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1.
AIM: To investigate the effect of neuropeptide Y (NPY) on intracellular free calcium(［Ca2+］i) and Ca2+ sarcoplasmic reticulum of cardiomyocytes in rats.METHODS: Cardiomyocytes of neonatal Sprague-Dawley rats were incubated with NPY at concentration of 100 nmol/L for 24 h. Fluorescent indicator Fluo-4 AM was used to detect ［Ca2+］i and Fluo-5N AM was used to detect Ca2+ in sarcoplasmic reticulum (SR). Calcium image was recorded by laser scanning confocal microscope. The SR Ca2+ load was estimated by caffeine-induced Ca2+ transient (CCT). RESULTS: 24 h after incubation with NPY, compared with control group, the concentration of ［Ca2+］i was significantly elevated (P<0.05), and the concentration of free Ca2+ in SR (［Ca2+］SR) was significantly decreased (P<0.05), and the peak of CCT was attenuated.CONCLUSION: Stimulation with NPY for 24 h causes redistribution of free calcium in rat cardiomyocytes, namely the elevation in ［Ca2+］i and decline in ［Ca2+］SR.  相似文献   

2.
AIM: To investigate the role of intracellular free Ca2+ concentration (［Ca2+］i) in the regulation of calcium-activated chloride (ClCa) channels in pulmonary artery smooth muscle cells (PASMCs) of rats under normoxic, acute and chronic hypoxic conditions. METHODS: Acute hypoxia-induced contraction was observed in rat pulmonary artery by using routine blood vascular perfusion in vitro. The fluorescence Ca2+ indicator Fura-2/AM was used to observe ［Ca2+］i of rat PASMCs in normal and chronic hypoxic condition. The influences of ClCa channels on PASMCs proliferation were assessed by MTT assay. RESULTS: (1) The ClCa channel blockers niflumic acid (NFA) and indaryloxyacetic acid (IAA-94) produced inhibitory effects on acute hypoxia-evoked contractions in pulmonary artery. (2) Under chronic hypoxic condition, ［Ca2+］i was increased. In normoxic condition, ［Ca2+］i was (123.63±18.98) nmol/L, and in hypoxic condition, ［Ca2+］i was (281.75±16.48)nmol/L (P<0.01). (3) In normoxic condition, ［Ca2+］i had no significant change and no effect on ClCa channels was observed (P>0.05). (4) Chronic hypoxic increased ［Ca2+］i which opened ClCa channels. The NFA and IAA-94 blocked them and decreased ［Ca2+］i from (281.75±16.48)nmol/L to (117.66±15.36)nmol/L (P<0.01). (5) MTT assay showed that in chronic hypoxic condition NFA and IAA-94 decreased the value of absorbing light degree (A value) from 0.459±0.058 to 0.224±0.025 (P<0.01). CONCLUSION: Hypoxia increased ［Ca2+］i which opened ClCa channels and had a positive-feedback to ［Ca2+］i. This may play an important role in hypoxic pulmonary hypertension. In chronic hypoxic condition, ClCa channel may play a role in the regulation of PASMCs proliferation.  相似文献   

3.
AIM:To study the effect of chronic hypoxia (CH) on the intracellular calcium (［2+］i) in pulmonary artery smooth muscle cells (PASMCs) and the role of L-type calcium channel and calcium store. METHODS:The rat chronic hypoxia model was set up and intervene the PASMCs with normal PSS, calcium-free PSS, nifedipine, and heparine respectively. The resting ［Ca2+］i was determined with the Fura-2/AM calcium imaging technique. RESULTS:(1) The ［Ca2+］i in CH group in normal PSS was higher than that in control group in normal PSS (P<0.05). The ［Ca2+］i in CH group in normal PSS was higher than that in calcium-free PSS (P<0.05). (2) No obvious change of ［Ca2+］i before and after application of nifedipine in PASMCs of CH groups was observed. (3) No difference of ［Ca2+］i before and after application of heparine in PASMCs of CH groups was detected. CONCLUSION:Chronic hypoxia increased the ［Ca2+］i in PASMCs. Chronic hypoxia induced increase in ［Ca2+］i may relate to the influx of extracellular calcium, but not due to the L-type calcium channel or the IP3R modulation only.  相似文献   

