中老年男性肥胖者阻塞性睡眠呼吸暂停低通气综合征与代谢综合征相关性研究

目的 探讨中老年男性肥胖者阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)与代谢综合征(metabolic syndrome,MS)及其组分之间的关系.方法 选择中老年男性肥胖患者154例,根据多导睡眠呼吸监测仪监测结果诊断OSAHS及病情严重程度,测定MS相关指标,应用统计学方法对OSAHS各组相关指标及OSAHS与MS之间的关系进行比较分析.结果 与对照组比较,重度OSAHS组高密度脂蛋白胆固醇明显降低[(1.03±0.29)mmol/L对(1.31±0.38)mmol/L,P＜0.05],血糖[(6.61±1.76)mmol/L对(5.47±0.64)mmol/L]、收缩压[(133±13)mm Hg对(125±12)mm Hg]及舒张压[(99±10)mm Hg对(80±5)mm Hg]明显升高(均P＜0.05);MS患病率轻度OSAHS组25.7%,中度OSAHS组46.5%,重度OSAHS组84.4%,均明显高于对照组16.1%(均P＜0.01);在OSAHS患者中,MS患病率是对照组的6.16倍.结论 中老年男性肥胖患者OSAHS是MS发病的独立危险因素.

Abstract：

Objective To explore the relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and metabolic syndrome (MS) in obese middle-aged and older men. Methods We selectively recruited 154 obese middle-aged and older men matched for body mass index (BMI) and age. The polysomnography was performed for diagnosing OSAHS and for discriminating disease severity. The BMI, waist circumference, blood pressure, plasma glucose and lipid profiles were measured and analyzed in all subjects. Appropriate statistical methods were used to compare the components of MS in each group. Logistic regression was taken to elucidate the relationship between OSAHS and MS. Results Compared to control group, severe OSAHS group had significantly lower high density lipoprotein cholesterol level [( 1.03 ± 0.29 ) mmol/L vs. ( 1.31 ± 0. 38) mmol/L,P＜0. 05] and higher fasting glucose [(6.61±1.76) mmol/L vs. (5.47±0.64) mmol/L, P＜0. 05]as well as higher systolic blood pressure [( 133 ± 13) mm Hg vs. ( 125 ± 12) mm Hg, P＜0. 05] and diastolic blood pressure [(99±10) mm Hg vs. (80±5) mm Hg, P＜0. 05]. The prevalence of MS was significantly higher in OSAHS group than in control group (mild OSAHS group: 25.7%,moderate OSAHS group: 46. 5%, severe OSAHS group: 84.4%, control group: 16. 1 %, all P＜0. 01). OSAHS was independently associated with an increased prevalence of MS Odds ratio, 6.16).Conclusions OSAHS is independently associated with MS in obese middle-aged and older men.     

异丙肾上腺素诱导慢性心力衰竭大鼠心肌醛固酮及其核受体的变化

目的 探讨异丙肾上腺素(isoproterenol,ISO)诱导的慢性心力衰竭SD大鼠心肌醛固酮及其核受体的变化.方法 将SD大鼠抽签随机分为心力衰竭组(9只)和对照组(10只),心力衰竭组皮下注射ISO,对照组皮下注射等量生理盐水,心功能采用超声心动图及血流动力学检查,放射免疫法测定血浆及心肌组织醛固酮水平,免疫印迹和免疫组化染色法检测盐皮质激素核受体蛋白表达的变化.结果 心力衰竭组与对照组比较心功能明显下降,左心室射血分数分别为(38.8±4.0)%与(79.4±4.6)%;左心室内压最大上升速率分别为(7164.4±502.6)mm Hg(1 mm Hg=0.133 kPa)/s与(10199.5±462.9)mm Hg/s(均P＜0.01).血浆及心肌组织醛固酮含量明显升高,分别为(0.63±0.06)μg/L与(0.30±0.07)μg/L、(0.41±0.05)μg/kg与(0.08±0.01)μg/kg(均P＜0.01),左心室心肌醛固酮核受体蛋白表达增高(P＜0.01).结论 ISO可诱导SD大鼠出现类似扩张型心肌病的慢性心力衰竭表现,在这种心力衰竭模型中其循环和左心室心肌醛固酮水平明显升高,心肌醛固酮核受体表达上调,可能在心力衰竭的发生、发展中起着重要作用.

Abstract：

Objective To investigate the changes of cardiac aldosterone and mineralocorticoid receptor (MR) in Sprague-dawley (SD) rats with chronic heart failure (CHF) induced by isoproterenol (ISO). Methods The SD rats were randomly divided into CHF group (n=9) and normal control(NC) group (n=10). The experimental CHF group was induced by subcutaneous injection of ISO, and the NC group received same dose injection of sodium chloride. The heart function was evaluated with both echocardiography and hemodynamics. The contents of aldosterone in both plasma and heart were assessed by radioimmunoassay. The expression of MR was measured by Western blot and immunohistochemistry staining. Results Compared with NC group, the heart function was decreased in CHF group, the left ventricular ejection fraction was (38.8%±4.0%) in CHF and(79. 4%±4.6%), in NC group. The maximal rate of increase of ventricular pressure (+dp/dtmax) was (7164.4±502.6) mm Hg(1 mm Hg=0.133 kPa)/s in CHF and (10199.5±462.9) mm Hg/s in NC group (both P＜0. 01 ). The contents of aldosterone both in plasma and heart were higher in CHF group than in NC group [(0.63±0.06)μg/L vs. (0.3±0.07) μg/L, (0.41±0.05) μg/kgvs. (0.08±0.01)μg/kg, both P＜0. 01]. The MR expression was increased in CHF group versus in NC group (P＜0.01). Conclusions The heart function is decreased in rats with CHF induced by ISO, which is similar to dilated cardiomyopathy. The higher levels of aldosterone both in circulation and in heart as and well as MR expression upregulation in heart may play important roles in the pathogenesis of CHF induced by ISO.     

