Objective To investigate the protective effects of ischemic postconditioning (IPo) on ischemiareperfusion (I/R) myocardium and the relationship with mitochondrial adenosine triphosphate (ATP) sensitive K+ channels (mitoKATP) and provide evidences to the development of druginduced postconditioning. Methods Langendorff models were established in 40 Wistar rats which were divided into 5 groups by random number table with 8 rats in each group. Normal control group(NC group): the rat hearts were continuously reperfused by KrebsHenseleit bicarbonate buffer (K-HB) for 100 min without any other treatment; I/R group: the rat hearts underwent a 40-min global ischemia followed by a 60-min reperfusion; IPo group: after a 40-min global ischemia, the process of 10-second reperfusion followed by a 10-second ischemia was repeated 6 times, then there was a continuous 58min reperfusion; 5-hydroxydecanoic acid(5-HD) group: after a 40min global ischemia, hearts with 5HD(100 μmol/L) K-HB were reperfused for 15min and then perfused without 5HD for 45min；IPo+5-HD group: after a 40-min global ischemia, the process that the isolated hearts with 5-HD(100 μmol/L) KHB were reperfused for 10second followed by a 10second ischemia was repeated 6 times, then the hearts with 5-HD(100 μmol/L) KHB were continuously [CM(159mm]perfused for 13-min followed by reperfusion without 5-HD(100 μmol/L) K-HB for 45-min. The cardiac function,coronary flow(CF), cardiac troponin I(cTnI) content in coronary effluent, the area of acute myocardial infarction (AMI) and myocardial ultrastructure were observed. Results Left ventricular developed pressure(74.3±3.3 mm Hg vs. 57.1±3.3 mm Hg,t=1300, P=0.000),+dp/dtmax(1 706.6±135.6 mm Hg/s vs. 1 313.3±96.2 mm Hg/s,t=6.28,P=0.000),－dp/dtmax(1 132.8±112.1 mm Hg/s vs. 575.7±67.7 mm Hg/s,t=13.48, P=0.000) and CF(6.49±0.30 ml/min vs. 3.70±0.24 ml/min,t=28.6,P=0.000) in IPo group were higher than those in I/R group. Left ventricular enddiastolic pressure(10.9±1.7mm Hg vs. 26.2±1.5 mm Hg,t=－19.21, P=0000)and cTnI content in coronary effluent (0.62±0.01 ng/ml vs. 0.71±0.01 ng/ml, t=-12.00,P=0.000) were lower than those in I/R group; the area of AMI decreased 20.8％ compared with that in I/R group (Plt;0.05). The myocardial protective effect in IPo+5HD group was similar with that in IPo group, but lower than that in IPo group. The electron microscope showed that IPo and IPo+5HD could reduce myocardial fiber damage and mitochondrial damage caused by I/R. Conclusion IPo can protect I/R myocardium, which is achieved mainly by activating mitoK-ATP channels.
Objective To investigate the effect of ischemic preconditioning(IPC) on myocardial ischemic reperfusion injury(I/R) of elderly rats. Methods Fiftysix Wistar rats, of which there were 28 aged from 21-23months(elderly rat) and 28 aged from 4-5months(young rat), were used to build isolated heart perfusion Langendorff model. The rats were divided into 7 groups with random number table（8 in each group）: adult control group, adult I/R group, adult IPC group, elderly control group, elderly I/R group, elderly IPC group and elderly enhanced IPC group. The control group underwent a 90-min perfusion without any intervention; the I/R group underwent a 30-min equilibration period, then a 30-min ischemia and a 30-min reperfusion; the IPC group underwent a 10-min equilibration period, then a 5-min ischemia for twice and a 5-min reperfusion, after that a 30-min ischemia and [CM(158-3mm]a 30-min reperfusion; the enhanced IPC group underwent a 10-min equilibration period, then a 5-min ischemia for 4-times and a 5-min reperfusion, after that a 30-min ischemia and a 30-min reperfusion. The recovery rates of cardiac output(CO), left ventricular developed pressure (LVDP), the maximum rising and descending rate of left ventricular pressure (±dp/dtmax) after a 30-min reperfusion were compared among groups. The activity of creatine kinase (CK) in coronary outflow, the level of malonyldialdehyde (MDA) and superoxide dismutase (SOD) before ischemia and after a 30min reperfusion were detected. The myocardial infarction areas were compared among groups. Results After a 30min reperfusion, compared with adult I/R group, in adult IPC group CK reduced significantly(89.48±18.72 U/L vs. 115.76±16.72 U/L，q=6.061，Plt;0.01)，the level of MDA decreased significantly（9.53±3.44 nmol/ml vs. 16.84±2.29 nmol/ml，q=7.732，Plt;0.01)，the level of SOD increased significantly（584.7±122.62 U/ml vs. 429.46±85.24 U/ml，q=4.754，Plt;0.01)，the recovery rates of CO,LVDP,+dp/dtmax and -dp/dtmax increased ignificantly(78.69%±9.68% vs. 65.10%±8.63%，83.61%±8.46% vs. 67.23±8.68%，81.68±8.68% vs. 67.89%±6.89%，89.79%±7.78% vs. 66.79%±8.46%，Plt;0.01), the myocardial infarction areas reduced significantly (5.25%±4.33% vs. 14.75%±8.02%,q=7.458，Plt;0.01)。There was no statistical significance between elderly IPC group and elderly I/R group in the above indexes（Pgt;0.05）.However, There was statistical significances between elderly enhanced IPC group and I/R group. CK reduced significantly (88.60±28.32 U/L vs. 105.76±9.64 U/L，q=5.620，Plt;0.01)，the level of MDA decreased significantly（8.38±3.36 nmol/ml vs. 16.80±3.06 nmol/ml，q=7.500，Plt;0.01)，the level of SOD increased significantly（558.87±78.66 U/ml vs. 433.75±86.65 U/ml，q=7.335，Plt;0.01)，the recovery rates of CO,LVDP,+dp/dtmax and -dp/dtmax increased significantly (77.99%±10.02% vs. 66.26%±9.78%，85.59%±6.67% vs. 73.90%±6.66%，83.87%±9.98% vs. 68.90%±8.68%，86.01%±766% vs. 70.39%±7.98%，Plt;0.01)， the myocardial infarction areas reduced significantly (795%±6.32% vs. 1568%±10.36%,q=8.680， Plt;0.01). 〖WTHZ〗Conclusion The protective effect of IPC on I/R elderly rat hearts has weakened. The enhanced IPC is able to regain the protective effect of IPC on elderly rat hearts.
