Cardioprotective effect of hyperkalemic cardioplegia in an aquaporin 7-deficient murine heart

Background Hyperkalemic cardioplegia using St. Thomas’ Hospital solution No. 2 (STH2) is commonly used to protect the myocardium during surgery. Mice deficient in the myocyte channel aquaporin 7 (AQP7) show significantly reduced glycerol and ATP contents and develop obesity; however, the influence of AQP7 on cardioplegia effectiveness remains unclear. Methods After determining the influence of ischemic duration on cardiac function, isolated hearts of male wild-type (WT) and AQP7-knockout (KO) mice (> 13 weeks old) were aerobically Langendorff-perfused with bicarbonate buffer, and randomly allocated to the control group (25 min of global ischemia) and STH2 group (5 min of STH2 infusion before 20 min of global ischemia, followed by 60 min of reperfusion). Results Final recovery of left ventricular developed pressure (LVDP) of WT and AQP7-KO hearts in the control group was 24.5 ± 12.4% and 20.6 ± 8.4%, respectively, which were significantly lower than those of the STH2 group (96.4 ± 12.7% and 92.9 ± 27.6%). Troponin T levels of WT and AQP-KO hearts significantly decreased in the STH2 groups (142.9 ± 27.2 and 219.9 ± 197.3) compared to those of the control (1725.0 ± 768.6 and 1710 ± 819.9). Conclusions AQP7 was not involved in the protective efficacy of STH2 in this mouse model, suggesting its clinical utility even in complications of metabolic disease.