| Background: Ischemic stimulation can induce formation of regional collateral circulation. It has clinical cardiovascular danger although high intensity training can improve collateral circulation formation. Our pilot researchs have demonstrated that physiological ischemic training (PIT) can improve collateral circulation formation and increase blood flow in pathological ischemic region, but the protective function of PIT is unclear.Object: The hypothesis of this article is coronary collateral circulation formation induced by PIT can protect myocardium as infarction happens.Methods: 35 New Zealand White rabbits were implanted water baloon constrictor in the left ventricular branch (LVB) to make controllable myocardial ischemic model, and left sciatic nerves were implanted platinum filament electrode for electrical stimulation as model for PIT. The rabbits were randomly, medially assigned to three groups: pure ischemia (PI) group, exercise training (ET) group, sham-operated (SO) group. The subjects in the PI group underwent pure-ischemia exercise to mimic the ischemia episode of the myocardial ischemic patients, the protocol is LVB occlusion for 2 min followed by reperfusion, twice a day. Rabbits in ET group underwent myocardial ischemia session, which was as same as that of the PI group. ET group also doing isometric contraction 4 min each session, twice a day. The protocols of the PI and ET groups were performed 5 days/wk for 4 weeks. The rabbits in the SO group remained inactive for 4 weeks.After four weeks training, the chests were opened again, and the LVB were ligated to make myocardial infarction model. Two hours after the infarction, to survival rabbits, infarct size was measured by magnetic resonance (MR) imaging. Echocardiogram were performed before and 3 days after infarction to measure left ventricular ejection fraction (LVEF). After the rabbits were sacrificed, immunohistochemistry were execute to measure capillary density (CD), and microspheres were detect to measure collateral circulation blood flow (CCBF). Result: mortality of fibrillation ventricular because of LVB ligation in ET, PI and SO group was 40%, 33% and 33%, respectively (P>0.05). The infarct size ET group (5.67±1.08%) is significantly lower than that of PI group (14.26±2.95%, P<0.01) and SO group (29.31±5.71%, P<0.01). Before infarction, there was no difference of LVEF level among groups (P>0.05). After infarction, ?LVEF% of ET group (8.39±1.53%) was significant lower than that of PI group (14.54±0.63%, P<0.01) and SO group (21.98±3.41%, P<0.01). ?LVEF% of PI group was significant lower than that of SO group (P<0.01).At the beginning of training, there was no significant difference of CCBF among groups (P>0.05). At the end point of training, the CCBF of ET group (73.76±4.38%) was significant higher than that of PI group (60.47±6.94%,P<0.01) and SO group (32.76±5.73%,P<0.01). End point CCBFof PI group was significant higher than SO group (P<0.01).CD in ET group (61.17±3.43capillaries/VF) is significantly higher than that of PI group (33.00±3.35 capillaries/VF , P<0.01) and SO group (19.50±2.74 capillaries/VF, P<0.01). CD of PI group is significantly higher than that of SO group (P<0.01) . CD has significant correlation with endpoint CCBF (r=0.91, P =0.000), infarct size (r=-0.91, P =0.000), and ?LVEF (r=-0.94, P =0.000). Conclusion: To controllable myocardial ischemic New Zealand White rabbits model, coronary collateral circulation formation induced by PIT can protect myocardium when myocardial infarction happening. |
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