Effect of Matrine on Human Ether à go-go Related Gene (HERG) Channels Expressed in Chinese Hamster Ovary Cells

Objective: To observe the effect of matrine on human ether à go-go related gene (HERG) potassium channels expressed in Chinese hamster ovary (CHO) cells and investigate whether HERG channel is a new target of the pharmacological effect of matrine on arrhythmia and tumor. Methods: HERG channel potassium current in CHO cell was recorded using whole-cell patch-clamp technique, and the influence of matrine on the current was explored. Results: Matrine inhibited HERG potassium current in a dose-dependent manner, and the 50% inhibitory concentration (IC50) was 411±23 μmol/L. Matrine had no significant effect on the activation kinetics, and mainly blocked HERG channels in their closed state. Conclusions: The blocking effect of matrine on HERG channels might be one of the mechanisms against arrythmias and tumors. Unlike most other blockers exerting blocking effect at the intracellular sites by entering the cell with the opening of HERG channel, matrine blocked HERG channels at the extracellular sites.     

Trichostatin A Regulates hGCN5 Expression and Cell Cycle on Daudi Cells in vitro

The expression of human general control of amino acid synthesis protein 5 (hGCN5) in human Burkitt's lymphoma Daudi cells in vitro, effects of Trichostatin A (TSA) on cell proliferation and apoptosis and the molecular mechanism of TSA inhibiting proliferation of Daudi cells were investigated. The effects of TSA on the growth of Daudi cells were studied by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium (MTT) assay. The effect of TSA on the cell cycle of Daudi cells was assayed by a propidium iodide method. Immunochemistry and Western blot were used to detect the expression of hGCN5. The proliferation of Daudi cells was decreased in TSA-treated group with a 24 h IC50 value of 415.3979μg/L. TSA induced apoptosis of Daudi cells in a time- and dose-dependent manner. Treatment with TSA (200 and 400μg/L) for 24 h, the apoptosis rates of Daudi cells were (14.74±2.04) % and (17.63±1.25) %, respectively. The cell cycle was arrested in G0/G1 phase (50, 100μg/L) and in G2/M phase (200μg/L) by treatment with TSA for 24 h. The expression of hGCN5 protein in Daudi cells was increased in 24 h TSA-treated group by immu-nochemistry and Western blot (P<0.05). It was suggested that TSA as HDACIs could increase the expression of hGCN5 in Daudi cells, and might play an important role in regulating the proliferation and apoptosis of B-NHL cell line Daudi cells.     

Effects of apigenin on cell proliferation of human pancreatic carcinoma cell line BxPC-3 in vitro

Objective： To observe the effects of apigenin on cell proliferation of human pancreatic carcinoma cell line BxPC-3 in vitro. Methods：The inhibitive effects of apigenin at different concentrations （0 μmol/L, 100 μmol/L, 200 μmoL/L, and 400 μmol/L） on human pancreatic carcinoma cell line BxPC-3 were detected by MTT assays, transmission electron microscope, agarose gel electrophoresis and flow cytometry. The immunohistochemistry was used to detect the expression of Bcl-2 and Bax gene. Results： Apigenin at different concentrations could inhibit the proliferation of human pancreatic carcinoma cell lines BxPC-3, and the inhibitive effect was dose-dependent. The cell cycle of pancreatic carcinoma cells was arrested at G2/M phase. The results of immunohistochemistry showed that the density of apigenin increased, and the expression of Bcl-2 gene was reduced gradually, At the same time the expression of Bax gene was enhanced. Conclusion ：Apigenin could inhibit the proliferation of human pancreatic carcinoma cell lines BxPC-3 in vitro. The effect of apoptosis was accompanied with the expression of Bcl-2 decrease and Bax increase.     