4.
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5.
AIM: To study the role of prostaglandin F2α (PGF2α) in cardiac hypertrophy and its relation with calcineurin (CaN) signal transduction pathway in vitro. METHODS: The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of PGF2α, and the hypertrophic response was assayed by measuring the cell diameter, protein content and atrial natriuretic factor (ANF) mRNA expression. For mechanism studies, the intracellular free calcium concentration (［Ca2+］i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator. ANF and CaN mRNA expressions, and the expressions of CaN and its downstream effectors, NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blotting, respectively.RESULTS: In cultured cardiomyocytes, PGF2α induced profound hypertrophic morphology change, the significant increase in cell diameter and protein content in a concentration-dependent manner compared with those in vehicle control (P<0.01). The same result was found in measuring the ［Ca2+］i in cardiomyocytes (P<0.01). PGF2α at concentration of 10-7 mol/L significantly promoted ANF and CaN mRNA expressions and the protein expressions of CaN/NFAT3/GATA4 compared with those in the vehicle control (P<0.05). Cyclosporin A, a CaN inhibitor, markedly inhibited the myocyte hypertrophy (P<0.01), reduced the increased ［Ca2+］i(P<0.01) and decreased the expressions of CaN mRNA and CaN/NFAT3/GATA4 proteins (P<0.05) compared with those of only PGF2α　10-7 mol/L treatment. CONCLUSION: Cardiomyocyte hypertrophy induced by PGF2α may be, at least in part, mediated by CaN signal transduction pathway activated by increasing ［Ca2+］i.  相似文献   

6.
AIM: To investigate the effects of high-fat diet on the level of intracellular free calcium (［Ca2+］i) and the activity of angiotensinⅠconverting enzyme (ACE) in alveolar macrophages (AMs) of rabbits.The association between asthma and high-fat diet was also observed.METHODS: Twelve male New Zealand rabbits were medially divided into normal diet group and 1.2% high-cholesterol diet group randomly.8 weeks later,bronchial alveolar lavage was performed in vitro.［Ca2+］i was determined by Fluo-2/am.The activity of ACE was detected with ultraviolet method.RESULTS: The levels of ［Ca2+］i in AMs greatly increased (P＜0.01).The activity of ACE both in BALF and in culture supernatants of AMs was all greatly increased compared with normal diet group (P＜0.01).In hypercholesterolemic group the number of macrophages in BALF showed a positive correlation with the content of cholesterol in serum,such as the level of ［Ca2+］i in AMs and the activity of ACE in the culture supernatants of AMs (all P＜0.05).CONCLUSION: The results suggest that AMs of rabbits may be activated by hyperlipoidemia and become ease to be stimulated.  相似文献   

7.
AIM:The mechanism of angiopoietin-1 (Ang-1) in mediating increase in intracellular free magnesium (［Mg2+］i) in human umbilical vein endothelial cells (HUVECs) was investigated in this study. METHODS:The change of ［Mg2+］i in HUVECs was quantitatively detected in intracellular cation measurement system via loaded with the fluorescent magnesium indicator mag-fura-2. RESULTS:Ang-1 increased ［Mg2+］i, and there was not any significant difference among the groups of 0 mmol/L and 1 mmol/L of extracellular Mg2+. Similar results were obtained in groups done with Ca2+. Pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) blocked the increase in ［Mg2+］i induced by Ang-1. However, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) had no effect on the Ang-1-induced ［Mg2+］i　increase. CONCLUSION:These results suggest that the increase in ［Mg2+］i by Ang-1 come from intracellular Mg2+ pools mediated by tyrosine kinase/PI3K -dependent signaling pathways.  相似文献   

8.
AIM: To explore the effects of salvianolic acid B (SalB) on the energy metabolism and hydrocephalus in mice with cerebral ischemia.METHODS: NIH mice were randomly divided into four groups: sham-operated group,cerebral ischemia group,SalB-treated group and nimodipine-treated group.The brain tissue energy charge (EC),phosphocreatine (PCr),the activity of ATPase,excitability amino acid (EAA) content and water content of brain were measured when cerebral ischemia for 30 min.RESULTS: EC (0.520±0.034),PCr content ［(98.344±13.249) μmol/g］,the activity of Na+-K+-ATPase ［(0.593±0.013)×103 U/g］ and Ca2+-ATPase ［(0.484±0.053)×103 U/g］ in SalB-treated group were significantly higher than those in cerebral ischemia group {EC (0.465±0.037),PCr content ［(81.614±9.919) μmol/g］ ,the activity of Na+-K+-ATPase ［(0.244±0.065)×103 U/g］,the activity of Ca2+-ATPase ［(0.321±0.086)×103 U/g］} (P<0.01).The glutamate (Glu) content ［(0.405±0.110) μmol/g］,aspartate (Asp) content ［(0.141±0.020) μmol/g］ and water content of brain ［(38.1±0.1)%］ in SalB-treated group were markedly lower than those in cerebral ischemia group ［ Glu content (0.550±0.140) μmol/g,Asp content (0.287±0.050) μmol/g,water content of brain (44.1±0.1)%］ (P<0.05,P<0.01).CONCLUSION: The increase in cerebral energy metabolism and the activity of ATPase,and decrease in EAA content in brain tissue are the mechanism of SalB alleviating hydrocephalus at the early stage of cerebral ischemia in mice.  相似文献   

