Abstract:Aim Cardiotrophin-1(CT-1) is a member of interleukin-6(IL-6) family of cytokines.CT-1 plays a role in inducing cardiomyocyte hypertrophy and promoting cardiomyocyte viability.We sought to elucidate effect of CT-1 inducing atrial natriuretic peptide (ANP) mRNA expression and its underlying mechanism in cultured neonatal rat cardiomyocyte. Methods The cardiomyocytes of neonatal rat were isolated and cultured with method of pre-plating for different time.The ANP gene of cardiomyocytes was measured with reverse transcription polymerase chain reaction(RT-PCR) approach. Results The ANP/GAPDH ratio of cardiac myocytes were increased by CT-1 in a dose-dependent manner(10-9,10-8 and 10-7 mol/L) in cultured neonatal rat cardiomyocytes.The ratio were respectively 1.18±0.14,1.58±0.20 and 2.03±0.30.And the ANP/GAPDH ratio were also augmented by CT-1 in a time-dependent manner(1,3,5 d,10-8 mol/L),respectively 1.16±0.18,1.47±0.17 and 1.97±0.24.Pretreatment of PD098059(50 μmol/L),a extracellular signal regulated kinase 1/2(ERK1/2) blocker,increased significantly ANP mRNA expression of cardiac myocytes induced by CT-1(ANP/GAPDH ratio 1.94±0.15),whereas Calphostin C,a protein kinase C(PKC) blocker,10 μmol/L,effected no significantly on this role induced by CT-1. Conclusion These results indicate that ANP mRNA expression induced by CT-1 increased significantly in a dose-dependent and a time-dependent manner in cultured neonatal rat cardiomyocytes.The MAPK(ERK1/2) signal pathway mediate the effect of CT-1.The PKC signaling molecule may no take part in directly the effect of CT-1.

Abstract:Aim To investigate the effects of serum from rats of different ageson endothelial progenitor cells(EPC) ability to differentiate into mature endothelial cells(EC). Methods Mononuclear cells were obtained from young(1 to 2 month-old) and old(19 to 26 month-old) Sprague-Dawley rats bone marrow by Ficoll density gradient centrifugation and cultured with medium DMEM/F12 in culture dishes,48 h later,the suspending cells were translocated to be cultured in other new flasks coated with fibronectin,the secondary attached cells were characterized as adherent cells which were double positive for DiI-acLDL uptake and lectin binding by direct fluorescent staining demonstrated under a laser scanning confocal microscope;serums from young and aged rats were collected and used to culture EPC.The experiments were divided into four groups: aged rat EPC+aged rat serum,aged rat EPC+young rat serum,young rat EPC+aged rat serum and young rat EPC+young rat serum.After incubation with DMEM/F12 containing 20% serum from young or aged rats(no feta1 blood serum was added),in vitro cultured EPC double positive for DiI-ac-LDL uptake and lectin binding were tested by laser scanning confocal microscopy,also were documented by demonstrating the expression of von Willebrand factor(vWF) with immunofluorescence,vascular endothelial growth factor receptor-2(KDR) and endothelial nitric oxide synthase(eNOS) mRNA expression with reverse transcription-polymerase chain reaction(RT-PCR) methods;in vitro vasculogenesis kit was used to test the participation of EPC to tube formation. Results Young rat serum significantly increases percentage of double-positive cells for DiI-ac-LDL and lectin binding in aged rat EPC cultured in EC conditioned-medium whereas aged rat serum obviously decreases such percentage in young rat EPC;young rat serum also markedly promotes EC conditioned-medium to induce vWF and eNOS(p<0.01) and KDR(p<0.05) expression in aged rats EPC;young rat serum obviously increases the ability of aged rats EPC to form tube structure in vitro after incubation with EC conditioned-medium(p<0.05). Conclusions Young serum significantly promotes EC conditioned medium-induced aged rats EPC differentiation into mature EC whereas EC differentiation of EPC from young rats can be partly inhibited by serum from aged rats;there maybe exist age-related changes of systemic factors in young and aged rat serum which modulate rat EPC differentiation.

