiology and cardiac surgical procedure, a job wanted for a very long time. it's of basic curiosity for clinicians in addition to study staff and scholars within the cardiac box.
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Sample text
57. 58. 59. 60. 61. 62. 63. 35 reflow: the role of iron in the pathogenesis of reperfusion injury. Circulation 1987: 76: 906- 15. Stewart JR, Blackwell WH , Crute SL et al. Inhibition of surgically induced ischemialreperfusion injury by oxygen free radical scavengers. J Thorac Cardiovasc Surg 1983: 86: 26272. Johnson DL , Horneffer PJ , Dinatale JM Jr et al. Free radical scavengers improve functional recovery of stunned myocardium in a model of surgical coronary revascularization. Surgery 1987: 102: 334- 40, Gardner TJ.
Prolonged depletion of ATP and of the adenine nucleotide pool due to delayed resynthesis of adenine nucleotides following reversible myocardial ischemic injury in dogs. J Mol Cell Cardiol 1981 ; 13: 229-39. Swain JL , Sabina RL, McHale PA et al. Prolonged myocardial nucleotide depletion after brief ischemia in the open-chest dog. Am J Physiol 1982; 242 : H818-H826. Neely JR, Grotyohann LW. Role of glycolytic products in damage to ischemic myocardium: dissociation of adenosine triphosphate levels and recovery of function of reperfused ischemic hearts .
Oxygen radicals have also been shown to interfere with the Na +_Ca 2+ exchange [140] and to inhibit the Na +-K+-ATPase activity [138]. Impairment of the Na +-K +-ATPase activity results in Na + overload, with consequent activation of the Na +_Ca 2+ exchange activity [84,85] . This impairment is prevented by antioxidants [139]. All of these observations imply that excessive production of oxyradicals could result in increased transarcolemmal calcium influx and cellular calcium overload. It is important to point out that the foregoing postulated mechanisms involve alterations in calcium homeostasis, and thus would reconcile the oxyradical hypothesis and the calcium overload hypothesis of stunning into one pathogenetic mechanism.