9.
AIM: To characterize the vasodilatatory effect of CH2Cl2 extract of flos magnoliae (CEF) on isolated rat thoracic aorta and to elucidate its possible mechanism. METHODS: The thoracic aorta was isolated from male Sprague-Dawley (SD) rats and the isometric tension of aortic rings with or without endothelium was measured. RESULTS: CEF (0.1-1 000 mg/L) produced concentration-dependent, endothelium-independent relaxations in phenylephrine (PE)-contracted aortic rings. The maximum relaxation induced by CEF was 78.68%±6.03% in endothelium intact rings and 64.98%±13.90% in endothelium removed rings while the forskolin (1 μmol/L)-induced vasodilation was obtained as 100%. The vasodilatatory effect of CEF was not statistically inhibited by 10 μmol/L glibenclamide (Glib), 3 mmol/L tetraethylammonium (TEA), 100 μmol/L BaCl2 and 10 μmol/L 1H- -oxadiazole- -quinoxalin-1-one (ODQ) in the preparations without endothelium. The CEF pre-treatment significantly inhibited vasoconstrictions to angiotensin Ⅱ (AngⅡ), prostaglandin F2α, (PGF2α), dopamine (Dopa), vasopressin (Vaso), 5-hydroxytryptamine (5-HT) and PE by 91.31%, 82.11%, 95.32%, 90.53%, 72.22% and 83.63%, respectively (P<0.01). In Ca2+-free medium treated endothelium removed aortic ring, incubation with CEF at concentration of 82 mg/L significantly attenuated intracellular Ca2+ release by PE. In Ca2+-free + high potassium medium incubated aortic rings without endothelium, CEF (82 mg/L) markedly inhibited potassium-stimulated Ca2+-dependent contraction which was mainly due to Ca2+ influx (P<0.01).CONCLUSION: CEF induced vasorelaxation is mainly related to interfering intracellular calcium homeostasis by blocking Ca2+ influx and intracellular Ca2+ release.  相似文献   

10.
AIM:To investigate the changes of intracellular calcium ion (Ca2+) concentration in mouse H9c2 (2-1) cells transfected with or without FK506 binding protein 12.6(FKBP12.6) gene by ultrasound mediated destruction of microbubbles. METHODS:The pcDNA3.1-FKBP12.6 plasmid, mingled with albumin-coated microbubbles agents, was transfected into H9c2 (2-1) cells by ultrasound-mediated destruction of microbubbles. The H9c2 (2-1) cell growth state was investigated by inverted microscope. The changes of intracellular Ca2+ concentration was determined by laser scanning confocal microscope. The FKBP12.6 protein expression was checked by immunohistochemistry. RESULTS:As compared with control cells, the H9c2 (2-1) cells, transfected with FKBP12.6 gene, grew better, had higher gross intracellular Ca2+ concentration. CONCLUSION:FKBP12.6 gene augments Ca2+ concentration in mouse H9c2 (2-1) cells, enhances the contractibility of the myocardial cell, which may be helpful to improve the myocardial dysfunction.  相似文献   