Abstract:Aim To obtain the nucleotide and amino acid sequences of ATP-binding cassette transporter A1(ABCA1) from tree shrew;identify the tissue distribution of ABCA1 in tree shrew. Methods The first strand of cDNA was transcripted from mRNA isolated from tree shrew liver.Benefiting from SMART-RACE technique,cDNA clones of tree shrew ABCA1 were obtained and the amino acid sequence was deduced from the sequencing cDNA.The tissue distribution of ABCA1 in tree shrew was identified by Real-Time PCR. Results The nucleotide sequence of tree shrew ABCA1 covered 7762 bp,including a 6786 bp coding region which encoded a 2261 amino acids protein.This protein shared the same length as the high identity(95%) with human ABCA1.ABCA1 was expressed in many tissues in tree shrew,the highest in lung,followed by liver,kidney and spleen in turn.This pattern was much different from that in human and mouse,which were high in liver whereas less in lung and spleen. Conclusion The feature of tree shrew ABCA1 distributed in tissues may have effects on its concentration and mass,lead to indirectly increase the produce of high density lipoprotein.

Abstract:Aim To explore the effect of valsartan on arterial compliance and indexes associated with apoptosis in aging rat and its possible action mechanism. Methods The healthy Wistar rat were divided into young group,aging group and valsartan group to detect malondialdehyde(MDA)and superoxide dismutase(SOD)level aorta plasma,and measure the compliance of rat carotid segment by constant liquid injection.Immunohistochemistry,RT-PCR and Western-Blot were used to analyze the expression of apoptosis-association genes B-cell lymphoma/leukemia-2(Bcl-2)、Cysteinylasparate specific proteinase-3(Caspase-3). Results Compared with the aging group,malondialdehyde concentration in valsartan group evidently declined(p<0.05),but superoxide dismutase markedly ascended(p<0.05).The carotid flexibility increased,especially flexibility area were significantly different(p<0.05).The percentage of Bcl-2 positive cell increased(p<0.05),but the percentage of Caspase-3 positive cell decreased(p<0.05).Bcl-2 mRNA and protein expression increased markedly(p<0.05),but Caspase-3 protein expression decreased evidently(p<0.01). Conclusions Vascular aging has its special physiologic function changes.One of its molecular mechanism might be associated with decreasing the expression level of Bcl-2 and increasing Caspase-3 protein.Valsartan may protect vascular from aging through up-regulating Bcl-2 gene expression and inhibiting Caspase-3 activation.

Abstract:Aim To observe the effect of calcitonin gene-related peptide(CGRP) on the proliferation or apoptosis of hyperplasia / hypertrophic vascular smooth muscle cells(HVSMC) induced by angiotensin Ⅱ(Ang Ⅱ),and explore whether the mechanism is related to the expression of caveolin-1 and caspase-3. Methods The HVSMC was established by quiet rat vascular smooth muscle cells incubated with Ang II for 24 hours.MTT and flow cytometry were used to determine the ability of proliferation of HVSMC induced by Ang II in the presence or absence of CGRP.Western blotting was used to determine the expression of caveolin-1 and caspase-3. Results Treatment with CGRP for 8 h could inhibit the viability,continuous proliferation of HVSMC induced by Ang II,but it could not significantly induce the HVSMC apoptosis.This effect of CGRP was concomitant with the increased expression of caveolin-1 and with no significant change on the expression of caspase-3. Conclusion CGRP could significantly inhibit the proliferation of HVSMC induced by AngⅡ,but not significantly induce apoptosis of HVSMC,the signal pathway of inhibitory effect of CGRP may be related to the increase of the caveolin1 expression.