脑钠肽联合组织多普勒检查对老年高血压患者左室肥厚及舒张功能受损的评估

目的 探讨老年原发性高血压患者左室肥厚(LVH)及舒张功能与脑钠肽(BNP)水平的关系.方法 140例老年原发性高血压患者,其中左室肥厚(LVH)组69例,非左室肥厚(NLVH)组71例,健康对照组50例.测定各组BNP浓度.常规脉冲多普勒测量二尖瓣口舒张早期血流速度(E)、舒张晚期血流速度(A),计算E/A值.应用定量组织速度成像(QTVI)技术测量左室壁二尖瓣环6个位点(侧壁和后间隔、前壁和下壁、前间隔和后壁)处的舒张早期峰值运动速度(Em)、舒张晚期峰值运动速度(Am),计算Em/Am值,同时计算6个位点平均速度(MEm、MAm)、MEm/MAm值及E/MEm值.比较3组间舒张功能指标的变化,以及BNP浓度与超声指标的关系.结果 高血压NLVH组、LVH组E/MEm(11.3±1.83、15.7±1.45)及BNP浓度[(61.64±37.18)ng/L、(138.65±30.23)ng/L]较对照组升高(P＜0.05及P＜0.01);MEm[(6.32±0.94)cm/s、(4.29±0.91)cm/s]及MEm/MAm值(0.76±0.19、0.51±0.11)较对照组减低(P＜0.05及P＜0.01);高血压组BNP浓度与E/A、MEm、MEm/MAm值显著负相关(r=-0.294、r=-0.387、r=-0.422,均P＜0.01),与LVMI及E/MEm值显著正相关(r=0.342及r=0.501,均P＜0.01).结论 高血压患者无论有无左室肥厚均有舒张功能减低,而LVH患者左室舒张功能障碍更为严重.联合血浆BNP浓度和超声指标有助于准确评估老年高血压患者左室肥厚和舒张功能.

Abstract：

Objective To investigate the clinical values of brain natriuretic peptide (BNP) in combination with TDI in diagnosing left ventricular hypertrophy (LVH) and impaired diastolic function in elderly hypertensive patients. Methods The 140 elderly hypertensive patients were divided into LVH group (n=69) and NLVH group (n=71). Control group consisted of 50 normal subjects. Plasma BNP level and index of echocardiography, including mitral peak flow velocity during early and late diastole (E, A), ratio of E/A, average peak velocities of six LV wall sites at mitral annuluses during early and late diastole (MEm, MAm), ratios of MEm/MAm and E/MEm were measured in all patients. The correlation of plasma BNP level with cardiac ultrasonographic findings was also examined. Results The level of BNP [(61.64±37.18)ng/L, (138. 65±30. 23)ng/L] and the ratio of E/MEm (11.3±1.83, 15.7±1.45) were significantly higher in NLVH group and LVH group than in normal group (P＜0. 05 or P＜0. 01). MEm [(6.32±0. 94)cm/s, (4.29±0. 91)cm/s]and MEm/MAm (0.76±0.19, 0.51±0. 11) were significantly lower in NLVH and LVH group than in normal group (P＜0.05 or P＜0. 01). The BNP level was negatively correlated with E/A, MEm and MEm/MAm (r=- 0. 294, r= 0. 387 and r= 0. 422, all P＜0. 01), and was positively correlated with LVMI and E/MEm (r=0.342, r=0.501, all P＜0.01). Conclusions Left ventricular diastolic function is impaired in elderly hypertension patients regardless of LVH or NLVH.Plasma BNP level in combination with echocardiography parameter is accurate to evaluate the LVHand impaired diastolic function in elderly hypertensive patients.     

过表达肌浆网钙ATP酶治疗实验性慢性缺血性心力衰竭

目的 研究肌浆网钙ATP酶2a(SERCA2a)基因过表达对慢性缺血性心力衰竭(心衰)心功能及心肌内质网应激(ERS)相关凋亡的影响.方法采用ameroid环束扎小型猪前降支制备慢性缺血性心衰模型.开胸心肌内注射重组腺相关病毒以过表达SERCA2a或对照报告基因绿色荧光蛋白.60 d后检测血流动力学、SERCA2a的表达和活性、心肌凋亡及ERS标志蛋白-分子伴侣GRp78、凋亡蛋白caspase-12的表达.结果基因转导后60 d,与心衰对照及报告基因组相比,转基因组SERCA2a蛋白表达和活性显著增高,心功能参数改善,心肌凋亡指数降低,伴GRP78和活化caspase12表达下降.结论过表达SERCA2a可改善慢性缺血性心衰的心脏功能,其机制可能涉及减轻ERS相关的心肌细胞凋亡.

Abstract：

Objective Chronic myocardial ischemia (CMI) has become the most importat cause of heart failure (HF) all over the world. The aim of the current study was to investigate the effects of Sarcoendoplasmic reticulum calcium ATPaee 2a (SERCA2a) gene transfer on cardiac function and endoplasmic reticulum stress (ERS) associated myocardial apoptosis in a minipig HF animal model induced by CMI. Methods HF was induced in minipigs by implantation of ameroid constrictor in the initial segment of left anterior descending (LAD) branch of coronary artery. After confirmation of myocardial perfusion defects and cardiac function impairment by myocardial perfusion imaging and echocardiography, animals were divided into 4 groups (n =4 each): HF group, HF + enhanced green fluorescent protein (EGFP) group,HF + SERCA2a group, and shamed animals as control group. A total amount of 1×1012 v.g. Of rAAV1EGFP or rAAV1-SERCA2a were injected intramyocardially to each animal of HF + EGFP and HF +SERCA2a groups. Sixty days after gene transfer, protein level and activity of SERCA2a were examined,cardiac functions and changes of serum inflammatory and neuro-hormonal factors were determined. Apoptotic index of the ischemic myocardium, protein levels of ER stress marker glucose regulated protein 78 ( GRP 78) and ER stress specific apoptotic marker caspase-12 were also assayed. Results At the study end,echocardiographic and hemodynamic measurements indicated a significant improvement of both cardiac systolic and diastolic function in HF + SERCA2a group compared with HF/HF + EGFP groups [LVEF (60.2±8.6)%vs (44.2±7.1)% and (46.8±6.7)%, Ev/Ay 1.28±0.24 vs 0.77 ±0.17 and 0.80±0.21, +dp/dtmax(2713.9 ±434.0) mm Hg/s ( 1 mm Hg =0.133 kPa) vs (1892.3 ±434.2) mm Hg/s and (1931.2±397.4)mm Hg/s, -dp/dtmax (1422.1±334.4) mm Hg/s vs (848.3±308.3) mm Hg/s and (849.5±278.3)mm Hg/s, P＜0.05], along with increase in both SERCA2a protein level (1.13±0.26 vs 0.73 ±0.17 and 0.64±0.18, P＜0.05) and activity [(16.2±5.5) IU/ml vs (7.9±3.1) IU/ml and (7.5 ±2.8)IU/ml, P ＜0.05] compared with HF/HF + EGFP groups. Serum concentrations of inflammatory factor tumor necrotic factor α [(382.3±114.4) ng/L vs (732.3±201.4) ng/L and (689.8±192 5) ng/L, P＜0. 05], neural-hormonal factors brain natriuretic peptide [(142.6±45.3) ng/L vs (422.3±113.6) ng/L and(393.7 ±103.3)ng/L, P＜0.01], endothelin-1 [(111.4 ±37.5)ng/L vs (193.5 ±54.3)ng/L and (201.0±72.1)ng/L,P＜0.05] and angiotensin Ⅱ[(189.7±65.2)μg/L vs (538.3 ± 135.2) μg/L and ( 525.5±144.1)μg/L, P＜0.01] were also significantly decreased in HF + SERCA2a group compared with HF/HF + EGFP groups. The apoptotic index [(12.71±4.11)% vs(23.22±7.23) % and (24.31±6.38)%, P＜0.05], protein levels of GRP78 (1.27±0.33 vs 3.23±1.14 and 4.18±1.13, P＜0.05)and protein level ratios of cleaved caspase-12 to total caspase-12[(4.62±1.93)% vs (9.71±2.70)% and (10.14±2.81)%, P＜0.05] were also significantly reduced in the ischemic myocardium of HF+SERCA2a group compared with the HF/HF + EGFP groups. Conclusion Overexpression of SERCA2a significantly improved cardiac systolic and diastolic function in this HF model partly through attenuation of ER stress related myocardial apoptosis, suggesting its therapeutic potential for CM1 related heart failure.     