11.
CHEN Xing-wu  XU Jun 《园艺学报》2007,23(6):1125-1129
AIM: To explore the role of endothelin-1 (ET-1) in initiating transdifferentiation of sub-epithelial fibroblasts (SEFs) into myofibroblasts and its ionic and signal transduction mechanism.METHODS: Human SEFs or SEFs plated in collagen gels were co-cultured with human bronchial epithelial cells (16HBE) treated with lipopolysaccharide (LPS) plus mechanical scratch. ET receptor A inhibitor (BQ123) or the inhibitors specific for p38 MAPK, ERK1/2 were added, repectively. The expression of α-smooth muscle actin (α-SMA) in the SEFs and contractility of the collagen gels containing with SEFs as well as the effects of p38 MAPK or ERK1/2 on α-SMA expression were evaluated. Using Ca2+ sensitive Fluo-3/AM, dynamic changes of intracellular calcium concentration (［Ca2+］i) were observed in the SEFs by laser confocal microscopy.RESULTS: Injured 16HBE induced the transdifferentiation of myofibroblasts, which expressd α-SMA and increased contractility. BQ123 blocked the induction to a certain extent. Injured 16HBE activated p38 MAPK and ERK1/2 pathways in SEFs, both inhibitors of p38 MAPK and ERK1/2 attenuated the induction of α-SMA by injured 16HBE. The addition of exogenous ET-1 enhanced α-SMA expression and activated p38 MAPK, ERK1/2 pathways in the SEFs. Additionally, ET-1 significantly facilitated Ca2+ inflow into the fibroblasts.CONCLUSION: Injured 16HBE induces the transdifferentiation of SEFs into myofibroblasts, which is involved in the activation of p38 MAPK and ERK1/2 pathways. The ET-induced influx of Ca2+ may be an early signal for initiating the myofibroblasts transdifferentiation.  相似文献   

12.
AIM: To explore the effects and mechanism of interleukin-2 (IL-2) on the positive effect of isoproterenol (ISO) in the isolated rat cardiomyocytes. METHODS: Enzymatically isolated cardiomyocytes were used. Peak twitch amplitude and maximal velocity of shortening/relaxation (±dL/dtmax) in the isolated cardiomyocytes were recorded with a microscope coupled to a charge-coupled device camera and ［Ca2+］i transients were determined with a fluorometric ratio method by using Fura-2/AM as Ca2+ indicators. RESULTS: ① ISO increased the peak twitch amplitude and ±dL/dtmax of the isolated cardiomyocytes. Perfusion for 15 min with IL-2 at 2×103 U/L, which had no effect at all, attenuated the enhancing effect of ISO on the peak twitch amplitude and ±dL/dtmax. ② ISO increased the ［Ca2+］i transients of the single ventricular myocytes in a dose dependent manner and the corresponding EC50 values of ISO was (0.12±0.01) μmol/L. Perfusion for 15 min with IL-2 at 2×103 U/L, which had no effect on the ［Ca2+］i transient at all, attenuated the enhancing effect of ISO and the corresponding EC50 was (0.44±0.06) μmol/L. ③ The electrically induced ［Ca2+］i transient was significantly increased by pretreatment with 20 mg/L cholera toxin for 12 h. The elevation of the ［Ca2+］i transient induced by cholera toxin was significantly attenuated by 2×103 U/L IL-2. ④ Forskolin (1 μmol/L), the activator of adenyl cyclase, significantly increased the electrically induced ［Ca2+］i transient, which was attenuated by IL-2 at 2×103 U/L. CONCLUSION: IL-2 inhibits the positive effect of isoproterenol in the isolated single ventricular myocytes, in which Gs protein and adenyl cyclase are involved.  相似文献   

13.
AIM: The effects of breviscapin on transient outward potassium current (Ito) and inward rectifier potassium current (IK1) channel in isolated ventricular myocytes of rats were determined. The mechanism of breviscapin at the ionic channel level was explored. METHODS: Single ventricular myocyte of rats was isolated by enzymatic dissociation. The whole-cell patch-clamp recording technique was used to record the change of Ito and IK1 channel current influenced by breviscapin. RESULTS: Breviscapin decreased the Ito channel current in a dose-dependent and voltage-dependent manner in ventricular myocytes of rats. (1) The current-voltage curve was significantly decreased. Breviscapin at concentrations of 0.02, 0.05, 0.08, 0.10 g·L-1 respectively decreased Ito current density (10.07±0.50)%, (27.47±2.36)%, (42.72%±2.50)% and (56.09±5.60)%. Ito was inhibited in a voltage-dependent manner, showing a significant attenuating effect at test potentials from 0 to + 50 mV. (2) The Ito activation curve, the activation curve and the recovery curve were not altered. (3) Breviscapin did not affect IK1. CONCLUSION: Breviscapin concentration-dependently decreases Ito channel current in ventricular myocytes of rat.  相似文献   