Cardioprotective effects of simvastatin on reversing electrical remodeling induced by myocardial ischemia-reperfusion in normocholesterolemic rabbits

Background Recent studies have revealed that pretreatment with statin is effective in preventing arrhythmia, but its electrophysiological mechanism is unclear. This study was conducted to investigate the cardioprotective effects of simvastatin on reversing electrical remodeling in left ventricular myocytes of rabbit heart undergoing ischemia-reperfusion, so as to explore the ionic mechanism responsible for the anti-arrhythmic effect of statin. Methods Forty-five rabbits were randomly divided into three groups： ischemic-reperfusion group （I-R）, simvastatin intervention group （Statin） and sham-operated control group （CON）. Anesthetized rabbits were subjected to 30-minute ischemia by ligation of the left anterior descending coronary artery and a 60-minute reperfusion after a 3-day administration of oral simvastatin of 5 mg-kg^-1.d^-1 in the Statin group or a placebo in the I-R group. Single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region dedved from the hearts in the I-R and Statin group and the same anatomical region in the CON animals. The whole cell patch-clamp technique was used to record membrane ionic currents, including sodium current （IRa）, L-type calcium current （Ica-L） and transient outward potassium current （Ito）. Simultaneously, the level of serum cholesterol was examined. Results There was no significant difference in the serum cholesterol concentration among the three groups. The peak IRa current density （at -30 mV） was significantly decreased in I-R （（22.46±5.32） pA/pF, n=12） compared with CON （（42.78±5.48） pA/pF, n=16, P〈0.01） and Statin （（40.66±5.89） pA/pF, n=15, P〈0.01）, while the peak IRa current density in the Statin group was not different from CON （P〉0.05）. The peak ICa-L current density （at 0 mV） was significantly increased in I-R （（4.34±0.92） pA/pF, n=15） compared with CON （（3.13±1.22） pA/pF, n=13, P〈0.05） and Statin （（3.46±0.85） pNpF, n=16, P〈0     

ROLE OF ERK1／2 KINASE IN CISPLATIN-INDUCED APOPTOSIS IN HUMAN OVARIAN CARCINOMA CELLS

Objective To investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells.Methods Cisplatin-induced apoptosis were stained with DAPI and was assessed microscopically in human epithelial adenocarcinoma ovarian cell line SKOV3 cells. ERK activation was determined by Western blotting using an anti-phosphoERK antibody to detect ERK activity. The effect of PD98059 on ERK activity induced by cisplatin was detected by MTT assay.Results Marked apoptosis of SKOV3 cells resulted from 48 hours treatment with 20 μg/mL cisplatin. Strong activation of ERK was led to by 15 μg/mL cisplatin. Dose response and time course of cisplatin induced apoptosis in SKOV3 cells.Cisplatin-induced ERK activation occurred at 12 hours and increased to highest induction at 24 hours by Western blotting.The effect of PD 98059 on ERK activity induced by cisplatin at the concentration of 100 μmol/L PD 98059. Statistically significant decreased in cell survival were observed with 100 μmol/L PD 98059 at 15 and 20 μg/mL cisplatin (P＜ 0.05).Conclusions Cisplatin activates the ERK signaling pathway in ovarian cancer cell line SKOV3. Inhibition of ERK activity enhances sensitivity to cisplatin cytotoxity in ovarian cancer cell line SKOV3. Evaluation of ERK activity could be useful in predicting which ovarian cancer will response most favorably to cisplatin therapy.     

Reversal of Multidrug Resistance and Inhibition of Phosphorylation of AKT in Human Ovarian Cancer Cell Line by Wild-type PTEN Gene