Abstract： Objective To investigate the protective effects of adenosine (ADO) on lung ischemia/reperfusion injury following heart-lung transplantation in canine. Methods Canine heart-lung transplantation was performed．Canines were divided into two groups: transplant control groupand ADO group. The changes of arterial partial pressure of oxygen(PaO2) after reperfusion in two groups at 30，60，90，120 min were observed．The tissue contents of nitric oxide (NO) were measured at 10 min before ischemia, 10 min and 120 min after ischemia; 10 min and 60 min after reperfusion．The lung tissue samples were obtained 1h after reperfusion．The tissue myeloperoxidase(MPO) activity,content of malondialdehyde(MDA), content of superoxide dismutase(SOD), wet/dry ratio of lung(W/D) were measured.Microscopic examination of lungs was also conducted. Results (1)In ADO group，PaO2 were significantly higher than that in control group at 30，60，90 and 120 min after reperfusion (Plt;0.05)．(2) The tissue contents of NO at 120 min after ischemia, 10 min and 60 min after reperfusion were significantly lower than that at 10 min before ischemia(Plt;0.05). In ADO group，the tissue contents of NO at 120 min after ischemia, 10 min and 60 min after reperfusion were higher than that in control group respectively(Plt;0.05). (3)The tissue MPO activity, content of MDA, W/D in ADO group were significantly lower than those in corresponding control group. The content of SOD in ADO group were higher than that in control group(Plt;0. 05)．(4)The microscopic examination showed that there were severe leukocyte infiltration and edema formation in the alveolar space in control group, but the changes were less severe in ADO group. Conclusion Administration of ADO in canine heart-lung transplantation can protect the donor lung against ischemia／reperfusion injury．
Objective To investigate the relationship between graded spinal cord ischemia/reperfusion injury and somatosensory evoked potentials(SEP),neurologic function score（NFS）and the histopathological changes of spinal cord. Methods Forty rabbits were randomized and equally divided into 4 groups: shamoperation group, ischemia for 30min, 45min and 60min groups. The spinal cord ischemiareperfusion injury model was created by occlusion of the abdominal aorta in rabbits. SEP was monitored before ischemia,5,10minutes after ischemia, 15, 30 minutes, 1,2, 24 and 48 hours after reperfusion. NFS was evaluated at 6,12,24 and 48 hours after reperfusion.The pathological changes of spinal cord were observed after reperfusion 48 hours. Results The pathological characters with mild,moderate and severe spinal cord ischemia/reperfusion injury could be simulated by declamping after 30， 45 and 60 minutes infrarenal aorta crossclamping. SEP amplitude returned to normal after reperfusion 15 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 30 minutes（Pgt;0.05）during mild spinal cord ischemia/reperfusion injury.SEP amplitude returned to normal after reperfusion 30 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 60 minutes（Pgt;0.05）during moderate spinal cord ischemia/reperfusion injury. SEP latency increased and SEP amplitude decreased during severe spinal cord ischemia/reperfusion injury,compared with other groups, there were significant differences in SEP latency and SEP amplitude by clamping the infrarenal aorta for 60min（Plt;0.01）. With graded spinal cord ischemia/reperfusion injury, compared with shamoperation group, spinal cord ischemiareperfusion groups had significant differences in NFS（Plt;0.01）. Conclusion SEP is much quicker in the recovery of amplitude than latency during spinal cord ischemia/reperfusion. SEP is a sensitive and accurate index for spinal cord function during ischemia/reperfusion injury. SEP monitoring spinal cord ischemia/reperfusion injury during operation provides experimental basis for clinical application.