Abstract:Aim To explore whether paraoxon,an active component of organophosphate,can directly injure vascular endothelial cells in vitro and to explore the potential mechanisms. Method The thorac aortic rings of healthy sprague-dawley rats and cultured human umbilical vein endothelial cells(hUVEC) were exposed to medium contained different concentrations(36.3 nmol/L～36.3 μmol/L) of paraoxon and co-incubation different time.Both endothelial-dependent and non-dependent relaxation of aortic rings in rats and endothelial monolayer permeability in acetylcholine(Ach)-induced endothelium dependent relaxation(EDR) and increased hUVEC was assayed. Results Paraoxon concentration and time-dependently inhibited permeability of the endothelial monolayer in hUVEC.Paraoxon also simultaneously resulted in a reduction of both superoxide dismutase(SOD) activity and nitric oxide(NO) content and an increase of malondialdehyde(MDA) content in both aortic tissues and cultured cellular medium.But sodium nitroprusside-induced endothelium-independent relaxation of aortic rings were not affected by paraoxon.The injurious effects of paraoxon to EDR was partly lessened by added L-arginine,but not done by pretreatment of atropine. Conclusion Paraoxon could directly injure vascular endothelium cells and EDR.The mechanisms of endothelial dysfunction induced by paraoxon may relate to trigger oxidative stress and formation of lipid peroxidation by oxidation-stress,and the increase of endothelial cell monolayer permeability.

Abstract:Aim To observe the functional changes in vascular endothelium of obstructive sleep apnea syndrome(OSA) animal models and investigate the association between OSA and coronary atherosclerosis. Methods 16 China swine were divided into obstructive sleep apnea(OSA) group and control group.OSA group was treated by injecting polyacrylamide hydrogel.Animals were sacrificed after 12 weeks.The descending anterior branch of coronary were prepared for examination by transmission electron microscopy.The changes in plasma concentrations of endothelin-1(ET-1) and nitric oxide(NO) were tested before making animal models and after 12 weeks. Results(1) There was a significant lower NO level(57.46±4.55 μmol/L vs.29.64±2.48 μmol/L),higher ET-1 level(46.84±5.39 ng/L vs.71.24±6.13 ng/L) and lower ratio of NO/ET-1(1.25±0.17 vs.0.42±0.02) than those before experiment in OSA group.No difference was found in control group(NO level 60.94±3.28 μmol/L vs.57.72±2.82 μmol/L,ET-1 level 49.24±5.13 ng/L vs.50.19±5.71 ng/L,NO/ET-1 1.25±0.13 vs.1.26±0.06).A marked difference(p<0.05) was showed when these values were compared in two groups.(2)Under electron microsocopy,endothelial cell in animals of OSA group became anomaly.Parts of them were degenerated and exfoliated.Basal lamina of endothelium was not in its integrity. Conclusions Experimental obstructive sleep apnea can injure endothelial cell of blood vessel and make them dysfunction,further initiate and accelerate the process of atherogenesis.

Abstract:Aim To study the feasibility of noninvasive detection of atherosclerotic unstable lesions with technetium-99m radiolabeled(99mTc-annexinV)by the single photon emission computed tomography(SPECT). Methods Atherosclerotic plaques animal models were produced in 5 rabbits by 15 weeks of cholesterol diet.Other 3 rabbits were fed on normal diet without manipulation as contrast.All animals were injected 99m Tc-annexin V 200 Ci/g,30 Ci/g and 16 Ci/g respectively.Atherosclerotic plaques images were performed by SPECT at 5,30,60,120 minutepoints after injection. Results In the control rabbits,little radiodistribution was found in aortic artery at 5th minute and clear away at 120th minute.The atherosclerotic plaque models can be seen explicit radiodistribution with varied inject doses at 5th minute.Furthermore, image agent was uptaken higher with more radioactivity dosage at 120th minute. Conclusion 99mTc-annexin V SPECT could be an attractive imaging method for the noninvasive detection of atherosclerotic plaques in vivo.