The reversing effect of wild-type PTEN gene on resistance of C13K cells to cisplatin and its inhibitory effect on the phosphorylation of protein kinase B (AKT) were studied. The expression of PTEN mRNA and protein in OV2008 cells and C13K cells were semi-quantitatively detected by using RT-PCR and Western blotting. Recombinant eukaryotic expression plasmid containing human wild-type PTEN gene was transfected into C13K cells by lipofectamine2000. The expression of PTEN mRNA was monitored by RT-PCR and the expression of PTEN, Akt, p-Akt protein were ana- lyzed by Western blotting in PTEN-transfected and non-transfected C13K cells. Proliferation and chemosensitivity of cells to DDP were measured by MTT, and cell apoptosis was detected by flow cytometry after treatment with cisplatin. The expression of PTEN mRNA and protein in OV2008 cells were significantly higher than those in C13K cells. After transfection with PTEN gene for 48 h, the expression of PTEN mRNA and protein in C13K cells were 2.04±0.10, 0.94±0.04 respectively and the expression of p-Akt protein ( 0.94±0.07) was lower than those in control groups (1.68±0.14, 1.66±0.10) (P< 0.05). The IC50 of DDP to C13K cells transfected with PTEN (7.2±0.3 μmol/L) was obviously lower than those of empty-vector transfected cells and non-transfected cells (12.7±0.4 μmol/l, 13.0±0.3 μmol/L) (P<0.05). The apopototis ratio of wild-type PTEN-transfected, empty vector transfected and non-transfected C13K cells were (41.65±0.87)%, (18.61±0.70)% and (15.28 ±0.80)% respectively, and the difference was statistically significant (P<0.05). PTEN gene plays an important role in ovarian cancer multidrug resistance. Transfection of PTEN could increase the ex- pression of PTEN and restore drug sensitivity to cisplatin in human ovarian cancer cell line C13K with multidrug-resistance by decreasing the expression of p-Akt.     

The Effect of Human Recombinant Interferon Gamma （hrIFN-γ） on hCG Secretion of Trophoblast and Protein Synthesis of Decidual Tissue in Vitro

In this study the effect of human recombinant interferon gamma (hrIFN-γ) on hCG secretion of human first trimester trophoblast and protein synthesis of decidual tissue was investigated in vitro. The results indicated that hrIFN-γ at the doses of 250 U/ml medium and 2500 U/ml medium decreased hCG secretion of trophoblast obviously (P ＜ 0. 0,5, P＜0. 01 ) in a dose dependent manner. The effect of hrIFN-γ on protein synthesis at the doses of 10 U to 1,000 U/ml medium inhibited the^3 H leucine incorporation obviously. The cpm values between control and experimental groups were significantly different (P ＜0. 05 ) in a dosedependent manner. Furthermore its inhibitory effect is in a dose-dependent manner and was neutralized by IFN-γ antiserum. The IFN-α at the doses used did not find any effect on protein synthesis in decidual tissue.     

Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in AngiotensinⅡ-induced Hypertrophic Myocardial CellsIn Vitro

Objective To explore the effect of atorvastatin on cardiac hypertrophy and to determine the potential mechanism involved. Methods Anin vitro cardiomyocyte hypertrophy from neonatal rats was induced with angiotensinⅡ (AngⅡ) stimulation. Before AngⅡ stimulation, the cultured rat cardiac myocytes were pretreated with atorvastatin at different concentrations (0.1, 1, and 10μmol/L). The following parameters were evaluated: the myocyte surface area,3H-leucine incorporation into myocytes, mRNA expressions of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase 9, matrix metalloproteinase 2, and interleukin-1β, mRNA and protein expressions of theδ/β peroxisome proliferator-activated receptor (PPAR) subtypes. Results It was shown that atorvastatin could ameliorate AngⅡ-induced neonatal cardiomyocyte hypertrophy in the area of cardiomyocytes,3H-leucine incorporation, and the expression of atrial natriuretic peptide and brain natriuretic peptide markedly. Meanwhile, atorvastatin also inhibited the augmented mRNA level of several cytokines in hypertrophic myocytes. Furthermore, the down-regulated expression of PPAR-δ/β at both the mRNA and protein levels in hypertrophic myocytes could be significantly reversed by atorvastatin treatment. Conclusions Atorvastatin could improve AngⅡ-induced cardiac hypertrophy and inhibit the expression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.     