降压达标干预对原发性高血压患者臂踝脉搏波传导速度的影响

目的 探讨原发性高血压患者降压干预对臂踝脉搏波传导速度(baPWV)的影响.方法 150例高血压患者接受包括缬沙坦80 mg/d在内的降压治疗6个月[降压达标定义为＜140/90 mm Hg(1 mm Hg=133 kPa)]和正常对照组135例,应用欧姆龙-VP1000自动测量baPWV,对其进行标准化的心血管病危险因素调查、体格检查及实验室检查.结果 高血压组baPWV为(2105.8±378.4)cm/s,高于正常对照组的(1371.5±1 76.5)cm/s(t=4.05,P＜0.001).高血压组和对照组的动脉硬化的检出率分别为82.0%和21.8%;高血压组患者的年龄(r=0.51,P＜0.001)、收缩压(r=0.53,P＜0.001)、脉压、(r=0.43,P＜0.05),脉压指数(PPI)(r=0.51,P＜0.05)、空腹血糖(r=0.39,P＜0.01)均与baPWV呈正相关;高血压组的baPWV由(2105.8±378.4)cm/s降低至(1704.2±332.0)cm/s(t=3.85,P＜0.05).降压达标组的baPWV[(1588.8±278.7)cm/s]明显低于未达标组[(1857.7±324.9)cm/s(t=3.67,P＜0.001)].结论 年龄和收缩压是高血压患者baPWV的主要影响因素,降压达标可以改善baPWV,减轻动脉僵硬度.

Abstract：

Objective To investigate the effect of antihypertensive therapy on brachial-ankle pulse wave velocity (baPWV) in patients with essential hypertension (EH). Methods The 150 EH patients (EH group)receiving antihypertensive therapy with valsartan 80 mg/d, and 135 healthy controls (control group) were enrolled in this study. Automatic pulse wave velocity (PWV)measurement system was employed to examine baPWV, and the investigation about cardiac risk factors, physical and laboratory examination was performed. The baPWV was used as an index to show artery stiffness.Results The baPWV was significantly higher in EH group than in control group [(2105.8±378.4) cm/svs. (1371.5±176.5) cm/s, t=4.05, P＜0.001]. The detection rate of atherosclerosis was 82.0% and 21.8% in EH and control group respectively. In EH group, there were positive relationships between age and baPWV (r= 0.51, P＜0. 001), SBP and baPWV (r=0.53, P＜0.001), pulse pressure (PP) and baPWV (r=0.43, P＜0. 05), PP index (PPI) and baPWV (r=0.51, P＜0.05), blood glucose and baPWV (r=0.39, P＜0.01). The baPWV decreased significantly from (2105.8±378.4) cm/s to (1704.2±332.0) cm/s (t=3.85, P＜0. 05) in EH group. The baPWV was significantly lower in the subgroup with a target BP than without a target BP in EH patients [(1588.8±278.7) vs. (1857.7±324.9) cm/s, t=3.67, P＜0.001].Conclusions The age and SBP are primary risk factors for baPWV in EH patients. The antihypertensive therapy can relieve baPWV with a target blood pressure.     

