| Objective To oberserve the protective effect and mechanism of ulinastatin and systemic ischemic preconditioning on myocardial ischemia reperfusion injury, and to further explore the principle that protective effect was strengthened of ulinastatin combining with systemic ischemic preconditioning on myocardial ischemia reperfusion injury .Methods adult New Zealand white rabbits of either sex(32) were randomly divided into 4 equal groups,8 rabbits in each group :the I/R group(n=8),the UTI group (n=8),the SIP group (n=8)and the UTI + SIP group (n=8). The I/R group was subjected to only 30-min left anterio coronary(LAD) occlusion followed by 120-min reperfusion. The UTI group was administered intravenously with UTI injection in dose of 10000u/kg 5-min before ischemia reperfusion ,after which the procedures were the same as those in the I/R group. The SIP group was induced by rapidly(5-min)withdrawing blood from femoral artery and maintaining the mean artery pressure at 50 mmHg for 10-min, afterwards, all of the withdrawn blood was re-infused, then the procedures were the same as those in the I/R group. The UTI+SIP group was received ulinastatin combining with SIP, then the procedures were the same as those in the I/R group. The model of SIP was withdrawing blood from femoral artery in 5-min and maintaining the mean artery pressure at 50 mmHg, lasting for 10- min (30- min in I/R and UTI). The model of myocardial ischemia reperfusion injury (I/R)was ligating the left anterio coronary(LAD) for 30-min,and reperfusing for 120-min. Rabbit heart rate and mean arterial pressure were recorded before ischemic, 30-min after ischemic, 30-min after reperfusion,120-min after reperfusion respectively. After 120-min reperfusion,a catheterization was put into the left ventricular to measure the left ventricular end diastolic pressure (LVDEP). 4ml×4 blood was drawn to measure the index variance of serous cardiac troponin I(cTnI) concentration,superoxide dismutase(SOD) activity, malondialdehyde(MDA) , nitric oxide(NO) ,TNF-αcontent at the same 4 time above. Cadiocyte ultrastructural pathological changes were observed with transmission electron microscope. Results 1, There were no significant differences among all the groups about the blood pressure and heart rate at Pre-I,but the blood pressure and heart rate were generally lower than that at Pre-I (P <0.05) and were no difference among 4 groups (P> 0.05) . 2, after 30-min of ischemia, 120-min reperfusion, the serum levels of SOD, NO decreased, MDA, TNF-α, cTnI were elevated. UTI, SIP, UTI+SIP groups compared to I/R group, the differences were significant (P <0.01 or P <0,05). 3,The results of the electronmicroscope:the necrosis of muscle fiber and extensive vacuolization of mitochondria could be observed in I/R group.The cell damage in UTI, SIP, groups was obviously slighter than that in I/R group. The muscle fiber was almostly normal with only a few vacuolizated mitochondria in UTI, SIP groups.The effects of UTI + SIP group was very obvious.Conclusions 1, Both UTI and SIP had a good effect on anti-myocardial ischemia reperfusion injury. 2,The use of combined UTI with SIP could enhance the capacity of anti-myocardial ischemia reperfusion injury further because they had a good collaborative function. 3, UTI and SIP played a protective effect on anti-myocardial ischemia-reperfusion injury. Their common mechanism might be regulating vascular tone, reducing leukocyte adhesion, improving microcirculation and removing oxygen free radicals by increasing the level of endogenous nitric oxide and inhibitting the expression of tumor necrosis factor.
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