ABSTRACT
Objective To observe the effects of ischemic postconditioning (I-postC) on lung injury after limb ischemia reperfusion (LIR) in rats, and to investigate the protective effect and the mechanisms. Methods Twenty-four Wistar rats were divided into three groups:control group (group Control), ischemia-reperfusion group (group IR) and ischemic postcondi?tioning group (group I-postC). Referring to routine method in our department, the model rats underwent 4-hour ischemia and 4-hour reperfusion of hind limbs were made. In group Control, the rubber band around the limb was loose,which did not block the blood flow. Rats in group I-postC were given repeated 3 times of 5 min ischemia-5 min reperfusion, and then did perfusion 4 h before reperfusion. The blood and lung samples were collected for detecting arterial gas of partial pressure of oxygen [p(O2)] and partial pressure of carbon dioxide [p(CO2)]. The plasma and lung tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD) and xanthine oxidase (XOD) were detected. The morphological changes of lung tissue were ob?served under light microscope and electron microscope. Results It was found that after suffering from ischemia-reperfu?sion, levels of p(O2) and p(CO2) decreased significantly. The activity of SOD in plasma and lung tissues decreased, but XOD and MDA increased significantly (P<0.05). With microscope, lung interstitial vascular dilation, infiltration of neutrophils, the width of the alveolar space, alveolar septal thickening and alveolar exudate were found. Compared with IR group, it was found that p(O2) and p(CO2) increased significantly in group I-postC. The activity of SOD in plasma and lung tissues in?creased, but XOD and MDA decreased significantly(P<0.05). The mild damage of pathological changes were found. Conclu?sion Ischemic postconditioning can reduce the lung injury after limb ischemia reperfusion in rats, which may be related to the inhibition of lipid peroxidation.
ABSTRACT
Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .