| Some clinic researches found out, compared with inpatients who developed acute myocardial infarction(AMI) but never developed angina pectoris(AP),the mortality and the incidence of severe heart failure and shock decreased obviously in those who often endured AP before the occurrence of AMI. Furthermore, the shrunken infarct size and improved venticular wall function also found in the patients who once endure AP, and all these results were independent of compensated branch flow seen by coronary angiography. Another study showed patients with AP after undergoing the 1st stress test, the threshold of AP will increse at the 2nd time. Preconditioning refers to the heart with a brief period of ischemia followed by reperfusion renders it very resi- stant to injury from a subsequent prolonged ischemia. The protection by precondition- ing mainly lies in limiting infarct size, reducing the incidence of ventricular arrhyth- mia and improving post-ischemic cardiac function. Because ischemia injury itself is a hurt to body, so it is unacceptable to apply it to the clincal treatment. Nowadays, instead of ischemia or biological methods, the research of inducing preconditioning mains by pharmacological means. Pharmacological preconditioning protection against heart injury is trigged by medicines which can mimic beneficial effects of cardiac ischemic preconditioning. Thatwould be helpful to probe the mechanism of IPC and develop novel access to treatment of the cardiovascular diseases.Endogenous hydrogen sulfide (H2S), which was considered as a novel gasotransmitter, maybe have important biological functions as a neuromodulator and signal transmitter. As neuron exciting, the inflow of Ca2+ activates cystathionine P -synthase (CBS ) which generates H2S by using L-cysteine as a main substrate. H2S regulated the function of neurological system by CAMP pathway. H2S also is an important endothelium derived relaxing factor(EDRF), which exerts its cardiovascular physiological effects by means of Katp channel or inhibiting extracellular Ca2+ inflow. However, it is unclear whether the endogenous H2S contributes to the protection of myocardial injury. To investigate the role of H2S on myocardial ischemic reperfusion injury in rats, we preconditioned rat hearts with NaHS to observe changes in morphology, hemodynamics and biochemistry of rats myocardium. So, we may find a new way to protect myocardial dysfunction after ischemic injury of heart, and find the mechanisms which support it.Methods: (D 64 Wistar rats(half male and half female) were included and divided averagely into four groups named sham operation group , myocardial ischemia/reperfusion(IR) model group, and two positive control NaHS groups at different doses of 5.6 P mol/kg and 14 u mol/kg at random., each group includes 16 rats. ? The rats in two control NaHS groups were injected intraperitoneally(i.p) with the NaHS at doses of 5.6 y mol/kg-d and 14 y mol/kg-d respectively for 5 days, while the same volume of physiological salt solution injected intraperitoneally in Sham and I/R model groups. (3) After 24 hours of the last injected intraperitoneally, all rats were subjected to openning chest and the left anterior desending coronary arteries (LAD) were ligated for 30min and undamped for 60min except the rats with only thread-drawing in Sham group. Electrocardiogram, hemodynamics of all rats were measured. One half rats of every group were injected Evans blue then the hearts were taken out and the atria and right ventricle were removed. After' refrigeration, the frozenheart was cut along the long axis into 1-mm- thick slices, and the slices were incubated in 1% triphenyltetrazolium chloride (TTC). The slices were immersed in 10% formalin overnight. The infarcted myocardium was dissected from the ischemic zone size under the illumination of a dissecting microscope. Ischemic zone size and infarct size and left ventricle were weighed. Heart tissue homogenate was made and then superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondia- ldehyde (MDA) and nitric oxide (NO) were measured in other half rats.Results: (D Hemodynamics Myocardial functional parameters, such as left ventricular systolic pressure(LVSP), maximum positive and negative change in pressure( + dp/dt) and left ventricular end-diastolic pressure(LVEDP) were similar among the 4 groups before the ligation of LAD (P>0.05). LVSP was significantly decreased in group I/R compared with group NaHSl^mol/kg (P<0.05), extremely significantly greater compared with group sham (P<0.01). But there are no significant differences between other groups (P>0.05). Furthermore, compared with NaHS5.6,?mol/kg group , ± dp/dt was higher in NaHS14^mol/kg group(P<0.05), and there is no differrnce between sham and NaHS14/?nol/kg group (P>0.05). Besides, there is significantly statistical difference between other each two groups(P<0.01) about ± dp/dt. As far as LVEDP was concerned, there is no differences between group sham and group NaHS14^mol/kg, but there is statistical significance between two NaHS control groups(P<0.05),and there is significantly statistical difference between other each two groups(P<0.01). (2) Morphology (Ischemic zone size and infarct size) Ischemic zone size was not different among the groups except Sham group[(40.14± 4.65)%, (39.78+3.84) % vs (39.24±8.60)%, P>0.05]]. Infarct size was significantly lower in group NaHSS^mol/kg and 14/jmol/kg vs I/R group[(27.77 + 6.04)%, (23.35 + 5.45)% vs (36.52+5.68)%, P<0.05, P<0.01] but there was no difference between two NaHS control groups(F>0.05 ). ?Biochemistry (SOD, GSH-Px, MDA and NO) Compared with Sham group, the level of myocardial SOD, GSH-Px were significantlydecreased (108.5±8.85 vs 143.1±8.10, 103.8±2.69 vs 135.5±4.66, P<0.01) but MDA increased markedly in the I/R group(20.76±1.53 vs 10.90±1.52, P<0.01). Between two NaHS control groups, the level of SOD has not a significantly statistical difference (129.4±6.05 vs 119.8±6.34, P>0.05). And the level of GSH-Px (128.9+5.21 vs 122.8±4.00, P<0.05) and MDA(13.29±1.85 vs 16.26±1.99, P<0.05) also has a statistical difference. The level of NO in I/R group was lower than Sham (1.33±0.43 vs 2.99±0.56, P<0.01), but it increased markedly in group NaHS 14^mol/kg and S.o^mol/kg compared with the I/R group(3.57±0.59, 2.31 ±0.25 vs 1.33+0.43, P<0.01). And there was significantly statistical difference of NO between two NaHS control groups (3.57+0.59 vs 2.31+0.25, P<0.01).Conclusions:1. These results demonstrated that pretreatment of rats with H2S had cardio-protective effects, which can limit myocardial infarct size.2. H2S increased antioxidants and inhibited lipid to peroxidate in rat hearts when they were subjected to ischemia/reperfusion injury.3. H2S increased the level of myocardic NO, which may be one of the mechanisms of its cardio-protective effects.
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