14.
AIM: To investigate the effect of pioglitazone (Pio) on glucose metabolism and peroxisome proliferators-activated receptor (PPAR)-γ expression in free fatty acid (FFA) -induced insulin resistance in rats. METHODS: A hyperinsulinaemic-euglycaemic clamp and ［3-3H］-glucose tracing technique were used in awake rats. Glucose metabolism in vivo and PPAR-γ in adipose tissue expression were assessed with elevation FFA by lipid infusion over 4 h in rats pretreated with or without Pio.RESULTS: During steady-state of clamp, there was a significant increase in plasma FFA in two lipid-infused groups, compared to control rats (P<0.01). The glucose infusion rates (GIR) in Pio-treated rats (P/L group), compared with controls, were significantly reduced ［(20.6±0.4) mg·kg-1·min-1 vs (33.6±0.6)mg·kg-1· min-1, P<0.01］, whereas the GIR was lower in the lipid group (L group) than that in the P/L group［(12.6±0.8) mg·kg-1·min-1 vs (20.6±0.4) mg·kg-1·min-1, P<0.01］. The hepatic glucose production (HGP) was significantly suppressed (85%) ［(18.3±2.1)mg· kg-1·min-1 (basal) vs (2.7±2.4)mg· kg-1·min-1, and (17.5±2.6) mg· kg-1·min-1 vs (2.6±1.0)mg· kg-1·min-1］, all P<0.01 during clamp in control and P/L groups. The suppressive effect of insulin on HGP was significantly blunted in L group［(17.3±2.1)mg· kg-1·min-1 vs (15.8±1.5)mg· kg-1·min-1］. The rate of glucose disappearance (GRd) was significantly reduced in two lipid-infused rats compared with controls［(26.6±1.6)mg· kg-1·min-1 and (23.2±0.9)mg· kg-1·min-1 vs (37.7±2.6)mg·kg-1·min-1,P<0.01］. The PPAR-γ expression of adipose tissue in P/L group was significantly upregulated. CONCLUSION: Lipid-infusion induces an acute insulin-resistance in vivo. Pio treatment upregulates the PPAR-γ of adipose tissue and suppresses HGP. Pio can protect partly against lipid-induced insulin resistance.  相似文献   

15.
AIM: In order to investigate the mechanisms involved in the vascular hyporeactivity after hemorrhagic shock, the changes of Ca2+ release from calcium store in vascular smooth muscle cells (VSMCs) with hypoxia were observed and the role of Ca2+ release from calcium store in the occurrence of vascular hyporeactivity to norepinephrine (NE) after hemorrhagic shock in rats was further explored.METHODS: A hemorrhagic shock model (40 mmHg for 2 h) in rats and a VSMCs hypoxic model were established. The changes of intracellular Ca2+ concentration in VSMCs were evaluated by fura3-AM and the role of IP3R and RyR mediated Ca2+ release from calcium store was further observed. The role of IP3R and RyR mediated Ca2+ release from Ca2+ store in the development of vascular hyporeactivity was measured with an isolated organ perfusion system. RESULTS: In the absence of extracellular Ca2+, NE upregulated by mobilizing Ca2+ release through calcium store. Compared to the normal control, the VSMCs had a slight increase when treated with hypoxia and NE-induced intracellular down-regulated, both without significant difference. Compared to the normal control cells, there was a significant change of Ca2+ release from calcium store in hypoxia-treated VSMCs, characterized by the significant increase in triggered by RyR-sensitive Ca2+ releasing activator caffeine. However, the increase in triggered by IP3R-mediated Ca2+ release agonist adenophostin A (10-5 mol/L) and ATP-Na2 (10-4 mol/L) had no significant difference in hypoxic VSMCs. Furthermore, the vascular reactivity to NE decreased in abdominal aorta in hemorrhagic shock (40 mmHg, 2 h) rats. The activation of IP3R mediated Ca2+ release with ATP-Na2 (10-4 mol/L) did not improve the vascular reactivity to NE, while inhibition of IP3R mediated Ca2+ release with heparin (104 U/L) significantly antagonized the vascular reactivity to NE in hemorrhagic shock rats. In addition, in normal K-H solution (with about 2.2 mmol/L) and Ca2+-free K-H solution, RyR antagonist ryanodine (10-5 mol/L) partly restored the vascular reactivity to NE in hemorrhagic shock rats, while RyR agonist caffeine(10-3 mol/L) further decreased the vascular reactivity. CONCLUSION: The over-activation of RyR-mediated Ca2+ release from calcium store is partly involved in the development of vascular hyporeactivity after hemorrhagic shock in rats.  相似文献   

