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.

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: 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: 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: To investigate the role of HO-1 in protection of rat hearts against anoxia/reoxygenation-induced injury and its underlying mechanism. METHODS: Cardiac contractility, lactate dehydrogenase (LDH) and infarct area were analyzed by the Langendorff method in isolated rat hearts. RESULTS: After intraperitoneal injection of HO-1 inducer hemin, CO concentration in rat blood enhanced (P

AIM: To explore the probable mechanisms of diabetes-induced arrhythmias. 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. All animals were observed by 2,4,6 and 8 weeks,respectively. Transmembrane potentials were recorded with conventional glass microelectrodes. RESULTS: Action potential duration(APD) at all level (APD10,APD20,APD30,APD50,APD70,APD90) was significantly lengthened in right ventricular papillary muscle from week 2 of diabetes. At week 8,APD was more lengthened at any level of repolarization than that at week 2. No differences were observed in the maximum rate of depolarization(V_ max ),overshoot(OS) and action potential amplitude(APA) as well as the resting membrane potential(RP) from the 2th to 8th week of diabetes. CONCLUSION: The results indicate that prolongation of APD may be prominently responsible for the increased incidence of cardiac re-entry-arrhythmias and sudden death,especially at late stages of diabetes.

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