Abstract:Aim To investigate the antiproliferative mechanisms of probucol in rat vascular smooth muscle cells(VSMC) stimulated by H₂O₂. Methods Effects of probucol on cell cycle,DNA synthesis,cell proliferation and apoptosis in the presence of H₂O₂ were observed by means of MTT test,cell number count,3 H-TdR incorporation,FCM and RT-PCR. Results Probucol significantly inhibited proliferation and DNA synthesis of VSMC stimulated by H₂O₂.Cell number,A value and 3 H-TdR incorporation in probucol+H₂O₂ group were reduced by 46.9%,45.0%,and 39.5%,respectively,compared with H₂O₂ group(p<0.05).Probucol protected against H₂O₂-induced VSMC proliferation through inducing cell growth arrest at G0/G1 phase.H₂O₂ increased extracellular signal-regulated kinase-1(ERK-1) mRNA transcriptional levels by about 6 times and decreased mitogen-activated protein kinases phosphatase-1(MKP-1) mRNA by 82.2%,respectively,compared with controls.Probucol down-regulated the increase in H₂O₂-stimulated ERK-1 mRNA level and up-regulated MKP-1 mRNA level decreased by H₂O₂.Probucol induced apoptosis of VSMC under H₂O₂-stimulated condition. Conclusion Probucol suppresses H₂O₂-stimulated VSMC proliferation by inhibition of cell cycle progression via down-regulating ERK-1 mRNA transcriptional level,as well as inducton of apoptosis of VSMC.

Abstract:Aim To determine the effects of irbesartan on gap junction remodeling and expression of connexin 43(Cx43) in left cardiac ventricle of congestive heart failure(CHF) rats. Methods A heart failure model of experimental pressure overload induced by surgical abdominal aortic stenosis in adult SD rats was used.The rats with heart failure were confirmed by measuring the hemodynamic parameters and divided randomly into the group treated with irbesartan(50 mg/kg) and placebo.Sham-operated(PS) group rats served as negative controls after 16 weeks.Sixteen weeks later,gap junction remodeling in left cardiac ventricle of rats in sham-operated group,the irbesartan group,and placebo group was characterized by immunoblotting and electron microscopy. Results Compared with Sham-operated group,the expression of Cx43 in left ventricles from failing hearts in the placebo group was decreased 25.7%(0.929±0.095 vs 1.250±0.083,p<0.05),the expression of Cx43 in left ventricles from irbesartan group increased to the same level of Sham-operated group.Electron microscopy of LV tissue revealed that in contrast to left ventricles myocytes from Sham-operated group,which showed Cx43 labeling largely confined to the intercalated disks,left ventricles myocytes from rats in placebo group showed dispersion of punctate Cx43 labeling over the entire cell surface.The proportion of Cx43 label at the intercalated disk decreased significantly.In rats from irbesartan group,the gap junction disorganization was markedly reduced. Conclusion In left ventricles from failing hearts,the expression of Cx43 decreased,while the expression of Cx43 in left ventricles from rats treated with irbesartan increased significantly.Meanwhile,Irbesartan can improve space-remodling of gap junction in failing hearts.

Abstract:Aim To discuss the regulation of expression of GATA-6 by nitric oxide/cGMP-dependent protein kinase I in vascular smooth muscle cells(VSMC) phenotypic modulation. Methods Cultured wistar rat aortic VSMC were used as an experimental model.Cell growth was determined by MTT assay.The mRNA and protein expression of GATA-6 and smooth muscle myosin heavy chain(sm-MHC) were assayed by RTPCR and Western blot analysis. Results The results showed that phenylephrineinduced proliferation of VSMC was inhibited by S-nitroso-N-Acetylpenicillamine (SNAP) and Sp-8-pCPT-cGMPs,but promoted by Rp-8-pCPT-cGMPs.The expression of GATA-6 and sm-MHC mRNA and protein were increased by SNAP and Sp-8-pCPT-cGMPs,and decreased by Rp-8-pCPT-cGMPs. Conclusions NO/PKG I can up-regulate the expression of GATA-6 and sm-MHC at the transcriptional and translational level.These findings demonstrate that NO/PKG I pathway is involved in the maintenance of the differentiated phenotype in VSMC.