16.
AIM:To observe the influence of captopril on intracellular free calcium concentration (［Ca2+］ i) and the involved ion channels mechanisms in cardiac myocytes of the neonatal rat undergone anoxia-reoxygenation injury.METHODS:The anoxia-reoxygenation model in cultured neonatal rat ventricular myocytes was established.Groups were divided into ① normal;② anoxia-reoxygenation;③anoxia-preconditioning (5 min anoxia+5 min reoxygenation);④ captopril preconditioning.Flou-3 /AM loading and flow cytometry technique were used to observe the ［Ca2+］i,and whole-cell patch clamp technique was used to record the L-type calcium current and Na+/Ca2+ exchange current.RESULTS:① Compared to normal group,［Ca2+］i in anoxia -reoxygenation group was increased significantly (789.42±9.05 vs 414.08±37.40,P<0.01),L-type calcium current density was decreased (P<0.01),the current-voltage curve was moved up,the inactivation curve was moved left and Na+/Ca2+ exchange current was increased in anoxia-deoxygenating.② Compared to anoxia-reoxygenation group,anoxia and captopril preconditioning resulted in a significant decrease in ［Ca2+］i (593.84±5.06,507.08±31.89 vs 789.42±9.05,P<0.01),and a significant increase in L-type calcium current density (P<0.01),the current-voltage curve was moved down,the inactivation curve was moved right and Na+/Ca2+ exchange current was decreased ③ Compared to normal oxygen condition,the anoxia and captopril precondition resulted in a lightly increase in ［Ca2+］i (507.08±31.89 vs 414.08±37.40,P<0.05) and Na+/Ca2+ exchange current.④ Compared to anoxia-preconditioning group,captopril-preconditioning resulted in no significant difference in all the markers mentioned above.CONCLUSIONS:The anoxia-reoxygenation injury in cardiac myocytes results in ［Ca2+］i abnormal increase and calcium overload by increasing Na+/Ca2+ exchange current.Late preconditioning in cardiac myocytes is triggered by transient and repeated anoxia and captopril,which slightly increases Na+/Ca2+ exchange current and ［Ca2+］i and restraines the abnormal increasing of Na+/Ca2+ exchange current and calcium overload induced by subsequenced anoxia-reoxygenation injury,so it plays an delayed protective role in cardiac myocytes.L-typed calcium passage is not involved in calcium overloaded and late preconditioning of calcium in myocytes during reperfusion.  相似文献   

17.
AIM: To evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury.METHODS: The subjects were divided into 2 groups: 110 ACS patients (group ACS) and 18 healthy persons (group control).One hundred and ten patients with ACS were divided into 3 sub-group: 51 patients with ST-segment elevated myocardial infarction (STEMI),28 patients with non-ST-segment elevated myocardial infarction (NSTEMI) and 31 patients with unstable angina (UA).Complement 3 (C3),complement 4 (C4),troponin T (TnT) as well as creatine kinase MB (CK-MB) were evaluated.RESULTS: Plasma C3 and C4 peak levels were significantly higher in patients with STEMI ［(1 525±302)mg/L and (423±123) mg/L］ and NSTEMI ［(1 516±289)mg/L and (396±68) mg/L］ than those in patients with UA ［(1 275±172)mg/L and (356±91) mg/L］ and the control subjects ［(1 072±196)mg/L and (182±73) mg/L］ (P<0.01 for all).Also,C3 and C4 serum levels in patients with UA were significantly higher than those in control subjects (P<0.01 for all).At one-week follow-up,plasma levels of C3 and C4 were significantly different among various days in patients with ACS (P<0.01).Plasma C3 and C4 levels in ACS showed a relationship with peak creatine kinase MB (CK-MB) and troponin T (TnT) levels (P<0.01).CONCLUSION: Plasma C3 and C4 levels are elevated in ACS in present study.The relationship between C3,C4 levels and ACS suggests that the complement activation is related to necrosis within the myocardium.  相似文献   

