Effects of hydrogen sulfide preconditioning on myocardial ischemia reperfusion injury in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effects of hydrogen sulfide preconditioning on myocardial ischemia reperfusion injury in rats.</p><p><b>METHODS</b>Sprague-Dawley male rats were divided into 4 groups with 10 in each group: in S group rats received sham operation; in IR group rats were given with NS (1.0 ml/kg iv) 24 h before ischemia; in H group rats were treated with NaHS (0.05 mg/kg iv) 24 h before ischemia; and in D group, NaHS-treated rats received 5-hydroxydecanoate (5-HD) 15 min before ischemia. Rats in IR group,H group and D group were subjected to ischemia by occlusion of coronary artery for 30 min followed by 2 h of reperfusion. At the end of the reperfusion,myocardial infarct size was measured. SAM-s was measured by Western blotting. Plasma SOD activity and MDA were determined at the end of reperfusion.</p><p><b>RESULTS</b>The infarct size was significantly lesser in H group (25.40 % ± 3.54%) than that in IR group (38.27% ±5.64%,P<0.05). The SAM-s protein expression in myocardium was significantly lower in H group than that in IR group. The plasma MDA content was significantly lower and SOD activity was higher in H group than those in IR group,but there was no difference between IR group and D group.</p><p><b>CONCLUSION</b>The hydrogen sulfide preconditioning attenuates myocardial IR injury possibly through down-regulating SAM-s expression,reducing the production of oxygen free radicals and enhancing anti-oxidize effect in rats.</p>

Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats.</p><p><b>METHODS</b>Sprague-Dawley male rats were randomly divided into 4 groups (n= 10 in each): Group S (sham operation group), Group IR (ischemia/reperfusion group), Group H (IR+ NaHS 0.05 mg/kg iv, 24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate (5-HD)15 min before ischemia. Animals in groups IR, H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS) was examined. Glutathione S-transferase (GST) was measured by Western blotting. The myocardial ultrastructures were observed under the electron microscopy.</p><p><b>RESULTS</b>The IS was significantly smaller in Group H than that in Group IR [(25.40 ± 3.54)% compared with (38.27 ± 5.64)%, P<0.05]. The GST expression in myocardium was significantly higher in Group H than that in Group IR. Microscopic examination showed less myocardial damage in Group H than in Group IR. The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pre-treatment.</p><p><b>CONCLUSION</b>The hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.</p>

Effects of hypertonic saline against focal cerebral ischemia-reperfusion injury in rats and the mechanism / 中华神经医学杂志

Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.

Effect of morphine postconditioning on myocardial ischemia-reperfusion injury in rabbits / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the protective effects of morphine postconditioning on myocardial ischemia-reperfusion (I/R)injury and the potential mechanisms in rabbits.</p><p><b>METHODS</b>Thirty-two New Zealand male white rabbits were randomly assigned into 4 groups: Group 1 (Sham), Group 2 (I/R), Group 3 (ischemic postconditioning), Group 4 (ischemia and morphine postconditioning). Group 1 was perfused for 160 min; Group 2 underwent 40 min ischemia and 120 min reperfusion; Group 3 underwent three cycles of 30 s reperfusion and 30 s left anterior descending coronary artery re-occlusion immediately after 40 min ischemia and before 120 min reperfusion; Group 4 was given morphine 1.0 mg/kg immediately after 40 min ischemia in 1 min and before 120 min reperfusion. Blood samples were taken from arterial line at 20 min before occlusion, 20 min after occlusion, 40 min after occlusion, 1 h after reperfusion and 2 h after reperfusion for determination of the plasma levels of cardiac troponin I (cTnI). At the end of the reperfusion, infarct size (IS) and area at risk were defined by Evans and TTC staining. Plasma SOD activity and MDA were determined at the end of reperfusion.</p><p><b>RESULT</b>The levels of cTnI were significantly lower during reperfusion in the two postconditioning groups than those in I/R group. The plasma MDA content was significantly lower and SOD activity was significantly higher in the two postconditioning groups than those in I/R group, but there was no difference between two postconditioning groups. Morphine significantly reduced infarct size of the left ventricular area at risk as compared with I/R group (P<0.05).</p><p><b>CONCLUSION</b>Morphine postconditioning is as effective as ischemic postconditioning in the protection of myocardium against I/R injury in rabbits. Decrease in oxygen free radicals and increased antioxidant activity might be involved in its mechanism.</p>