Effects of Atractylodes Macrocephala on the Cytomembrane Ca^2＋-activated K^＋ Currents in Cells of Human Pregnant Myometrial Smooth Muscles

The study examined the inhibitory effect of Atractylodes macrocephala(AM) on the uterine contraction during premature delivery and explored its electrophysiological mechanism by studying the effects of AM on the Ca2 -activated K currents of pregnant human myometrial smooth muscle cells with or without the treatment with interleukin-6.Single cells were acutely isolated from pregnant human myometrial smooth muscles.Whole-cell Ca2 -activated K currents were recorded by using an Axopatch1-D amplifier.The cells were divided into three groups: group A in which AM was added into perfusate,group B,in which interleukin-6 was added into perfusate) and group C in which AM was added into perfusate after addition of interleukin-6.IL-6 10 ng/mL inhibited BKca by 36.9%±13.7% as compared with control(P<0.01).AM at 2 mg/mL raised BKca by 36.7%±22.6% or 45.2%±13.7% with or without the treatment of IL-6,respectively(P<0.01).It is concluded that AM was able to enhance the BKca of pregnant human myometrial smooth muscle cells treated or un-treated with interleukin-6 and its effect on the BKca IL-treated cells was stronger that its effect on BKca of untreated cells.Our results suggested that AM can help to maintain the membrane potentials and the resting status of pregnant human myometrial smooth muscle cells.     

风湿性心脏瓣膜病患者钾离子通道特性变化的实验研究

目的:探讨风湿性心脏瓣膜病(简称风心病)患者心房组织细胞Kvl.5钾通道的变化。方法:将风心病患者分为窦性心律组(SR)、阵发性房颤组(PAF)和慢性房颤组(CAF)。应用全细胞膜片钳技术记录各组单个右心耳组织细胞超快速延迟整流钾电流(ultrarapid delayed rectifier current,IKur)的表达。结果:指令电压为+10~+50mV时,慢性房颤组(n=22)IKur密度较窦性心律组(n=25)明显降低。阵发性房颤组(n=23)IKur密度与窦性心律组差异无统计学意义(P>0.05);其中,在+50mV时,电流由窦性心律组(8.98+1.69)PA/pF降为房颤组的(4.17+1.82)PA/pF(P<0.01),降低幅度为(53.6+1.4)%。阵发性房颤组(8.21+1.54)PA/pF与窦性心律组差异无统计学意义(P>0.05),与慢性房颤组差异有统计学意义(P<0.01)。结论:Ikur密度在发生慢性房颤的风心患者心房肌细胞中密度明显下降,提示Kv1.5钾通道的变化与风心病房颤的发生有关。     

法乐四联症儿童肥厚右心室细胞瞬间外向钾电流的研究

目的观察压力增高导致的人肥厚心室组织离子通道的特性.方法应用酶解分离技术从法乐四联症(F4)患儿的心脏右室得到单个细胞,应用膜片钳全细胞记录技术观察了细胞Ito1的特征.结果将钙电流阻断后,去极化至-20mV～+60mV时均可记录到Itn1,激活后电流衰减速度不随去极化程度的增强而改变,在0、20、40、60mV时分别为123ms±6ms、131ms±10ms、122ms±6ms、122ms±6ms,去极化至60mV时的电流密度为4.7pA/pF±0.8pA/pF,半数最大激活电位为4.1mV±2.8mV,半数最大失活电位出现在-41mV±4mV,失活后再激活的恢复时间常数为83ms±4ms.这种电流可被10mM4-AP基本抑制.结论肥厚的人右室细胞存在Itn1,通道动力学特征与成人心房肌细胞类似.     

