Abstract
Biochemical and morphological damage in the ischemic myocardium result from increased activity of proteases, particularly lysosomal enzymes. The concentration of lysosomal enzymes increases in the both myocardium in response to ischemia and the systemic circulation in response to extracorporeal circulation. Cold cardioplegia minimizes the effects of ischemia during open heart surgery. It has been reported that aprotinin protects the myocardium from ischemia followed by reperfusion by suppressing the release of lysosomal enzymes2,3.
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Reference
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© 1988 Plenum Press, New York
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Sunamori, M., Innami, R., Fujiwara, H., Yokoyama, M., Suzuki, A. (1988). Significant Role of Protease Inhibition by Aprotinin in Myocardial Protection from Prolonged Cardioplegia with Hypothermia. In: Hörl, W.H., Heidland, A. (eds) Proteases II. Advances in Experimental Medicine and Biology, vol 240. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1057-0_48
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DOI: https://doi.org/10.1007/978-1-4613-1057-0_48
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8313-3
Online ISBN: 978-1-4613-1057-0
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