过表达肌浆网钙ATP酶治疗实验性慢性缺血性心力衰竭

Objective Chronic myocardial ischemia (CMI) has become the most importat cause of heart failure (HF) all over the world. The aim of the current study was to investigate the effects of Sarcoendoplasmic reticulum calcium ATPaee 2a (SERCA2a) gene transfer on cardiac function and endoplasmic reticulum stress (ERS) associated myocardial apoptosis in a minipig HF animal model induced by CMI. Methods HF was induced in minipigs by implantation of ameroid constrictor in the initial segment of left anterior descending (LAD) branch of coronary artery. After confirmation of myocardial perfusion defects and cardiac function impairment by myocardial perfusion imaging and echocardiography, animals were divided into 4 groups (n =4 each): HF group, HF + enhanced green fluorescent protein (EGFP) group,HF + SERCA2a group, and shamed animals as control group. A total amount of 1×1012 v.g. Of rAAV1EGFP or rAAV1-SERCA2a were injected intramyocardially to each animal of HF + EGFP and HF +SERCA2a groups. Sixty days after gene transfer, protein level and activity of SERCA2a were examined,cardiac functions and changes of serum inflammatory and neuro-hormonal factors were determined. Apoptotic index of the ischemic myocardium, protein levels of ER stress marker glucose regulated protein 78 ( GRP 78) and ER stress specific apoptotic marker caspase-12 were also assayed. Results At the study end,echocardiographic and hemodynamic measurements indicated a significant improvement of both cardiac systolic and diastolic function in HF + SERCA2a group compared with HF/HF + EGFP groups [LVEF (60.2±8.6)%vs (44.2±7.1)% and (46.8±6.7)%, Ev/Ay 1.28±0.24 vs 0.77 ±0.17 and 0.80±0.21, +dp/dtmax(2713.9 ±434.0) mm Hg/s ( 1 mm Hg =0.133 kPa) vs (1892.3 ±434.2) mm Hg/s and (1931.2±397.4)mm Hg/s, -dp/dtmax (1422.1±334.4) mm Hg/s vs (848.3±308.3) mm Hg/s and (849.5±278.3)mm Hg/s, P＜0.05], along with increase in both SERCA2a protein level (1.13±0.26 vs 0.73 ±0.17 and 0.64±0.18, P＜0.05) and activity [(16.2±5.5) IU/ml vs (7.9±3.1) IU/ml and (7.5 ±2.8)IU/ml, P ＜0.05] compared with HF/HF + EGFP groups. Serum concentrations of inflammatory factor tumor necrotic factor α [(382.3±114.4) ng/L vs (732.3±201.4) ng/L and (689.8±192 5) ng/L, P＜0. 05], neural-hormonal factors brain natriuretic peptide [(142.6±45.3) ng/L vs (422.3±113.6) ng/L and(393.7 ±103.3)ng/L, P＜0.01], endothelin-1 [(111.4 ±37.5)ng/L vs (193.5 ±54.3)ng/L and (201.0±72.1)ng/L,P＜0.05] and angiotensin Ⅱ[(189.7±65.2)μg/L vs (538.3 ± 135.2) μg/L and ( 525.5±144.1)μg/L, P＜0.01] were also significantly decreased in HF + SERCA2a group compared with HF/HF + EGFP groups. The apoptotic index [(12.71±4.11)% vs(23.22±7.23) % and (24.31±6.38)%, P＜0.05], protein levels of GRP78 (1.27±0.33 vs 3.23±1.14 and 4.18±1.13, P＜0.05)and protein level ratios of cleaved caspase-12 to total caspase-12[(4.62±1.93)% vs (9.71±2.70)% and (10.14±2.81)%, P＜0.05] were also significantly reduced in the ischemic myocardium of HF+SERCA2a group compared with the HF/HF + EGFP groups. Conclusion Overexpression of SERCA2a significantly improved cardiac systolic and diastolic function in this HF model partly through attenuation of ER stress related myocardial apoptosis, suggesting its therapeutic potential for CM1 related heart failure.     

过表达肌浆网钙ATP酶治疗实验性慢性缺血性心力衰竭

Objective Chronic myocardial ischemia (CMI) has become the most importat cause of heart failure (HF) all over the world. The aim of the current study was to investigate the effects of Sarcoendoplasmic reticulum calcium ATPaee 2a (SERCA2a) gene transfer on cardiac function and endoplasmic reticulum stress (ERS) associated myocardial apoptosis in a minipig HF animal model induced by CMI. Methods HF was induced in minipigs by implantation of ameroid constrictor in the initial segment of left anterior descending (LAD) branch of coronary artery. After confirmation of myocardial perfusion defects and cardiac function impairment by myocardial perfusion imaging and echocardiography, animals were divided into 4 groups (n =4 each): HF group, HF + enhanced green fluorescent protein (EGFP) group,HF + SERCA2a group, and shamed animals as control group. A total amount of 1×1012 v.g. Of rAAV1EGFP or rAAV1-SERCA2a were injected intramyocardially to each animal of HF + EGFP and HF +SERCA2a groups. Sixty days after gene transfer, protein level and activity of SERCA2a were examined,cardiac functions and changes of serum inflammatory and neuro-hormonal factors were determined. Apoptotic index of the ischemic myocardium, protein levels of ER stress marker glucose regulated protein 78 ( GRP 78) and ER stress specific apoptotic marker caspase-12 were also assayed. Results At the study end,echocardiographic and hemodynamic measurements indicated a significant improvement of both cardiac systolic and diastolic function in HF + SERCA2a group compared with HF/HF + EGFP groups [LVEF (60.2±8.6)%vs (44.2±7.1)% and (46.8±6.7)%, Ev/Ay 1.28±0.24 vs 0.77 ±0.17 and 0.80±0.21, +dp/dtmax(2713.9 ±434.0) mm Hg/s ( 1 mm Hg =0.133 kPa) vs (1892.3 ±434.2) mm Hg/s and (1931.2±397.4)mm Hg/s, -dp/dtmax (1422.1±334.4) mm Hg/s vs (848.3±308.3) mm Hg/s and (849.5±278.3)mm Hg/s, P＜0.05], along with increase in both SERCA2a protein level (1.13±0.26 vs 0.73 ±0.17 and 0.64±0.18, P＜0.05) and activity [(16.2±5.5) IU/ml vs (7.9±3.1) IU/ml and (7.5 ±2.8)IU/ml, P ＜0.05] compared with HF/HF + EGFP groups. Serum concentrations of inflammatory factor tumor necrotic factor α [(382.3±114.4) ng/L vs (732.3±201.4) ng/L and (689.8±192 5) ng/L, P＜0. 05], neural-hormonal factors brain natriuretic peptide [(142.6±45.3) ng/L vs (422.3±113.6) ng/L and(393.7 ±103.3)ng/L, P＜0.01], endothelin-1 [(111.4 ±37.5)ng/L vs (193.5 ±54.3)ng/L and (201.0±72.1)ng/L,P＜0.05] and angiotensin Ⅱ[(189.7±65.2)μg/L vs (538.3 ± 135.2) μg/L and ( 525.5±144.1)μg/L, P＜0.01] were also significantly decreased in HF + SERCA2a group compared with HF/HF + EGFP groups. The apoptotic index [(12.71±4.11)% vs(23.22±7.23) % and (24.31±6.38)%, P＜0.05], protein levels of GRP78 (1.27±0.33 vs 3.23±1.14 and 4.18±1.13, P＜0.05)and protein level ratios of cleaved caspase-12 to total caspase-12[(4.62±1.93)% vs (9.71±2.70)% and (10.14±2.81)%, P＜0.05] were also significantly reduced in the ischemic myocardium of HF+SERCA2a group compared with the HF/HF + EGFP groups. Conclusion Overexpression of SERCA2a significantly improved cardiac systolic and diastolic function in this HF model partly through attenuation of ER stress related myocardial apoptosis, suggesting its therapeutic potential for CM1 related heart failure.     