姜黄素对大鼠心室肌细胞快钠流和L型钙流的影响

目的：研究姜黄素对大鼠心室肌细胞快钠流（INa）和L型钙流（ICa-L）的影响。方法：采用急性酶解分离法获得大鼠心室肌细胞,以全细胞膜片钳技术记录快钠流（INa）和L型钙流（ICa-L）,观察50μmol/L姜黄素对INa和ICa-L的影响。结果：50μmol/L姜黄素对INa和ICa-L的抑制率分别是71.9%±6.3%（P〈0.01）和-1.7%±13.1%（P〉0.05）。它使INa电流密度-电压曲线上移,但不改变激活电位和反转电位,对ICa-L的电流密度-电压曲线无明显影响。结论：50μmol/L姜黄素对大鼠心室肌细胞INa有较强抑制作用,对ICa-L无明显影响。     

三七皂苷R1对心房颤动大鼠心肌炎症相关因子和金属基质蛋白酶表达的影响

【目的】研究三七皂苷R1对心房颤动大鼠细胞间黏附分子-1（ICAM-1）、肿瘤坏死因子-α（TNF-α）、金属基质蛋白酶-2（MMP-2）和金属机制蛋白酶-2抑制因子（TIMP-2）的影响，探讨三七皂苷R1防治心房颤动的机制。【方法】将102只大鼠根据随机数字法分为对照组、心房颤动组和三七皂苷R1组，每组34只。采用尾静脉注射乙酰胆碱-氯化钙建立心房颤动大鼠模型。三七皂苷R1组大鼠腹腔注射2mL三七皂苷R1水溶液。心电图测定心房颤动持续时间，Masson染色观察心肌纤维化程度，免疫组化法测定心房组织MMP-2和TIMP-2蛋白表达，酶联免疫吸附实验（ELISA）测定血清ICAM-1、TNF-α、MMP-2和TIMP-2水平，免疫印迹法（Western blotting）测定心房组织ICAM-1、TNF-α和Ⅰ型胶原蛋白水平。【结果】三七皂苷R1治疗前，两组心房颤动持续时间比较差异无统计学意义（P>0.05）；治疗后，三七皂苷R1组心房颤动持续时间（6.37±2.02）s，低于治疗前和心房颤动组（P<0.05）。Masson染色显示：对照组大鼠心房肌间质胶原纤维量正常；心房颤动组大鼠心房肌间质见大量胶原纤维；三七皂苷R1组大鼠心房肌间质见片、点状胶原纤维。与对照组比较，心房颤动组和三七皂苷R1组大鼠血清ICAM-1、TNF-α、MMP-2水平升高［（137.52±16.59）10-6g/L、（14.25±1.08）10-6g/L、（435.26±17.63）10-9g/L；（109.25±14.62）10-6g/L、（12.31±1.27）10-6g/L、（288.47±15.52）10-9g/L］（P<0.05），TIMP-2水平降低［（3541.27±331.24）10-9g/L；（3975.46±313.24）10-9g/L］（P<0.05），心房组织ICAM-1、TNF-α和Ⅰ型胶原蛋白水平（0.23±0.07、0.51±0.09、0.63±0.14；0.15±0.06、0.22±0.07、0.27±0.12）升高（P<0.05），心房组织MMP-2蛋白光密度值（0.35±0.07；0.18±0.06）升高（P<0.05），TIMP-2蛋白光密度值（0.11±0.04；0.18±0.03）降低（P<0.05）；与心房颤动组比较，三七皂苷R1组大鼠血清ICAM-1、TNF-α、MMP-2水平降低（P<0.05），TIMP-2水平升高（P<0.05），心房组织ICAM-1、TNF-α和Ⅰ型胶原蛋白水平降低（P<0.05），心房组织MMP-2蛋白光密度值降低（P<0.05），TIMP-2蛋白光密度值升高（P<0.05）。【结论】三七皂苷R1通过降低心房颤动大鼠血清和心房组织ICAM-1、TNF-α、MMP-2水平，升高TIMP-2水平发挥对心房颤动的防治作用。     