18.
AIM: To study the electrical heterogeneity of transient outward potassium current (Ito) in left and right ventricular myocytes of cardiomyopathy rat. METHODS: The rats were peritoneally injected with L-thyroxine 0.5 mg/kg for 10 d to establish the model of ventricular hypertrophy. The right and left ventricular parts of the heart were separated and the ventricular myocytes were prepared by step digestion using enzyme solution. Ito was recorded by using whole cell patch clamp technique. The change of the electrical heterogeneity was determined. RESULTS: The electrical heterogeneity of Ito existed in the normal myocytes of left and right ventricles. In the myocytes of left and right ventricles isolated from the cardiomyopathy rats, the electrical heterogeneity was enhanced obviously and showed statistical difference. At +40 mV depolarizing test potential, the current density of Ito in the myocytes of right ventricle was increased from (9.23±0.84) pA/pF to (11.19±1.73) pA/pF, while the current density of Ito in the myocytes of left ventricle was decreased from (6.99±1.14) pA/pF to (4.95 ±1.84) pA/pF and the dispersion was increased. The V1/2 of right ventricle steady inactivation was increased significantly ［from (-68.85±1.37) mV to (-49.86±0.69) mV］. The time constant τ of de-inactivation changed significantly ［τleft=(79.16±7.04) ms,τright=(53.19±3.72) ms］. CONCLUSION: Enhanced electrical heterogeneity of Ito in the left and right ventricular myocytes of cardiomyopathy rat may represent one of the important ionic mechanisms for some arrhythmia caused by myocardial hypertrophy.  相似文献   

19.
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-PGF1α,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<0.05］.Piroxicam (3 mg/kg) increased systolic function (LVDP 73%±10% vs 61%±11%,P<0.05),but exacerbated diastolic function ［LVEDP （29.00±5.61）mmHg vs （23.16±3.57） mmHg,P<0.01］ in H2O2 treated rat hearts.Nimesulide also protected rat hearts against superoxide anion and hydroxyl free radical injury.Nimesulide and piroxicam had no effect on the content of 6-Keto-PGF1α in rat hearts.Mitochondrial ATP sensitive potassium channel (mitoKATP) inhibitor 5-HD blocked the improvement of contractility (LVDP and ±dp/dtmax) induced by nimesulide in H2O2 treated rat hearts (53%±12% vs 69%±3%,58%±11% vs 72%±7% and 37%±8% vs 51%±4% respectively,P<0.01).CONCLUSION: The results suggests that COX-2 inhibitor nimesulide can protect rat hearts against oxidative injury.The protection is independent of COX activity.Activation of mitoKATP may be involved in nimsulide-induced cardioprotection in rat hearts.  相似文献   

20.
AIM: To investigate the effects of different concentrations of curcuma aromatica oil on learning and memory in rats exposed to chronic hypoxia. METHODS: The rats were divided randomly into the control, chronic hypoxia and chronic hypoxia with low (LC), middle (MC) and high (HC) concentrations of curcuma aromatica oil groups. After 29 d, all animals were examined to obtain the scores of leaning and memory. The SOD activity and MDA content were determined in the serum and hippocampus, the ［Ca2+］i in hippocampus was also detected. The staining and expression of p-calcium/calmodulin-dependent protein kinase II (p-CaMKII) in the hippocampus was observed and measured. RESULTS: ① In the chronic hypoxia group, the latency to find the hidden platform remarkably prolonged and the MDA content was obviously higher, but the SOD activity was significantly lower. Meanwhile, hippocampal ［Ca2+］i was markedly increased. The immunostaining of p-CaMKII was much weaker in hippocampus as well as its expressions (P<0.01). ② The latency to find the hidden platform was remarkably shorter in groups with MC and HC (P<0.05). The MDA content was obviously lower among groups treated with curcuma aromatica, but SOD activity was significantly higher in groups with MC and HC. Meanwhile, hippocampal ［Ca2+］i was markedly decreased in all groups treated with curcuma aromatica oil (P<0.01). The hippocampal immunostaining of p-CaMKII was much stronger in the MC and HC as well as its expression (P<0.05，P<0.01). Under the electron microscope, synaptic boundaries were not distinct, the edema of dendrite spine and axon was seen, synaptic vesicles and postsynaptic densities (PSD) were disappeared in the chronic hypoxia group. With rising of the concentration of curcuma aromatica oil, the edema of synapse and mitochondria was mitigated and the PSD was increased gradually. CONCLUSION: Curcuma aromatica oil might enhance learning and memory capacities of rats exposed to chronic hypoxia by cleaning up and antagonizing the production of the free radical and increasing the p-CaMKII expression in PSD. The effects are dose-dependent.  相似文献   

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