0 05) 3 hours after myocardial infarction,and remarkably decreased (P

Objective To inquire into the effects of cardiac ? 1 -adrenergic receptor on myocardial remodeling and modulating calcium channel. Methods The models of myocardial remodeling after myocardial infarction in Wistar rats were used to study the expression changes of cardiac collagen subtype Ⅰ,Ⅲ,fibronectin (FN) with immunohistochemistry,and changes of T-type calcium channel,L-type calcium channel and ? 1 -adrenergic receptor mRNA expressions by reverse transcription and polymerase chain reaction(RT-PCR) and in situ hybridization. Cardiac total Ca 2+ was tested by atomic absorption/flame emission spectrophotometer. Results Cardiac collagenⅠ,collagen Ⅲ,FN protein expressions in betaloc group were remarkably decreased (P

Objective To inquire into the correlation of cardiac AT 1 receptor,? 1 receptor with PKC/MAPKs(protein kinase C/mitogen-activated protein kinase) signal transduction pathway during myocardial remodeling.Methods Twenty-four Wistar rats were randomly divided into four groups-sham group,infarcted group,losartan group and betaloc group.Except sham group,left anterior descending coronary artery was ligated for 21 days.In the other three groups,expression changes of cardiac collagen subtype Ⅰ,Ⅲ,fibronectin(FN),c-fos,ERK 1 (extracellular signal-regulated kinase,ERK)and PKC proteins were studied with immunohistochemistry and computer image analysis. c-fos mRNA expression was tested by reverse transcription and polymerase chain reaction(RT-PCR).Results Expressions of collagen Ⅰ,collagen Ⅲ , FN,c-fos,ERK 1 and PKC proteins were significantly enhanced(P

Adriamycin is an effective and broad-spectrum anthracycline antineoplastic agent.However,long-term therapy with adriamycin is associated with a high incidence of cumulative and irreversible cardiomyopathy. Mechanisms about adriamycin-induced cardiotoxieity are complicated, including oxidative stress,mitochondrionopathy,cardiac apoptosis,and so on.For the past few years,a series of measures aye used,which attenuate the cardiotoxicity and uninfluence the antitumor effects.The review focuses on the mechanism and prevention of adriamycin-induced cardiotoxicity in order to improve the long term survival rate of neoplastic patient.

Objective To inquire into T-type calcium channel effects on RyR and IP 3R of sarcoplasmic reticulum in atrial myocytes during atrial fibrillation.Methods Ten dogs underwent continuous rapid atrial pacing (500 beats/min) to create persistent atrial fibrillation.In five rapidly-paced dogs,mibefradil dihydrochloride was given beginning 2 days after pacemaker implantation,continuing until the twenty-fourth week.A group of size-matched dogs (n=5) without given mibefradil was used as a pure atrial fibrillation group.Another group of size-matched dogs (n=5) without pacemaker implantation was used as a control group.Canine atrial myocytes isolated by enzymatic dissociation were used to study T-type Ca 2+ channel blocker effects on expression and function changes of RyR and IP 3R in atrial myocytes by confocal microscopy.Results RyR/IP 3R ratio (0.2965?0.01812) was markedly lower than that of control group (2.7043?0.2293),but there was no difference compared with that of atrial fibrillation group (0.2472?0.1355).Ca 2+transient of atrial myocytes was nremarkably changed (1.3031?0.1056)(P