拮抗或激活促肾上腺皮质激素释放因子受体对肠易激综合征大鼠内脏敏感性及结肠动力的影响

目的 探讨促肾上腺皮质激素释放因子(CRF)及其受体对肠易激综合征大鼠内脏敏感性及结肠动力的影响.方法 SD大鼠60只,随机平均分入空白组(不做处理)、模型组(特殊气味条件刺激和肢体束缚直肠刺激非条件刺激轮替致敏)、干预对照组(造模前侧脑室注射0.9%NaC1)、干预一组(造模前侧脑室注射CRF-R1拮抗剂)和干预二组(造模前侧腑室注射CRF-R2激动剂).采用腹部收缩反射(AWR)评分标准评估各组大鼠肠道敏感性,记录各组大鼠结肠快、慢波波动率、最大振幅、收缩波数及振幅指数等电生理活动改变.采用SPSS16.0统计软件分析,计量资料采用方差分析,等级资料采用秩和检验.结果 以AWR=3分时所需的直肠注水量作为评价指标,模型组大鼠[(0.90±0.11)ml]较空白组[(1.23±0.07)ml]内脏敏感性增高(F＝82.586,P＜0.01);结肠电生理活动增强,造模成功.干预对照组直肠注水量为(0.81±0.11)ml,与模型组[(0.90±0.11)ml]差异无统计学意义(F＝3.734,P＞0.05),干预一组[(1.28±0.07)ml,F＝161.878,P＜0.01]和干预二组[(1.22±0.05)ml,F＝121.564,P＜0.01]较干预对照组内脏敏感性降低.干预对照组大鼠结肠快、慢波波动率、最大振幅、收缩波数及振幅指数等电生理活动与模型组无明显差异(P均＞0.05);干预一组和干预二组大鼠结肠电生理活动均较干预对照组明显减弱(均P＜0.05).结论 CRF在IBS发病中起重要作用,抑制CRF-R1或激活CRF-R2可降低1BS大鼠内脏敏感性并抑制结肠运动.

Abstract：

Objective To explore the effect of corticotropin releasing factor (CRF) and its receptor on visceral sensitivity and colon motility of irritable bowel syndrome (IBS) rats. Methods sixty SD rats were divided randomly and equally into control group (without treatment),model group (sensitized in turn with camphor odor as conditional stimulation and physical restraint in combination with rectal distention pressure as non-conditional stimulation),treatment control group (injected physiological saline into lateral ventricles before treatment),treatment group 1 (injected CRF-R1antagonist into lateral ventricles before treatment),treatment group 2 (injected CRF-R2 agonist into lateral ventricles before treatment). Then the rats' visceral sensitivity were assessed by AWR,and colonic electricity activities such as volatility,maximum amplitude of fast wave and slow wave,interdigestive number of contraction wave and index of contraction were recorded. The data was analyzed with SPSS 16. 0 software. Results By the amount of ractal water injection to reach AWR=3 as the evaluation index,model group [(0. 90±0. 11) ml] showed higher visceral sensitivity than that of control group [(1. 23±0. 07) ml,F=82. 586,P＜0. 01],and colonic electricity activity increased (P＜0. 05),model was successfully set up. There was no significant difference of the amount of ractal water injection between model group [(0. 90±0. 11) ml] and treatment control group [(0. 81±0. 11) ml,F=3. 734,P＞0. 05]. Compared with treatment control group,the visceral sensitivity decreased in treatment group 1 [(1. 28±0. 07) ml,F=161. 878,P＜0. 01] and treatment group 2 [(1. 22±0.05) ml,F=121. 564,P＜0. 01]. There was no significant difference between treatment control group and model group in electricity activities such as volatility,maximum amplitude of fast wave and slow wave,interdigestive number of contraction wave and index of contraction (all P＞0. 05). While the electricity activities was weakened in treatment group 1 and 2 compared with the treatment control group (all P＜0. 05). Conclusions CRF plays an important role in the pathogenesis of IBS. Inhibition of CRF-R1 or activation of CRF-R2 may lower visceral hypersensitivity and decrease colon motility of rats.     

Mechanism of Profilin-1 in regulating eNOS/NO signaling pathway and its role in hypertensive myocardial hypertension

Objective:To explore the mechanism of Profilin-1 in regulating eNOS/NO pathway and its role in the development of myocardial hypertrophy.Methods:Spontaneously hypertensive rats(SHR) aged 5 weeks were injected with different adenovirus vectors to induce Profilin-1expression knockdown(SHR-I) or over express(SHR-H) or to use as control(SHR-C).All these treatment were compared with Wistar-Kyoto rats(SKY) treated with control adenovirus vectors(WKY-C).The same injection was executed at the sixth week during the experiment of 12 weeks.After experiment,the left ventricular weight-to-heart weight ratio(LVW/HW)and left ventricular long axis(LVLA) were measured.Meanwhile.NO contents in blood and myocardium,Profilin-1,eNOS and Caveolin-3 niRNA and protein levels and phosphorylated eNOS(P-eNOS) protein level in myocardium were determined.Results:Compared with WKY-C group,the SHR-C group was statistically higher in LVW/HW(0.79±0.03).LVLA(11.82±0.58 mm) and Profilin-1 niRNA and prolein level(P0.05).but lower in NO content[(18.63±6.23) μmol/L| in blood and[(2.71±0.17) μmol/L]in myocardium).eNOS activity and Caveolin-3 expression(P0.05).The over expressing Profilin-1 led SHR-H group to a higher value of LVW/HW[(0.93±0.03) mm and LVLA(14.17±0.69) mm]in comparison with SHR-C group(P0.05).and to a lower value of NO content(in myocardium).eNOS activity and Caveolin-3 expression(P0.05):however,this phenomenon was reversed by the knockdown Profilin-1 expression(SHR-I group).Conclusions:Profilin-1 expression,being negative in regulating Caveolin-3 expression and eNOS/NO pathway activity,promotes the development of myocardial hypertrophy which can be reversed by Profilin-1 silencing.     