Abstract:Aim To observe the effects of Ligan compounds in Fructus Forsythiae on ischemia/reperfusion(IR) rats models and the expression of endothelin3(ET-3) and glial fibrillary acidic protein(GFAP) in the models' hippocampus CA1 area,and to study the neurons'protection of Ligan compounds in Fructus Forsythiae and its value of treatment on ischemia/reperfusion imparement. Methods Forty-eight adult male mice were randomly divided into three groups: ①Ischemia/reperfusion group(n=24),the mice were subdivided into 1 day,3 days,5 days and 10 days(1 d,3 d,5 d and 10 d) subgroups according to reperfusion time after 7 minutes bilateral common cariod artery(BCCA) occlusion;② Ligan compounds in Fructus Forsythiae treatment group,the mice were given Ligan compounds in Fructus Forsythiae pre-operation and postoperation(n=18);③Sham-operated group(n=6) which was control group,only was exposed their BCCA,but not given 7 minutes BCCA occlusion.The expression of ET-3 immunoactivity were detected in the rats' hippocampus CA1 area by immuno-histochemisty. Results The number of ET-3 and GFAP immune positive cells in ischemia/reperfusion models'hippocampus CA1 area was increased compared with sham-group(p<0.01),the peak-time was the fifth day.While the number of ET-3 and GFAP immune positive cells in Ligan compounds in Fructus Forsythiae treatment group models'hippocampus CA1 area was decreased obviously compared with ischemia/reperfusion group. Conclusion The expressions of ET-3 and GFAP were up-regulated after IR,ET-3 is perhaps a destroying factor during reperfusion,astrocytic activation participated in the pathological process,while Ligan compounds can inhibit the process by getting rid of free radicals and exert the brain protection.

Abstract:Aim To investigate the association of apolipoproteinA5(ApoA5) gene polymorphisms of patients with coronary heart disease(CHD)and the degree of coronary artery stenosis. Methods Using polymerase chain reaction-restriction fragmentpolymorphisms of patients with CHD and the degree of length polymorphism methods,the genotypes of 260 patients with CHD confirmed by coronary angiography were analyzed,the levels of coronary artery stenosis were characterized by the numbers of diseased vessels and Gensini scores. Results Serum triglyceride level of the patients with ApoA5-1131CC genotype and c.553T allele carriers were obviously higher than that of the patients with ApoA5 c.553GG genotype and-1131T allele carriers,but the Gensini scores were not significantly different among them,and the distribution for the genotyopes of ApoA5 genetic variants were also not statistically different among variable number of coronary diseased vessels.The number of coronary diseased vessels and Gensini scores had strongly positive correlation with the presence of diabetes(r=0.141 and 0.143,p<0.05),and obviously negative correlation with the level of serum high density lipoprotein cholesterol(r=-0.129 and-0.164,p<0.05). Conclusions ApoA5 gene polymorphisms are remarkably associated with the level of triglyceride,but not the extent of coronary artery stenosis among CHD patients.

