| Objective The study aimed to examine whether L-carnitine was able to improve postischemia cardiac function and myocardial cell energy metabolism, reduce the leakage of myocardial enzyme and the level of malondialdehyde of myocardial tissue in ischemia/reperfused isolated rat hearts, and discussed the protective mechanism. Methods Male wistar rats weighing 230~280g were anesthetized with intra-peritoneal pentobarbital sodium(30mg/kg). The chests were opened, and the hearts were rapidly excised and mounted on modified Langendorff apparatus. Six hearts were continuously perfused for 85 min, comparisons of this group's left ventricular function and enzyme leakage were made in order to assess the stability of the apparatus over the perfusion period; Thirty-two hearts were randomly divided into four groups, n=8 in each: control group (CON group), ischemia/reperfusion group (I/R group) and two experimental groups (CAR1 group and CAR2 group). At a constant perfusion pressure of 75mmHg, the hearts in CON group were perfused continuously for 35 min with oxygenized Krebs-Henseleit (K-H) solution without being subjected to ischemia in order to measure baseline bioenergetics. All hearts in I/R group, CAR1 group and CAR2 group were perfused for 15 min. After this period, 0.5mmol/L (CAR1 group) and 5mmol/L (CAR2 group) L-carnitine were respectively added into K-H solution. After 20 min, perfusion was completed and the hearts were thensubjected to no-flow global normothermic ischemia for 20 min, following ischemia, hearts were reperfused with the same solution for 30 min. In the I/R group, the same procedures were performed without using L-carnitine. LVDP, ±dp/dtmax and coronary flow in I/R group, CAR1 group and CAR2 group were recorded at 15th min of perfusion, before ischemia, at 10th min, 20th min and 30th min of reperfusion. CK and LDH were measured before ischemia and at 30th min of reperfusion. After the Langendorff-experiment, the left ventricular myocardium was dissected, homogenized and reconditioned, then the content of myocardial MDA was determined. In CON group, I/R group and CAR2 group, the tissue of apex of heart was excised and stored in liquid nitrogen tar. ATP, ADP, AMP were determined with high performance liquid chromatography. The levels of total adenine nucleotide and energy charge were calculated. Results (1) In the six hearts which were used to evaluate the stability of the modified Langendorff apparutas, the change in LVDP, +dp/dtmax and -dp/dtmax from 15th min of perfusion to 85th min was approximately 9.3%, 9.7 and 11.8%, and there was no increase in CK and LDH release at both the two time intervals (P>0.05). (2) Before ischemia, there were no significant differences about heart function, coronary flow and the leakage of enzyme among I/R group, CAR1 group and CAR2 group(P>0.05). Postischemia recovery of LVDP, ±dp/dtmax and CF was significantly improved in the group with 5mmol/L L-carnitine(P<0.05, PO.01), but not with 0.5mmol/L L-carnitine (P>0.05). After 30 min of reperfusin, 5mmol/L L-carnitine lowered MDA level (PO.01) and the leakage of CK and LDH(P<0.01, PO.05). however, there were no significant differencs between I/R group and CAR1 group (/>>0.05). (3) After 20 min... |
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