丙泊酚复合不同阿片类药物在老年人结肠镜检查中的镇静效果

目的 探讨丙泊酚复合不同阿片类药物应用于老年人结肠镜检查镇静的效果.方法 60例老年结肠镜受检者随机分为3组,均采用靶控输注方法给予丙泊酚,其中20例单次推注芬太尼(芬太尼组),靶控输注舒芬太尼(舒芬太尼组)、瑞芬太尼(瑞芬太尼组)各20例.记录患者血流动力学改变、镇静深度和不良事件.结果 3组受检患者一般情况、血流动力学改变、镇静深度和不良事件比较差异无统计学意义(均P＞0.05).检查后恢复时间芬太尼组[(21.3±4.6)min]长于舒芬太尼组[(19.9±3.3)min]和瑞芬太尼组[(15.9±1.8)min],且与瑞芬太尼组比较差异有统计学意义(均P＜0.05).结论 丙泊酚复合3种阿片类药物均可安全有效地用于老年人结肠镜检查,但使用瑞芬太尼受检者恢复更为迅速.

Abstract：

Objective To explore the feasibility and safety of fentanyl, sufentanil or remifentanil combined with target-controlled infusion (TCI) of propofol for sedation in the elderly undergoing colonoscopy. Methods In this prospective randomized study, 60 patients undergoing colonoscopy and propofol TCI were randomly assigned to group F (fentanyl), group S (sufentanil) and group R (remifentanil)(each n=20). Patients in group F received a single bolus of fentanyl, while those in group S and group R received TCI sufentanil and remifentanil separately. The blood pressure, heart rate, blood oxygen content and Bispectral index (BIS) were monitored, and all the complications were recorded. Results All patients were adequately sedated. There were no significant differences in general conditions, hemodynamics changes, sedation depth and adverse event among the three groups (all P＞0.05). Time for recovery was longer in group F [(21.3±4.6) min] than in group S [(19.9±3.3) min] and group R [(15.9±1.8) min, P＜0.05]. Conclusions For the elderly undergoing colonoscopy, sedation with fentanyl, sufentanil or remifentanil combined with propofol TCI is feasible and safe. It is more excellent for the remifentanil group at shorter discharge time.     

分侧肺通气时不同呼气末正压和潮气量对单侧肺损伤犬循环的影响

目的 观察不同步分侧肺通气和同步分侧肺通气对单侧急性肺损伤(ALI)犬循环的影响.方法 取健康杂种犬12只,建立盐酸所致单侧肺损伤动物模型,行容积控制通气,将犬按随机数字表法分为不同步分侧肺通气组(NS组)和同步分侧肺通气组(S组).参数:患侧潮气量3.5 ml/kg保持不变,呼气末正压(PEEP)选择15、20、25 cm H2O(1 cm H2O=0.098 kPa);患侧PEEP 10 cm H2O不变,潮气量用随机数字表法选择5、7.5、10 ml/kg.健侧通气参数始终不变,检测不同通气条件下两组犬血流动力学和氧动力学指标.结果 (1)患侧潮气量3.5 ml/kg不变,PEEP为15、20 cm H2O时,两组血流动力学和氧动力学参数差异无统计学意义.当患侧PEEP为25 cm H2O时,NS组心率、体循环平均压(mABP)、心输出量、氧合指数和混合静脉血氧饱和度(SvO2)分别为(98±8)次/min、(84±6)mm Hg(1 mm Hg=0.133 kPa)、(1.10±0.13)L/min、(199±14)mm Hg和(55±6)%,明显低于S组[分别为(124±9)次/min、(103±7)mm Hg、(1.52±0.28)L/min、(221±15)mm Hg和(62±4)%,t值分别为-7.852、-16.561、-15.043、-13.314和-5.653,均P＜0.01].(2)患侧PEEP 10 cm H2O不变,潮气量分别为5、7.5 ml/kg时,两组的血流动力学和氧动力学参数比较差异无统计学意义.当患侧潮气量为10 ml/kg时,NS组HR、mABP、心输出量、氧合指数和SvO2均低于S组(均P＜0.01).结论 在本实验动物模型中,患侧与健侧所用PEEP水平相差≤20 cm H2O或患侧潮气量≤7.5 ml/kg时,同步和非同步分侧肺通气均能保持循环稳定.若需要更高水平PEEP时,建议选用同步分侧肺通气.     

缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性的影响

目的 比较缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性及一氧化氮、内皮素的影响.方法选取61例2、3级老年高血压患者,随机分为两组,分别给予缬沙坦+氨氯地平或缬沙坦+氢氯噻嗪行降压治疗,观察入选时、治疗第8周和第16周各种相关指示的变化.人选时检测血脂、空腹血糖、血尿酸,试验各个阶段监测24 h动态血压,检测血浆一氧化氮、内皮素水平.结果在患者入选时、治疗第8周和第16周三个时间点,缬沙坦+氨氯地平组和缬沙坦+氢氯噻嗪组24 h血压及白昼血压比较差异无统计学意义.治疗第16周,缬沙坦+氨氯地平组晨峰收缩压较缬沙坦+氢氯嚷嗪组明显降低[(22.6±8.8)mm Hg(1 mm Hg=0.133 kPa)比(26.3±13.7)mm Hg,P＜0.05];缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组24 h收缩压变异性(SBPV)进行性降低[缬沙坦+氨氯地平组:(12.5±2.8)mm Hg比(10.2 ±2.2)mm Hg比(8.8±1.6)mm Hg,P＜0.01;缬沙坦±氢氯噻嗪组:(12.5±2.5)mmHg比(10.7±2.2)mm Hg比(9.6±2.0)mmHg,P＜0.01],缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组白昼SBPV明显降低[缬沙坦+氨氯地平组:(12.2±3.0)mm Hg比(10.1±2.3)mm Hg比(8.4±1.9)mm Hg,P＜0.01;缬沙坦+氢氯噻嗪组:(11.8±2.7)mm Hg比(10.4±1.9)mm Hg比(9.6±2.2)mm Hg,P＜0.01],缬沙坦+氨氯地平组24 h舒张压变异性(DBPV)显著降低[(15.5±3.4)mm Hg比(13.0±3.5)mm Hg比(12.3±2.5)mm Hg,P＜0.01],缬沙坦+氢氯噻嗪组24 h DBPV无显著性变化;缬沙坦+氨氯地平组第16周白昼SBPV低于缬沙坦+氢氯噻嗪组[(8.4±1.9)mm Hg比(9.6 ±2.2)mm Hg,p＜0.05],缬沙坦+氨氯地平第8周、第16周的24 h DBPV、白昼DBPV低于缬沙坦+氢氯噻嗪组(P ＜0.01～0.05);缬沙坦+氨氯地平组一氧化氮进行性升高[(27.3±13.6)μmol/L比(47.2±16.3)μmol/L比(69.5±18.9)μmol/L,P＜0.01]、内皮素进行性降低[(45.3±8.0)ng/L比(37.4±3.9)ng/L比(34.2±4.4)ng/L,P＜0.01];缬沙坦+氢氯噻嗪组一氧化氮进行性升高[(33.5±13.9)μmol/L 比(49.7±21.9)μmol/L比(66.7 ±24.7)μmol/L,P＜0.01]、内皮素显著降低[(46.6±10.4)ng/L比(37.0±5.4)ng/L比(36.1±8.2)ng/L,P＜0.01].治疗第8周,缬沙坦+氨氯地平组收缩压变异性的降幅与一氧化氮的升幅有相关性(r =0.401,P=0.025).结论缬沙坦联合氨氯地平或氢氯噻嗪均能降低老年高血压患者血压变异性、改善血管内皮功能,缬沙坦联合氨氯地平可能更适合于老年高血压患者.     