Objective To inquire into T-type calcium channel effects on atrial electrical remodelling and its mechanisms during atrial fibrillation.Methods Animal experiment was performed in Peking University Pepole's Hospital from Feb.2002 to Oct.2006.Fifteen adult cross-bred dogs were used in the experiment.Ten dogs underwent continuous rapid atrial pacing(500 beats/min)for twenty-four weeks to create persistent atrial fibrillation.In five rapidly-paced dogs,50mg pure powder/day of mibefradil dihydrochloride was given from the second day after pacemaker implantation and continued until the twenty-fourth week.A group of size-matched dogs(n=5)without being given mibefradil was used as a pure atrial fibrillation group.Another group of size-matched dogs(n=5)without pacemaker implantation was used as a control group.Atrial fibrillation duration was determined by electrophysiological study.Canine atrial myocytes were isolated by enzymatic dissociation and intracellular Ca2+ cytosolic transient was studied with confocal imaging.Results (1)The preoperation atrial effective refractory period was 280/90~110 ms.In the twenty-fourth week after rapid atrial pacing,atrial effective refractory period was obviously extended(2000/1400~1700 ms)in the T-type Ca2+ channel blocker group compared with the preoperation one.In the twenty-fourth week,the induced rate of persistent atrial fibrillation was 75% in atrial fibrillation group,whereas the persistent atrial fibrillation occurred in only one case(20%)in the T-type Ca2+ channel blocker group.(2)Intracellular Ca2+ concentration of atrial myocytes was unremarkably changed in control group after blocking L-type Ca2+ channel(1.17?0.09 OD ratio),whereas the intracellular Ca2+ concentration was obviously enhanced(2.35?1.05 OD ratio)(P

40 weeks old SHR did not differ from that in slices of age matched WKY. B max was increased in the same brain region of SHR when compared to WKY. That rats of 4 5 weeks were in prehypertensive stage;rats of 10 12 weeks and above were at the stage of establishing hypertensive stage. Conclusion: The difference between SHR and normotensive rats in 5 HT 1A receptor binding in various brain regions may be related to the development of hypertension. When blood pressure changes,binding capacity of 5 HT 1A receptor in CNS changes accordingly.

A GC method is described for measuring fentanyl in man plasma. Fentanyl was extracted at basic pH with cyclohexane-isobutyl alcohol (197:3) with Ro21-2212 added as internal standard and fentanyl derivative as earner. The drug was back-extracted in H2SO4, then the extract was made basic and recxtracted with ethyl ether-dichloromethane (9:1). The organic phase was evaporated at 40℃ under N2 and the residue was dissolved in ethanol. A. portion (2?l) was analyzed on a wide-bore capillary column (10 m ? 0.53 mm) of HP-1 (2.65 ?m), operated at 255℃ with N2 as carrier gas (8 ml/min) and N -P detector. The calibration graph was linear within the ranges of 0.25-100 ng/ml with a corelation coefficient of 0.9996 and the detected limit was 0.2 ng/ml. Mean recovery was 99.02% ? 6.81%. The coefficient of variation for the within- and between-run were all less than 8%. No interference was found from endogenous compounds, metabolites of parent drug or other commonly used drugs. The method was applied to therapeutic drug monitoring and pharmacokinetic studies.

AIM: To study the effect of proliferating cell nucler antigen antisense oligonucleotide on ex vivo expansion of cord blood CD34~+ hematopoietic stem/progenitor cells.METHODS: CD34~+ cells were purified from fresh cord blood by immunomagnetic beads.CD34~+ cells were incubated in liquid culture system with different concentrations of(PCNA-ASODN).Using flow cytometry,the number of different kinds of stem/progenitor cells and PCNA expression were measured after CD34~+ cell incubation.RESULTS: PCNA was lowly expressed in low experiential group,with a positive rate of(27.2?3.6)% and(19.0?1.5)%,the positive rate of control group was(53.8?8.3)%(P

Objective To investigate the expression and significance of interleukin-1β and C-reactive pro-tein(CRP)in atrial fibrillation(AF).Methods Sixteen mongrel dogs were randomly divided into two groups:pa-cing group(n=8)and control group(n=8).High frequency pacing was performed in the pacing group with perma-nent pacernaker but not in the control group.After pacing for 24 weeks,tissue samples were obtained from the left and right atria.The levels of IL-1βand CRP in atria were detected by immunohistochemistry.Results Compared to the control group,the expression level of IL-1β and CRP were significantly enhanced(P<0.05)in atrial tissues during AF.Conclusion IL-1β and CRP may participate in atrial fibrillation formation and play a role in generation and maintaining the artrial fibrillation.