Abstract:Aim To investigate the polymorphisms and haplotypes in α-fibrinogen and β-fibrinogen gene and their relationship to coronary heart disease(CHD). Methods Plasma fibrinogen level was measured by turbidmetric assay. The TaqI polymorphism in α-fibrinogen gene and the single nucleotide polymorphisms-455G/A,-249C/T,-148C/T,+1689T/G,BsmAIG/C,448G/A,BclIG/A and HinfIA/C in β-fibrinogen gene were characterized by PCR-RFLP in one hundred and twenty one cases of CHD and one hundred and thirty healthy individuals from Hainan Han population.Haplotypes were estimated by the EH+program.The statistical differences of allelic,genotype and haplotype frequencies between the case group and the control were estimated by Chi square test. Results The allelic frequencies of the polymorphisms-455A,-148T,448A were 0.343,0.351 and 0.326 in CHD group,whereas the allelic frequencies of the polymorphisms-455A,-148T,448A were 0.254,0.254 and 0.242 in the control.The allelic frequencies of-455A,-148T,448A were higher in the CHD group than in the control(p<0.05).The allelic frequencies of the other six polymorphisms were not significantly different between the CHD group and the control(p>0.05).The odds ratios(OR) with the rare alleles of A-455 、T-148 and A448 were 1.53,1.59 and 1.51 respectively.Haplotypes constructed from the nine polymorphisms showed that the frequency haplotype H16 with β-455G,β-249C,β-148C,β+1689T,βBsmAI G,β448G,βBclI G,βHinfI A and αTaqI T2 were lower in the CHD group than in the control.Among the haplotypes constructed from polymorphisms including-455G/A,-249C/T,-148C/T in the promoter region of β-fibrinogen gene,haplotype h1 with-455G,-249C and-148 C alleles appeared more frequently in control group(p<0.01),whereas haplotype h5 with-455A,-249C and-148C and haplotype h6 with-455A,-249C and-148T occurred more frequently in the CHD group(p<0.01). Conclusions The results of multi-allele and haplotype analysis indicated that the polymorphisms-455G/A,-148 C/T and 448G/A in beta fibrinogen gene were associated with CHD in Hainan Han population.The allele with-455A,-148 T and 448 A may represents a genetic risk factor for CHD.

Abstract:Aim To investigate the association between paraoxonase-2 gene 311 Cys/Ser polymorphism and macrovascular disease in combination with paraoxonase-1 gene 192 Gln/Arg polymorphism in type 2 diabetes mellitus patients. Methods A case-control study of 272 Chinese subjects was performed.Genomic DNA was extracted from the subjects' peripheral blood leukocytes.The paraoxonase-1 gene 192 Gln/Arg and paraoxonase-2 gene 311 Cys/Ser polymorphisms were determined by PCR analysis.In addition,the association was investigated between paraoxonase-2 gene 311 Cys/Ser polymorphism and macrovascular disease in combination with paraoxonase-1 gene 192 Gln/Arg polymorphism in control group and type 2 diabetes mellitus complicated with macrovascular disease group. Results Paraoxonase-1 gene 192 Gln/Arg and paraoxonase-2 gene 311 Cys/Ser polymorphisms were detected in population of Qingdao.The genetype distribution(QQ,QR and RR) of paraoxonase-1 gene 192 Gln/Arg polymorphism showed no significant differences between type 2 diabetes mellitus complicated with macrovascular disease group and the other two groups(type 2 diabetes mellitus group & healthy subjects).But the genetype distribution(CC,CS and SS) of paraoxonase-2 gene 311 Cys/Ser polymorphism showed significant differences between type 2 diabetes mellitus complicated with macrovascular disease group and the other two groups,the former had a significantly higher S allele frequency(p<0.05 or p<0.01).The linkage analysis of paraoxonase2 gene 311 Cys/Ser and paraoxonase-1 gene 192 Gln/Arg gene polymorphisms further emphasized that paraoxonase-2 gene 311 S allele was an independent risk factor leading to type 2 diabetes mellitus complicated with macrovascular disease.When both of the paraoxonase-2 gene 311 S allele and the paraoxonase-1 gene 192 R allele existed,the OR of paraoxonase-2 gene 311 S allele for type 2 diabetes mellitus complicated with macrovascular disease was significantly higher(Or=49.494,95%CI: 0.907～2 701.872). Conclusions The paraoxonase-2 gene 311 Cys/Ser polymor-phism is associated with type 2 diabetes mellitus complicated with macrovascular disease in Qingdao's population.S allele may be a risk factor for type 2 diabetes mellitus complicated with macrovascular disease.Meanwhile,detecting the paraoxonase-1 gene 192 R allele may provide a more precise method to predict or diagnose type 2 diabetes mellitus complicated with macrovascular disease.