原发性高血压超声心动图的性别差异

目的研究高血压病人超声心动图的性别差异.方法1～2级原发性高血压病人108例,其中女性病例组(PGf) 52例,男性病例组(PGm)56例;正常血压者42例作对照,其中女性对照组(CGf) 20例,男性对照组(CGm)22例.所有受试者用Aspen电脑声像仪行超声心动图检查.检测受试者左心房和左心室结构和功能的相关指标,测值取5个心动周期测值的平均值.指标数据以(-x±s)表示,以t检验进行统计学分析.结果与PGm相比,PGf的超声心动图具有以下特点LAID、MVa较大[(37.24±5.88 vs 32.14±3.80)mm,P＜0.01和(84.18±12.13 vs 81.71±12.30)cm/s,P＜0.05];LV-MI[(119.26±22.33)g/m2vs(128.17±27.00)g/m2,P＜0.05]、EF(75.13%±6.69%vs 83.00%±3.68%,P＜0.01)、FS(41.67%±7.99%vs 49.03%±7.35%,P＜0.01)、MVe[(68.28±8.66)cm/s vs(73.73±11.46)cm/s,P＜0.05]和MVe/a(0.83±0.08 vs 0.93±0.11,P＜0.01)均较小.CGf和CGm之间的上述指标差别无显著性.结论高血压病人的超声心动图存在性别差异,女性高血压病人较男性更易出现心脏结构和功能损害.     

缬沙坦对心力衰竭家兔钙调蛋白依赖性蛋白激酶Ⅱ的影响

目的 探讨家兔慢性心力衰竭(心衰)时心肌钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)蛋白表达及活性的改变及血管紧张素Ⅱ受体拮抗剂缬沙坦长期干预的意义.方法 27只家兔随机分为3组,假手术组、心衰组和缬沙坦组各9只,通过超容量负荷联合压力负荷建立家兔心衰模型,于术后7周观察左心室结构、血液动力学的变化及CaMK Ⅱ的表达和活性的改变.结果 与假手术组比较,心衰组左室重量指数(LVMI)、左窒舒张末压显著升高(P＜0.05),左室短轴缩短率及左室射血分数明显降低(P＜0.05);与心衰组比较,缬沙坦组左室重量指数、左室舒张未压显著降低(P＜0.05),左室短轴缩短率及左室射血分数明显升高(P＜0.05);心衰组CaMK Ⅱ蛋白表达及活性显著高于假手术组(P＜0.05);缬沙坦组CaMKⅡ蛋白表达及活性显著低于心衰组(P＜0.05).结论 缬沙坦长期干预心衰,能够改善心脏舒缩功能,可能与其降低CaMK Ⅱ蛋白表达及活性有关.     

瑞舒伐他汀干预野百合碱诱导大鼠肺动脉高压的实验研究

目的 探讨他汀类药物改善内皮细胞功能、抗增殖等降脂外作用在防治肺动脉高压中的作用及可能机制.方法 雄性SD大鼠,体重(255.7±12.5)g,皮下注射野百合碱诱导大鼠形成肺动脉高压,肺动脉高压形成前后分别接受瑞舒伐他汀预防和治疗.预防实验:32只SD大鼠随机分为4组,分别为瑞舒伐他汀低剂量(2 mg·kg-1·d-1)预防组(n=8)、瑞舒伐他汀高剂量(10 mg·kg-1·d-1)预防组(n=8)、肺动脉高压4周组(n=8)和正常对照4周组(n=8),野百合碱注射当日起预防组每日予瑞舒伐他汀灌胃至第4周末,正常对照组、肺动脉高压4周组仅予生理盐水灌胃.治疗实验:52只SD大鼠随机分为4组,分别为瑞舒伐他汀低剂量(2 mg·kg-1·d-1)治疗组(n=12)、瑞舒伐他汀高剂量(10 mg·kg-1·d-1)治疗组(n=12)、肺动脉高压8周组(n=20)和正常对照8周组(n=8),野百合碱注射4周后治疗组每日予瑞舒伐他汀灌胃至第8周末,正常对照组、肺动脉高压8周组仅予生理盐水灌胃.比较各组生存率、平均肺动脉压(mPAP)、肺小动脉管壁厚度、右心室肥厚程度,比较肺小动脉增殖细胞核抗原(PCNA)、内皮型一氧化氮合酶(eNOS)蛋白表达水平,比较肺组织Rho激酶1(ROCK-1)、eNOS mRNA表达水平.结果 预防实验大鼠均存活,肺动脉高压形成之后瑞舒伐他汀治疗能改善生存率(瑞舒伐他汀低剂量治疗组、瑞舒伐他汀高剂量治疗组与肺动脉高压8周组比较为58%、75%比30%,P均＜0.05);肺动脉高压形成之前和之后瑞舒伐他汀预防和治疗均能降低mPAP[预防实验:瑞舒伐他汀低剂量预防组、瑞舒伐他汀高剂量预防组与肺动脉高压4周组比较为(27.53±3.43)mm Hg(1 mm Hg=0.133 kPa)、(25.72±1.76)mm Hg比(36.05±2.45)mm Hg,P均＜0.01;治疗实验:瑞舒伐他汀低剂量治疗组、瑞舒伐他汀高剂量治疗组与肺动脉高压8周组比较为(30.39±3.17)mm Hg、(27.59±1.99)mmHg比(40.68±1.39)mm Hg,P均＜0.01],减轻肺小动脉管壁增厚、右心室肥厚程度(P均＜0.01),下调肺小动脉平滑肌细胞PCNA表达(P均＜0.01),上调内皮细胞eNOS表达(P均＜0.05),抑制ROCK-1基因表达(P均＜0.05),有一定的剂量依赖性(P均＜0.05).结论 瑞舒伐他汀防治肺动脉高压可能是通过抑制ROCK-1基因表达,抑制肺动脉平滑肌增殖和恢复内皮细胞功能等机制来实现的.

