AIM: To investigate the electrophysiological changes of diabetic myocardium and effects of cyclovirobuxine D (CVB-D) on its electrophysiology. METHODS: Diabetes was induced in male SD rats, using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. Animal electrocardiogram (ECG) was recorded by 2 weeks. Effects of CVB-D on isolated right ventricular papillary muscle from experimental diabetic rats and control group were observed by recording the transmembrane potentials with conventional glass microelectrodes. RESULTS: QT intervals in ECG and action potential duration (APD) at all levels were significantly lengthened in myocardium from week 2 of diabetes. Within the concentration of 13.3-63.3 ?mol?L~(-1), CVB-D prologated APD of diabetes in dose-dependent manner and more than that of control. Within the concentration of 33.3-63.3 ?mol?L~(-1), CVB-D depressed RP, APA, V_(max) and OS of diabetes in dose-dependent way and more than that of control. In addition, CVB-D at concentration of 20 ?mol?L~(-1) prologated APD in a time-dependent manner. The most prologation of APD was attained about 40 min in control, while more than 40 min in diabetes. CONCLUSION: The results show that QT intervals in ECG and APD at all levels are significantly lengthened in myocardium from week 2 of diabetes. CVB-D prolongates APD and inhibits RP, APA, OS and V_(max) more in diabetes than in control.

AIM:To investigate whether nimesulide a selective cyclooxygenase 2 (COX-2) inhibitor and piroxicam (an inhibitor of COX-1) protect the rat hearts against oxidative stress induced by hydrogen peroxide, superoxide anion or hydroxyl free radical. METHODS: Cardiac contractility, lactate dehydrogenase (LDH) and malondialdehyde (MDA) were analyzed by the Langendorff method in isolated rat hearts. Production of 6-Keto-PGF1?, a marker of COX activity, was measured in isolated rat hearts. RESULTS: Rat hearts were exposed to hydrogen peroxide (H2O2), pyrogallol (which produced superoxide anion) or Vit C+Fe2+ (which produced hydroxyl free radical) for 10 min followed by reperfusion for 30 min. H2O2 decreased cardiac contractility and increased LDH release, which was inhibited by nimesulide (3 mg/kg) LVDP 72%?10% vs 61%?11%, LDH (5.5?2.5)U/L vs (8.0?2.1)U/L, P

AIM: The effects of low-glucose on long-term potentiation (LTP) in the CA1 region of hippocapal slices of immature (15-16 days old) and adult (56-63 days old) rats were examined. METHODS: The technique of electrophysiology was used, and the slopes of the field excitatory postsynaptic potentials (S-EPSP) were measured. RESULTS: When slices were exposed to glucose medium at concentrations of 3 or 1.5 mmol/L, S-EPSP decreased significantly. In the slices from adult rats, only short-term potentiation was elicited by high frequency stimulation in the medium of 3 or 1.5 mmol/L glucose. However, in the slices from immature rats, LTP was still induced in the medium of 3 mmol/L glucose. CONCLUSION: Low-glucose medium depressed the synaptic transmission. In terms of the synaptic plasticity, the low-glucose endurance in immature rats was stronger than that in adult rats.

AIM: To investigate the effect of interleukin-2 (IL-2) on the intracellular calcium in electrically stimulated adult rat ventricular myocytes during anoxia and reoxygenation. METHODS: The isolated cardiac ventricular myocytes were exposed to 5 min anoxia followed by 10 min reoxygenation. Chemical anoxia was introduced by Krebs-Henseleit (K-H) solution containing 10 -3 mol/L sodium dithionite. The spectrofluorometric method was used to verify intracellular calcium transient with fura-2/AM as calcium fluorescence probe. RESULTS: It was shown that during anoxia, the amplitude of Ca 2+ transient was decreased, diastolic [Ca 2+ ] i, time to peak and time to relaxation of Ca 2+ transient were increased. All the parameters were got back but did not returned to the pre-anoxia level during reoxygenation. IL-2 at 2?10 5 U/L administrated during anoxia aggravated the effect of rexoxygenation on [Ca 2+ ] i transient. Pretreatment with a specific ? opioid antagonist, nor-BNI (10 -8 mol/L), abolished the effect induced by IL-2 during anoxia on the [Ca 2+ ] i transients, whereas specific ? opioid antagonist, naltrindole (10 -6 mol/L), did not cancel the effect. CONCLUSION: It is concluded that administration of IL-2 during anoxia aggravated the effect of reoxygenation on the [Ca 2+ ] i transients of isolated ventricular myocytes, which was mediated by cardiac ? opioid receptor pathway.