Preconditioning of morphine protects rabbit myocardium from ischemia-reperfusion injury / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the protective effects of preconditioning morphine on rabbit myocardium during ischemia-reperfusion.</p><p><b>METHODS</b>Thirty New Zealand male white rabbits were randomly assigned to three groups: control, I/R and morphine groups. In morphine group 1.0 mg/kg morphine was given preoperationaly, in control and I/R groups 1.0 ml/kg NS was given. Twenty-four hours later rabbits in morphine and I/R groups underwent 40 min of coronary occlusion followed by 2 hours of reperfusion; for control group only sham operation was performed. At the end of the reperfusion, infarct size (IS) and area at risk (AAR) were defined by Evans blue and TTC staining. At the end of the reperfusion blood samples were taken for determination of plasma SOD activity and MDA levels. The heart was harvested and levels of the HSP27 were determined by Western blot, and the heart ultrastructures were observed under the electron microscopy.</p><p><b>RESULTS</b>Compared with I/R group,morphine significantly reduced infarct size (21.5%+/-2.4% Compared with 37.8%+/-1.7%, P<0.05). The morphine had a lower level of MDA and higher levels of SOD and HSP27 than those in I/R.</p><p><b>CONCLUSION</b>Preconditioning of morphine demonstrates cardioprotective effect on ischemia/reperfusion injury, which may be associated with increased HSP27 levels in the heart.</p>

Effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury in rabbits / 中南大学学报(医学版)

OBJECTIVE@#To investigate the protective effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury and the potential mechanism in rabbits.@*METHODS@#Thirty New Zealand male white rabbits were randomly assigned to 3 groups: Control group; I/R group; and 2.0% isoflurane group. Isoflurane group was exposed to 2.0% isoflurane-100% oxygen for 2 hours. Control group and I/R group were exposed to 100% oxygen for 2 hours and served as untreated controls. Twenty-four hours later I/R group and isoflurane group underwent 40 minutes of coronary occlusion followed by 2 hours of reperfusion. Blood samples were taken from the arterial line at 20 minutes before the occlusion(T1), 20 minutes after the occlusion(T2), 40 minutes after the occlusion(T3), 1 hours after the reperfusion(T4), and 2 hours after the reperfusion(T5) to determine the plasma level of TNF-alpha. At the end of the reperfusion, infarct size and area at risk were defined by Evans and TTC staining. The heart was harvested and levels of the p38MAPK activity were determined by Western blot, and ultrastructures were observed under the electron microscope.@*RESULTS@#The p38MAPK activity of isoflurane group was significantly lower than that of I/R group (P<0.05). Isoflurane significantly (P<0.05) reduced the infarct size(19.7%+/-2.8% in isoflurane group) of the left ventricular area at risk as compared with the controls (37.8%+/-1.7% in I/R group).The injury of I/R group was worse than that of isoflurane group under the light microscope. Isoflurane group had a lower level of TNF-alpha than I/R group.@*CONCLUSION@#Isoflurane can inhibit p38MAPK activity during myocardial ischemia reperfusion and modulate the cytokine expression, which may be one of the molecular mechanisms of isoflurane delayed preconditioning on cardioprotection.

