Objective To determine the protection effects and mechanisms for immature myocardium with limbs ischemic preconditioning (LIP). Methods Using the Langendorff perfusion apparatus to perfuse isolated hearts, we randomly divided 30 Japanese longeared white rabbits into 5 groups, each having 6 rabbits. For the I/R group，after the perfusion model was established, the isolated hearts underwent 15 min of perfusion with KH solution before working for another 15 min . Then perfusion was stopped to cause ischemia for 45 min before reperfusion for 15 min and working for another 30 min . For E1 group, the model was established by 3×LIP (double limbs obstructed for 5 min followed by 5 min reperfusion for 3 times) and then procedures of the I/R group were carried out. For E2 group, before procedures of the E1group were done, superoxide dismutase (SOD) was injected till LIP was completed. For E3 group, intravenous protein kinase C (PKC) polymyxin (PMB) was injected for 10 minutes before E1 procedures were repeated. For E4 group, intravenous mitochondrial ATPsensitive K+ channels (mitoKATP) blocker 5-hydroxydecanoate was injected for 10 min before E1 procedures were carried out. The left ventricular function recovery, myocardial water content (MWC), creatine kinase (CK) and lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) and ATP content, SOD activity and superoxygen negative ion (O2 ·-) content were tested. Results Left ventricular recovery in E1 group was better than other groups (Plt;0.05). ATP content and SOD activity in E1 group were also better than all other groups (Plt;0.05). MWC in E1 group was lower than other groups (Plt;0.05). MDA content, CK and LDH leakage in E1 group were also lower than other groups (Plt;0.05). There was no significant difference of the above indications among I/R,E2,E3 and E4 groups, while the difference of O2·- content in E1,E3 and E4 groups before and after preconditioning was significant. Conclusion LIP has obvious protective effects for immature myocardium and the mechanisms are probably through PKC stimulation and opening of mitoKATP.
Objective To investigate the role of mitochondrial adenosine triphosphatesensitive potassium channel(mitoKATP) in immature myocardial ischemic preconditioning, and to provide evidence for immature myocardial protection. Methods Langendorff isolated heart infused model was used in the experiment. Twentyfour rabbits (aged from 14 to 21 days) were randomly divided into 4 groups：ischemiareperfusion group（I/R group）, myocardial ischemic preconditioning group(E1 group), 5hydroxydecanoate(5-HD) group (E2 group) and Diazoxide (Diaz) group(E3 group). Hemodynamics recovery rate, myocardial water content(MWC), the leakage rates of serum creatine kinase and lactate dehydrogenase, adenosine triphosphate content, superoxide dismutase activity, malondialdehyde content, myocardial cell Ca2+ content and myocardial mitochondrial Ca2+ content, myocardial mitochondrial Ca2+-ATPase activity, the adenosine triphosphate(ATP) synthesizing ability of myocardial mitochondria were tested, and myocardial ultrastructure was observed via electron microscopy. Results The hemodynamics recovery rate, myocardial water content(P＜0.05), adenosine triphosphate content, superoxide dismutase activity, myocardial mitochondrial Ca2+-adenosine triphosphyatase(ATPase) activity and the ATP synthesizing ability of myocardial mitochondria of the rabbits in E1 and E3 group were significantly better than that in I/R group and E2 group(P＜0.05). Malondialdehyde content, the leakage rates of serum creatine kinase and lactate dehydrogenase, myocardial cell Ca2+ content and myocardial mitochondrial Ca2+ content of the rabbits in E1 group and E3 group were significantly lower than that in I/R group and E2 group (P＜0.05). The myocardial ultrastructure injury in E1 and E3 group were significantly reduced compared with that in I/R and E2 group. Conclusion Myocardial ischemic preconditioning has significant protective effects on immature myocardium. Its mechanism may be related to the activation of mitoKATP.
Objective To investigate the immature myocardial protection effects with renal ischemic preconditioning. Methods 18 neonatal rabbits were randomly divided into three groups. Ischemic/reperfusion(I/R) group underwent 45 min ischemia followed with 45 min reperfusion after Langendorff model performed. Cardiac ischemic preconditioning(CIP) group underwent 45 min ischemia followed with 45 min reperfusion after 5 min ischemia and then 5 min reperfusion for two times. Renal ischemic preconditioning(RIP) group underwent 45 min ischemia followed with 45 min reperfusion after renal artery obstruction for 5 min and 5 min reperfusion for three times.The left ventricular function recovery,myocardial water content(MWC), lactate dehydrogenase (LDH) and creatine kinase(CK) leakage, malondialdehyde(MDA) content,adenosine triphosphate(ATP) content, superoxide dismutase(SOD) activity, myocardial cell Ca2+ ［Ca2+］c content,mitochondrial Ca 2+ content ［Ca2+］m,synthesizing ATP activity of mitochondria ［ATP］m and Ca2+ATPase activity of mitochondria ［Ca2+ATPase］m were tested. Results The recovery of postischemic heart function in RIP group and CIP group were higher than that I/R group(Plt;0.01). There were no significant difference of HR, AF in three groups （Pgt;0.05）. There were significant difference of CF，CO，LVSP and LVEDP in RIP group and CIP group than those I/R group（Plt;0.01）. There were significant difference of MWC, CK, LDH, ATP content, MDA, SOD activity, ［Ca2+］c content, ［Ca2+ATPase］m， ［Ca2+］m and ［ATP］m in RIP group than those I/R group（Plt;0.01). There were no significant difference between RIP group and CIP group upon every index (Pgt;0.05). Conclusion RIP has the same cardioprotection to immature myocardium as ischemic preconditioning.