AIM: The objectives of the present study were to examine the effect of iron on relaxation of isolated rat aortic rings,and to elucidate the underlying mechanism. METHODS: The thoracic aortic rings of male Sprague-Dawley rats were mounted on bath system. Vasodilatation of aortic rings preconstricted with 10 -6 mol/L of phenylephrine (PE) was measured. RESULTS: (1) Exposure of endothelium-intact aortic rings to ferric ammonium citrate (FAC) for 30 min caused a significant reduction in the relaxation response to acetylcholine (ACh). Pretreatment with L-arginine (L-Arg) before incubation with FAC did not reverse the inhibition of relaxation response to ACh completely. (2) In endothelium-intact aortic rings,L-Arg relaxed the PE preconstricted vessels. Exposure to FAC for 30 min caused the decrease in the relaxation response to L-Arg. There was no difference in the relaxation response to nitric oxide donor,sodium nitroprusside, between endothelium-denuded arteries treated with or without FAC. (3) Dimethyl sulfoxide had no effect on the inhibition of relaxation to ACh by FAC in endothelium-intact rings. Pretreatment of arteries with glutathione and catalase prevented the decrease in relaxation responses to ACh induced by FAC. (4) The nitric oxide synthase activity was (56.49?2.49)?10 3U/g protein in normal aorta with endothelium,while after incubation with FAC for 30 min,it reduced to (25.15?5.75)?10 3U/g protein ( P

AIM: To test whether ischemic preconditioning (IPC) del ays ischemia-induced electrical uncoupling by activation of mitochondrial ATP-se nsitive potassium channels (mitoK ATP ). METHODS: Adult rat hearts perfused on a Langendorf f apparatus were subjected to 40 min ischemia followed by 30 min reperfusion. C han ges in coupling were monitored by measuring whole-tissue resistance. RES ULTS: IP C delayed the onset of uncoupling campared to ischemic control; Blocking mitoK ATP channels before the IPC protocol abolished the delay of uncoupling. The specif ic mitoK ATP channel opener diazoxide mimicked the protective effect of IPC . The delay induced by diazoxide was reduced by 5-HD, L-type Ca 2+ channel inhibitor verapamil and a free radical scavenger N-(2-mercaptopropionyl)glycine. CONCLUSIONS: IPC delays the onset of cellular electrical uncoup ling induced by acute ischemia, in which activation of the mitoK ATP channe ls may be involved.

Objective To investigate the role of HO-1 in the protection of rat heart from anoxia/reoxygenation induced injury and its underlying mechanism.Methods LVEDP,LVDP and dp/dtmax were analyzed by the Langendorff method in isolated rat heart.Lactate dehydrogenase(LDH), infarct area,COHb and 6-keto-PGF1? were further determined in the experiment.Results After intraperitoneal injection of HO-1 inducer hemin,CO concentration in rat blood enhanced(P

AIM: To analyze and compare the changes of pressure phase plane(PPP) derived τ and K on isolated rat heart during ischemia/reperfusion, and to explore the value of PPP derived τ and K for evaluation of left ventricular diastolic dysfunction. METHODS: LVEDP, -d(p/dt)_(max), τ and K were measured and calculated during ischemia/reperfusion in Sprague-Dawley rat hearts. Meanwhile, the level of lactate dehydrogenase (LDH) in the coronary effluent was measured, and the ultrastructure changes in myocardium were observed under electron microscope. RESULTS: Compared with control group, τ increased and K reduced significantly in each ischemic group in a time dependent manner (P<0.05). With prolonged ischemia, τ was even higher and K was even lower (P<0.05). Compared with control group, except ischemia 15 min, LDH in other groups increased significantly at 10 min and 20 min after reperfusion (P<0.05). Compared with ischemia 30 min, LDH of ischemia 45 min and ischemia 60 min were even higher at 10 min and 20 min after reperfusion (P<0.05). With prolonged ischemia, the abnormal changes of the myocardial ultrastructure were observed. CONCLUSION: PPP derived τ and K may be promising indexes for quantitative assessment of left ventricular diastolic function on isolated) rat heart during ischemia/reperfusion, and indication of the severity of ischemia/reperfusion injury.

AIM: To explore the protective effect of curcumin on high glucose-induced decrease in contraction of isolated rat aortic rings, and to elucidate its underlying mechanism. METHODS: The thoracic aortic rings with endothelium of male Sprague-Dawley rats were mounted on a bath system. Isometric contractions of aortic rings were measured. HO activity was also evaluated. RESULTS: (1)Four hours after incubated with 44 mmol/L of glucose (high glucose),the vascular contraction responses to phenylephrine (PE) decreased compared to control group (containing 11 mmol/L of glucose). (2)Coincubation with curcumin (3×10~(-11)-3×10~(-10) mol/L) and high glucose,the high glucose-induced decrease in contraction responses to PE of arteries was partly inhibited. (3)Four hours after incubation with curcumin,the HO activity in thoracic aorta increased. ZnPP,an inhibitor of HO-1,completely abrogated the protection effect of curcumin. (4)Methylene blue,an inhibitor of guanylate cyclase (GC),partly abolished the protective effect of curcumin. CONCLUSION: Curcumin prevents the high glucose-induced decrease in contraction responses to PE in intact aortic rings. The mechanism might be mainly involved in the activation of HO-1 and GC.