Abstract
Overexpression of HKI and HKII in cultured cells protects against oxidant-induced cell death. It is unknown whether cardiac alterations of HKII affect ischemia-reperfusion injury in the whole heart. In the present study we examined ischemia-reperfusion injury in isolated hearts of partial HKII (+/−) knockout (HKKO) and wild-type mice (WT). Langendorff-perfused hearts (HKKO: n=7; WT: n=8) were subjected to 40 min low-flow (5% of baseline flow) ischemia and 120 min reperfusion. Necrosis was determined by lactate dehydrogenase (LDH) enzyme release during the reperfusion period. At baseline, no significant differences were observed between groups: end-diastolic pressure (EDP) is 7.5 ± 1.0 mm Hg, developed left ventricular pressure (DLVP) is 98.7 ± 4.6 mm Hg, heart rate is 369 ± 12 beats/min and flow is 15.1 ± 1.4 ml/min/gww. Following 120 min reperfusion, recovery of DLVP was 68.3 ± 8.3 % (WT) versus 55.6 ± 9.1% (HKKO) and EDP was 11.6 ± 3.7 mm Hg (WT) versus 29.0 ± 6.8 mm Hg (HKKO). Between groups contracture development during ischemia reached EDP >10 mm Hg at different time points: 34 min for WT and 12 min for HKKO. LDH release was 1.8 ± 0.35 versus 3.3 ± 0.75 μmol/gww/120 min reperfusion for WT versus HKKO, respectively. The data suggest for the first time that HKII may be an important mediator of ischemia-reperfusion damage in the intact heart.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
