Why the study?
Does in vivo ischemia-reperfusion injury improve long-term preservation and post-transplant function in rat hearts?
Does in vivo ischemia-reperfusion injury improve long-term preservation and post-transplant function in rat hearts?
Prior ischemia-reperfusion injury induces HSP70 expression and protects rat hearts during long-term preservation and subsequent transplantation.
Hypothesis-generating for ischemia-reperfusion preconditioning in experimental heart preservation; leaves open translation to clinical transplantation.
281 It is unknown whether ischemia-reperfusion injured hearts may sustain long term preservation and function well after transplantation. To answer this question, thoracotomy of Lewis rats (225±25 g) was performed under ventilation. The left anterior descending coronary artery (LAD) was ligated at 2 mm from its origin for 15 minutes (min), untied for 45 min, religated for 15 min and untied again (Group LAD). Control group was sham operated. Hearts were excised at 48 hours after surgery, and then preserved for 24 hours by continuous perfusion of oxygenated Krebs-Henseleit buffer (pH 7.40) in a Langendorff system at room temperature, followed by transplantation (to Lewis) to carotid artery and jugular vein. At one hour after transplantation the maximum rate of left ventricular (LV) pressure rise (+dP/dtmax) was measured by balloon method. LV was harvested for analyzing mRNA of heat shock protein 70 (HSP70) and ATP. Results are: TableData shows Group LAD had better recovery of LV contractility, ATP, and higher HSP70 mRNA than sham group. LV twice ischemia-reperfusion induced a 10-fold increase of HSP70 mRNA expression, which could relate to such a protection of myocardium from preservation. Results suggest hearts subjected to a certain ischemia-reperfusion may still sustain long term preservation and function well after transplantation. This information may be important for transplantation physician.
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Tan et al. (1998) studied this question.
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