Abstract:Aim To investigate the relationship between coronary atherosclerosis and aortic pulse pressure(APP) in patients with essential hypertension. Methods A total of 300 untreated hypertensive patients were recruited for a first diagnostic coronary angiogram.The following data were collected: invasive intra-aortic systolic and diastolic blood pressure(BP),APP,extent of coronary artery disease,clinical and laboratory characteristics. Results In the whole population,aortic systolic BP and APP were significantly higher in CAD group than no CAD group(150.3±26.5 mm Hg vs 145.6±23.3 mm Hg,p<0.05) and(77.1±22.7 mm Hg vs.70.4±19.3 mm Hg,p<0.05).The ratio of stroke volume(SV) to APP was markedly lower in CAD group(1.15±0.44 mL/mmHg vs 1.31±0.50 mL/mmHg,p<0.05).In addition,CAD group is characterized by higher values of fasting glucose(122.3±24.0 mg/dL vs 95.6±24.4 mg/dL,p<0.01) and serum creatinine(1.06±0.19 mg/dL vs.0.99±0.14 mg/dL,p<0.01),and lower values of HDL cholesterol(47.7±11.7 mg/dL vs.54.9±15.6 mg/dL,p<0.01). Conclusions Atherosclerosis may further aggravate the aortic stiffness in hypertensive patients,therefore result in higher aortic PP.Atherosclerosis can also impair the renal function of hypertensive patients,and bring lipid metabolic disorder.

Abstract:Aim To investigate the effects of pioglitazone on serum matrix metalloproteinase-9 (MMP-9) and C-reactive protein(CRP) concentration in the elderly patients with acute myocardial infarction(AMI) and type-2 diabetic mellitus. Methods 37 cases of AMI patients accompanied with type-2 diabetic mellitus were divided into two groups according to the administration of pioglitazone previously: pioglitazone group(17 cases) and AMI group(20 cases).23 aged people of health physical examination were enrolled as health control group.The concentrations of serum MMP-9 and CRP were measured in all of the patients. Results The concentration of serum MMP-9 and CRP in AMI group were higher than those in health control group(396.5±67.3 μg/L vs 290.8±75.5 μg/L,8.73±2.59 mg/L vs 3.21±1.11 mg/L).The concentration of serum MMP-9(339.2±79.8 μg/L) and CRP(6.33±2.25 mg/L) in pioglitazone group were lower than those in AMI group. Conclusion Pioglitazone can lower the concentration of serum MMP-9 and CRP level.Pioglitazone has additional cardiovascular effects beside the improvement of insulin resistance.

Abstract:Aim To observe the myocardium damage caused by diabetic ketoacidosis with myocardial enzymogram and electrocardiogram and confirm their clinical significances. Methods 44 hospitalized patients had their vein blood drawn for determinating myocardial enzymogram which included creatine phosphokinase(CPK),creatinine phosphokinase-MB(CPK-MB),aspartate aminotransferases(AST) and cardiac troponin I(cTn-I);Meanwhile,the changes of electrocardiogram were recorded. The changes of myocardial enzymogram and electrocardiogram at acute stage were compared with those at catabatic stage. Results 44 patients with diabetic ketoacidosis had significantly higher levels of myocardial enzymogram at acute stage than those at catabatic stage(p<0.05).CPK-MB and CPK values of 44 patients at acute stage had no correlation(r=0.12,p>0.05).28(63.6%) patients with abnormal electrocardiogram changes at acute stage,and the major abnormities were 18(40.9%) sinus tachycardia,14(31.8%) ST-T change.The levels of myocardial enzymogram with abnormal electrocardiogram changes at acute stage were significantly higher than those with normal electrocardiogram changes(p<0.05). Conclusions The levels of myocardial enzymogram caused by diabetic ketoacidosis might be abnormally higher.There was transient and nonspecial damage to myocardium.The occurence of arrhythmia varied with the damage of diabetic ketoacidosis to myocardium.