心房颤动患者心型脂肪酸结合蛋白检测的临床价值

目的： 评价定量检测血清心型脂肪酸结合蛋白(heart type-fatty acid binding protein,H-FABP)对心房颤动患者检测的临床价值。方法： 采用酶联免疫吸附试验一步夹心法检测196名健康体检者、196例心房颤动患者的血清H-FABP,同时测定心肌肌钙蛋白I(cardiac troponin I,cTnI)、肌酸激酶同工酶-MB (creatine kinase isoenzyme MB,CK-MB),并作比较。结果： 房颤组治疗前、治疗后及对照组的H-FABP值分别为（2.8±1.3）μg/L,（2.3±1.4）μg/L和（1.6±1.1）μg/L;cTnI值分别为（0.26±0.05）μg/L,（0.23±0.06）μg/L和（0.05±0.02）μg/L;CK-MB值分别为(12.8±3.6) U/L,(13.6±3.1)U/L和(12.1±2.7) U/L。血浆H-FABP水平房颤组治疗前、治疗后及与对照组比较,差异均有统计学意义(P<0.05);血浆cTnI水平在房颤治疗前、治疗后比较差异无统计学意义(P>0.05),与对照组比较差异有统计学意义（P<0.05）;血浆CK-MB水平房颤组治疗前、治疗后及与对照组比较差异均无统计学意义(P>0.05)。结论： 检测血清H-FABP对心房颤动患者有较重要的临床价值。     

胡椒碱对H2O2所致兔心房肌细胞瞬时外向钾电流异常的保护作用

目的研究胡椒碱对H2O2引起的兔单个心房肌细胞瞬时外向钾电流(Ito)异常的保护作用。方法采用全细胞膜片钳技术分析50μmol/L的H2O2对兔单个心房肌细胞Ito的影响,并研究预先应用7μmol/L的胡椒碱对其的保护作用。结果 7μmol/L胡椒碱对正常兔心房肌细胞Ito及其通道动力学无显著影响。在50μmol/L H2O2作用下,兔心房肌细胞Ito峰值由(39.3±5.4)pA/pF降低至(32.8±2.0)pA/pF(P<0.05),电流-电压曲线下移,通道稳态激活曲线右移,通道稳态失活曲线及恢复时间不变,关闭态失活加速。预先给予7μmol/L胡椒碱,明显减轻H2O2对Ito的抑制作用(P<0.01),并可减轻H2O2对瞬时外向钾通道动力学的异常影响。结论胡椒碱可减轻氧化应激对心房肌细胞Ito的影响。     

术前纤维蛋白原单次目标给药对PLIF术中出血及凝血功能的影响

目的：探讨术前纤维蛋白原（FIB）单次目标给药,对腰椎后路减压椎间植骨融合内固定术（PLIF）术中出血及凝血功能的影响。方法选择腰椎间盘突出症（LDH）择期做 PLIF 的患者60例,依据术前 FIB 水平分为 FIB≥3．0 g／L 组（NC 组, n＝20）和低 FIB 组（FIB＜3．0 g／L,n＝40）,低 FIB 组再分为低 FIB 对照组（LC 组,n＝20）和术前 FIB 单次给药组（PF 组,n＝20）。PF 组于麻醉诱导完成后输入纤维蛋白原;LC、NC 组于麻醉诱导完成后输入纤维蛋白原剂量所需溶媒等容积的生理盐水。3组患者于给药前、后测定凝血4项及用凝血和血小板功能分析仪测定激活凝血时间（ACT）、凝血速率（CR）、血小板功能（PF）,术毕称量出血量。结果FIB 在给药后 PF 组为（3．75±0．23）g／L,明显高于 NC 组（2．62±0．33）g／L 和 LC 组（2．23±0．22）g／L, 3组比较差异有统计学意义（P ＜0．05）;CR 值在给药后 PF 组为（21．42±7．15）U／min,高于 NC 组（18．21±5．62）U／min 和 LC组（15．21±5．63）U／min。PF 组出血量为（516．74±135．53）g,低于 NC 组（660．71±119．34）g 和 LC 组（726．72±160．47）g,3组比较差异有统计学意义（P ＜0．05）。结论术前 FIB 单次目标给药可以有效提高 FIB 水平及凝血功能,减少围术期出血量。     