Effect of fructose-1,6-diphosphete on myocardial preservation during pulmonary operations / 中南大学学报(医学版)

OBJECTIVE@#To investigate the effect of fructose-1,6-diphosphete(FDP) on myocardial preservation in pulmonary operations.@*METHODS@#One hundred and six patients undergoing selective pulmonary lobectomy or segmentectomy were randomly divided into 2 groups with 53 patients each. FDP 200 mg/kg was infused intravenously before anesthesia in the FDP group, while 5% glucose with the same volume was given instead of FDP in the control group. ECGs were monitored from before the anesthesia to 72 h after the operation;the time and type of arrhythmia were recorded. Blood samples were taken before the operation (T0), immediately after the operation(T1), at 24 h(T2),48 h(T3)and 72 h(T(4)) after the operation to determine plasma creatine kinase isoenzyme MB(CK-MB) and cardiac troponin I(cTnI) concentrations.@*RESULTS@#The incidence of arrhythmia in FDP group (35 times) was significantly lower than that in the control group(67 times). The incidence of all types of arrhythmia in the FDP group was also significantly lower than that in the control group. The concentrations of CK-MB and cTnI in the FDP group were significantly lower than those in the control group at T1, T2, T3, and T4.@*CONCLUSION@#FDP is effective for myocardial preservation in pulmonary operations.

Effect of morphine on dorsal horn projection neurons in neuropathic pain rats / 中南大学学报(医学版)

OBJECTIVE@#To explore the inhibitory effect of spinal topical morphine on the dorsal horn projection neurons in nerve-injured rats and its mechanism.@*METHODS@#Single-unit activity of dorsal horn projection neurons was recorded in anesthetized L(5)/L(6) nerve-ligated rats. Allodynia was determined by a behavior test in nerve-injured rats. The evoked neuronal responses to mechanical stimuli applied to the receptive field were determined before and after the spinal topical application of morphine, bicuculline plus morphine, strychnine plus morphine, and both bicuculline and strychnine plus morphine in normal, sham operation, and nerve-injured rats.@*RESULTS@#Spinal topical application of 10 micromol/L morphine significantly inhibited the evoked responses of dorsal horn projection neurons in normal, sham, operation and nerve-injured rats. However, the inhibitory effect of morphine was significantly reduced in nerve-injured rats compared with that in normal and sham operation rats. Furthermore, the topical application of 20 micromol/L bicuculline had little effect on the inhibitory effect of morphine in nerve-injured rats but it almost abolished the effect of morphine in normal and sham operation rats. The glycine receptor antagonist strychnine at 4 micromol/L significantly decreased the effect of morphine in nerve-injured, normal, and sham operation rats.@*CONCLUSION@#The loss of tonic GABAergic inhibition contributes to the reduced inhibitory effect of morphine on dorsal horn projection neurons in nerve-injured rats.

Effect of chloroquine on the apoptosis of intestinal mucosa epithelial cells and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats / 中南大学学报(医学版)

OBJECTIVE@#To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats.@*METHODS@#The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained.@*RESULTS@#Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05).@*CONCLUSION@#Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.

Effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats / 中南大学学报(医学版)

OBJECTIVE@#To investigate the effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats.@*METHODS@#The total hepatic ischemia-reperfusion model was built after blocking of the hepatic porta, suprahepatic and infrahepatic vena cava. Ninety Sprague-Dawley rats were assigned randomly into 3 groups: Sham operation group (Group A, n=30); total hepatic ischemia group (Group B, n=30); and aminoguanidine treatment group (Group C, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different time phases: 20 minutes after the total hepatic vascular exclusion (T0), 4 hours after the reperfusion (T1), and 48 hours after the survival Group A and Group B were intravenously injected with normal saline ( mL/kg) while Group C was injected with aminoguanidine (20 mg/kg) dissolved in normal saline (1 mL/kg) 10 minutes before the open of the abdomin. The levels of portal blood nitric oxide ( O) endotoxin ( ET), tumor necrosis factor-alpha (TNF-alpha at T0 and T1 were detected; 48 hours survival rates and the lung wet/dry weight ratio were counted; and the histological changes of the lung tissues were observed.@*RESULTS@#Compared with Group A, the levels of portal vein NO, ET, and TNF-alpha T0 and T1 in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). But those indexes of Group C were lower than those of Group B (P < 0.05). The 48-hour survival rate in Group C was higher than that in Group B (P < 0.05). The lung wet/dry weight ratio in Group C was lower than in Group B (P < 0.05) and the histological change of Group C was slighter than that in Group B.@*CONCLUSION@#Aminoguanidine has the protective effects on the lungs against the total hepatic ischemia-reperfusion induced injury.