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Objective To evaluate the effects of preconditioning and postconditioning with fructose?1, 6?bisphosphate (FBP) on ischemia?reperfusion (I∕R) injury in isolated rat hearts. Methods Healthy male Sprague?Dawley rats, aged 5-6 months, weighing 210-240 kg, were heparinized and anesthetized with isoflurane. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with K?H solution saturated with 95% O2 and 5% CO2 at 37-38 ℃ in a Langendorff apparatus. Sixty isolated rat hearts were randomly divided into 4 groups ( n= 15 each ) using a random number table: control group ( group C) , FBP preconditioning group ( group Fpr) , I∕R group, and FBP postconditioning group ( group Fpo) . After 30 min of stabilization, the hearts were continuously perfused with K?H solution for 100 min in group C, with K?H solution for 10 min in the other three groups, or with K?H solution containing FBP 5 mmol∕L for 10 min in group Fpr. In I∕R, Fpr and Fpo groups, the hearts were perfused with cardioplegic solution 20 ml to induce cardiac arrest, and perfusion was stopped at the same time. After 30 min of suspension of perfusion, I∕R and Fpr groups were perfused with K?H solution for 60 min, and group Fpo was first perfused with K?H solution containing FBP 5 mmol∕L for 10 min, and then perfused with K?H solution for 50 min. At the end of stabilization ( T0 ) , at 1 min before suspension of perfusion ( T1 ) , and at 5, 15, 30 and 60 min of reperfusion ( T2?5 ) , heart rate ( HR ) , left ventricular developed pressure (LVDP), and left ventricular end?diastolic pressure (LVEDP) were recorded. At T0 and T5, the coronary flow ( CF) was measured, and the coronary effluent was collected for determination of creatine kinase ( CK) and lactic dehydrogenase ( LDH) activities. The histopathologic changes of myocardium were examined with light microscope at T5 . Results Compared to group C, HR and LVDP were significantly decreased, and LVEDP was increased at T2-5 in I∕R, Fpr and Fpo groups, the CF was decreased at T5 in I∕R and Fpr groups, and CK and LDH activities in coronary effluent were increased in I∕R, Fpr and Fpo groups. Compared to group I∕R, HR and LVDP were significantly decreased, and LVEDP was increased at T2-4 , and the CF was increased, and CK and LDH activities in coronary effluent were decreased at T5 in Fpr and Fpo groups. Compared to group Fpr, HR and LVDP were significantly increased, and LVEDP was decreased at T2-5 , and the CF was increased, and CK and LDH activities in coronary effluent were decreased at T5 in Fpo group. The histopathologic changes of myocardium were significantly mitigated in group Fpo compared with group Fpr. Conclusion Both FBP postconditioning and preconditioning can reduce I∕R injury and improve cardiac function in isolated rat hearts, and FBP postconditioning offers better effect than FBP preconditioning.
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Objective To investigate the effect of fructose-1,6-diphosphate (FDP) pretreatment on myocardial connexin 43 (Cx43) in a rat model of acute myocardial ischemia.Methods Thirty-six male Sprague Dawley rats (aged 8-12 weeks and weighing 220-280 g) were randomly divided into three groups (n =12 each):sham operation group (group S),ischemia group (group Ⅰ) and FDP + ischemia group (group F).The animals were anesthetized with intraperitoneal injection of 10％ chloral hydrate 40 mg/100 g,then tracheostomized and mechanically ventilated.Acute myocardial ischemia was induced by occlusion of the left anterior descending coronary artery for 30 minutes.Myocardial ischemia was verified by elevation of the S-T segment on echocardiogram (EGG).In group F,FDP 100 mg/kg was injected intravenously 10 minutes before ischemia.The hearts were removed after 30 minutes of myocardial ischemia.The myocardial infarct size (IS) and area at risk (AAR) were measured and the IS/AAR ratio was calculated.The expression of myocardial Cx43 protein was determined by immunohistochemestry and analysis of mean optical density.Results The severities of arrhythmia were significantly higher in groups F and I than in group S,while lower in group F than in group Ⅰ (P＜ 0.05).The IS/AAR ratio was significantly lower in group F than in group Ⅰ.The myocardial Cx43 protein expression was down-regulated in group Ⅰ and group F as compared with group S,and was significantly lower in group Ⅰ than in group F.Conclusion FDP pretreatment can protect myocardium against acute ischemia by up-regulation of myocardial Cx43 expression.
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Objective To investigate the effect of fructose-1,6-diphosphate (FDP) pretreatment on myocardial connexin43 (Cx43) in a rat model of acute myocardial ischemia.Methods Thirty-six male 8-12 week old SD rata weighing 220-280 g were randomly divided into 3 groups (n=12 each):group Ⅰ sham operation (group S);group Ⅱ ischemia(group Ⅰ)and group Ⅲ FDP+ischemia(group F).The animals were anesthetized with intraperitoneal 10%chloral hydrate 40 mg/100 g,tracheostomized and mechanically ventilated.Acute myocardial ischemia was induced by occlusion of left anterior descending coronary artery for 30 min.Myocardial ischemia was;verified by elevation of S-T segment on ECG.In group F FDP 100 mg/kg was injected iv at 10 min before ischemia.Arrhythmia was recorded within 30 min after occlusion and the severity of arrbythmia was aggesged.The hearts were removed after 30 min myocardial ischemia.The Left ventricle area (LVA),myocardial infarct area (IA) and area at risk (AAR) were measured and AAR/LVA and IA/AAR ratios were calculated.The expression of myocardial Cx43 protein was determined by immuno-histochemestry and analysis of mean optical density.Results The severity of arrhythmia was significantly higher in group F and I than in gropu S.while lower in group F than in group I(P<0.05).The IA,IA/AAR ratio was significantly lower in group F than in group I.The myocardial Cx43 protein expression was down-regulated in group I and F as compared with group S.and was significantly lower in group I than in group F.Conclusion FDP pretreatment can protect myocardium against acute ischemia by up-regulation of myocardial Cx43 expression.
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Objective To investigate effects of combined use of glycogen synthase kinase (GSK) -3 inhibitor and fructose-1,6-diphosphate (FDP) on liver trauma in rats. Methods After crea-tion of liver trauma model in 49 Sprague-Dawley rats, 42 rats were randomly divided into control group (NaCl group), FDP group and FGI Group (FDP and GSK-3 inhibitor in combination group). Then, each group was randomly subdivided into pre-ischemia group and 4-hour reperfusion group on account of time point when animals were sacrificed before and after iachemia. The other seven rats set as sham operation group (SH group) were sacrificed at 4-hour reperfusion time point. The AST and ALT levels in hlood and glycogen content, SOD vitality and MDA content in liver tissues were determined. Results At pre-is-chemia time point, liver glycogen content in three groups was in order of control group < FDP group < FGI group (P <0.01). At 4-hour reperfusion time point, blood ALT and AST levels in four groups were in order of control group > FDP group > FGI group > SH group (P < 0.01), while SOD vitality in liver tissues of four groups was in order of control group < FDP group < FGI group < SH group (P < 0.01) and MDA content in four groups was in order of control group > FDP group > FGI group > SH group (P < 0.01). Conclusions Combined use of FDP and GSK-3 inhibitor can enhance the protective effect of FDP on liver rupture, as may relate to the mechanism that GSK-3 inhibitor can effectively enhance glycogen synthesis of FDP as substrate before liver ischemia so that the liver glycogen storage is increased in a short period of time and hence post-traumatic warm ischemia-reperfusion injury is alleviated in the liver of rats.