阿魏酸钠对大鼠胸主动脉的非内皮依赖性血管舒张作用

目的研究阿魏酸钠对离体大鼠胸主动脉的影响。方法以等长张力的形式记录鼠主动脉及去内皮鼠主动脉对去氧肾上腺素和高钾的反应,以及阿魏酸钠对鼠主动脉及去内皮鼠主动脉的舒张作用。结果阿魏酸钠(0.1～30 mmol/L)能使预先用浓度为(2.73±0.02)的去氧肾上腺素和浓度为(2.57±0.06)的高钾预收缩的离体主动脉环舒张(P<0.05);机械去除内皮后,阿魏酸钠对主动脉环的舒张效应没有明显改变。结论阿魏酸钠是一种非内皮依赖性的血管平滑肌细胞松弛剂。     

早期肠内营养支持对急性缺血性卒中伴吞咽困难患者的影响

目的探讨早期肠内营养支持对急性缺血性脑卒中伴吞咽困难患者的营养状况及肺部感染的影响。方法将急性缺血性脑卒中伴吞咽困难患者58例随机分为2组：标准营养组30例,采用能全力按83．74～125．60J／（kg·d）标准配制,经鼻饲管滴注;匀浆膳食组28例,采用自行混制而成匀浆汤液200mL／次,经鼻饲管注入,4～6次／d。分别于入院第1、10天测定血清白蛋白（ALB）、血清前白蛋白（PA）,观察2组患者营养指标的变化以及肺部感染发生率。结果标准营养组入院治疗第10天与入院第1天比较ALB、PA值下降不明显（均P〉0．05）;匀浆膳食组入院治疗第10天与入院第1天比较,ALB[（34．3±2．1）g／L vs （38．8±2．1）g／L]、PA[（158．3±22．1）mg／L vs （198．6±30．8）mg／L]均有降低（均P〈0．05）。入院第10天,标准营养组ALB为（38．5±2．2）g／L、PA为（192．8±26．4）mg／L,均高于匀浆膳食组[ALB（34．3±2．1）g／L、PA（158．3±22．1）mg／L]（均P〈0．05）。标准营养组肺部感染发生率明显低于匀浆膳食组（26．7％VS35．7％,P〈0．05）;肺部感染患者其人院时ALB低于无并发肺部感染患者[（33．4±5．6）g／L vs （42．5±3．7）g／LP〈0．05]。结论早期肠内营养可减缓急性缺血性脑卒中并发吞咽困难患者营养状况恶化,降低肺部感染的发生率。     

Effect of didrovaltrate on l-calcium current in rabbit ventricular myocytes

OBJECTIVE:To investigate the effect of didrovaltrate on L-type calcium current(I Ca-L) in rabbit ventricular myocytes.METHODS:We used the whole cell patch clamp recording technique.RESULTS:Didrovaltrate at concentrations of 30 μg/L and 100 μg/L significantly decreased peak I Ca-L(I Ca-Lmax) from(6.01±0.48) pA/pF to(3.45±0.27) pA/pF and(2.16 ± 0.19) pA/pF(42.6% and 64.1%,n=8,P< 0.01),respectively.Didrovaltrate shifted upwards the current-voltage curves of I Ca-L without changing their active,peak and reverse potentials.Didrovaltrate affected the steady-state inactivation of I Ca-L.The half activation potential(V 1/2) was significantly shifted from(-26 ± 2) to(-36 ± 3) mV(n=6,P<0.05),with a significant change in the slope factor(k)(from 8.8 ± 0.8 to 11.1 ± 0.9,n=6,P<0.05).Didrovaltrate did not affect the activation curve.CONCLUSION:Didrovaltrate blocks I Ca-L in a concentration-dependent manner and probably inhibits I Ca-L in its inactive state,which may contribute to its cardiovascular effect.