Abstract：

Objective To investigate the effects of rosuvastatin on monocrotaline (MCT)-induced pulmonary artery hypertension in rats. Methods Pulmonary arterial hypertension was induced by a single subcutaneous injection of monocrotaline (50 mg/kg) in rats. In the prevention protocol, 32 male SpragueDawley rats were randomly divided into four groups ( n = 8 each): low-dose rosuvastatin prevention group (2 mg · kg-1 · d-1 ), high-dose rosuvastatin prevention group ( 10 mg· kg-1 · d-1 ), pulmonary arterial hypertension group, normal control group. Beginning on the MCT injection day, rats were treated with rosuvastatin by daily gavage for 4 weeks. Normal control group and pulmonary arterial hypertension group received vehicle by garage. In the treatment protocol, 52 male Sprague-Dawley rats were randomly dividedinto four groups (n = 13 each): low-dose rosuvastatin treatment group (2 mg · kg-1 · d-1), high-dose rosuvastatin treatment group( 10 mg · kg-1 · d-1), pulmonary arterial hypertension group, normal control group. Four weeks after MCT injection, rats were treated with rnsuvastatin by daily gavage for 4 weeks.Normal control group and pulmonary arterial hypertension group received vehicle by gavage. At the end of study, survival rates, mean pulmonary arterial pressure (mPAP), wall thickness of small pulmonary artery and right ventricular hypertrophy among groups were compared. The expression levels of proliferating cell nuclear antigen (P CNA) and endothelial nitricoxide synthase (eNOS) protein in small pulmonary artery,the expression levels of Rho kinase 1 ( ROCK-1 ) and eNOS mRNA in lung tissue were also detected. Results All rats in the prevention protocol survived. Rosuvastatin treatment improved survival in the treatment protocol (58%, 75% vs. 30%, P ＜0. 05 ). Rosuvastatin therapy in both preventment or treatment protocols significantly lowered mPAP [prevention protocol: ( 27.53 ± 3.43 ), ( 25.72 ± 1.76 ) vs. ( 36. 05 ± 2. 45 )mm Hg(1 mm Hg =0. 133 kPa), P ＜0.01; treatment protocol: (30. 39 ±3. 17), (27.59 ±1.99) vs.(40. 68 ± 1.39) mm Hg, P ＜0. 01], reduced thickening of small pulmonary artery wall (P ＜0. 01 ) and right ventricular hypertrophy ( P ＜ 0. 01 ). Rosuvastatin also inhibited PCNA expression of SMC ( P ＜0. 01 ), restored eNOS expression of EC ( P ＜ 0. 05) and inhibited ROCK-1 mRNA expressions in lung tissue (P ＜ 0. 05 ). Conclusions Rosuvastatin therapy reduced mPAP in monocrotaline-induced pulmonary arterial hypertension rat model and this effect is linked with inhibition of ROCK-I expression, inhibition of smooth muscle cell proliferation and restoration of endothelial cell functions.     

骨髓间充质干细胞对大鼠梗死心肌胶原重构的双重调节作用

目的 探讨骨髓间充质干细胞(MSC)对梗死心肌胶原重构的调节作用。方法 采用结扎冠状动脉前降支的方法复制大鼠心肌梗死(MI)模型,随机分为假手术组（仅穿线不结扎冠状动脉,n=8）、MI+ PBS组（结扎冠状动脉+心肌注射PBS溶液,n=8）和MI+ MSC组（结扎冠状动脉+心肌注射MSC,n=8）。通过心脏超声检查、血液动力学检查和组织学染色方法分别检测左心室射血分数(LVEF)、短轴缩短率(FS)、左心室收缩末压力(LVSP)、左心室舒张末压力(LVEDP)、左心室压最大升降速率（±dp/dtmax）、心肌梗死面积和梗死扩张指数等指标,评价MSC对大鼠心功能及心室重构的影响。同时采用免疫组化、RT-PCR、Western blot等方法,测量胶原蛋白表达情况。结果 (1)MI大鼠心室重构和心脏功能指标的检测结果：MI+ MSC组大鼠心肌梗死面积显著小于MI+ PBS组[(38.27±2.70)％比(46.20±3.17)％,t=5.386,P＜0.001],FS显著高于MI+ PBS组[(29.98±4.50)％比(23.43 ±3.34)％,t=-3.305,P=0.005],LVSP显著高于MI+ PBS组[(113.63±10.81)mm Hg(1 mm Hg=0.133 kPa)比（99.25±16.76）mm Hg,P＜0.05],LVEDP显著低于MI+PBS组[(12.10±4.28) mm Hg比(20.08±4.26) mm Hg,P＜0.05],+dp/dtmax显著高于MI+ PBS组[（4616.63±363.34）mum Hg/s比(3912.75±248.79) mm Hg/s,P＜0.05],- dp/dtmax显著高于MI+ PBS组[(4254.63±324.34) mm Hg/s比（3530.88±309.71）mm Hg/s,P＜0.05]。(2)Ⅰ型和Ⅲ型胶原蛋白表达水平的检测结果：MI+ MSC组大鼠梗死区Ⅰ型和Ⅲ型胶原蛋白表达均显著高于MI+ PBS组,而非梗死区Ⅰ型和Ⅲ型胶原蛋白表达均显著低于MI+ PBS组（P均＜0.05）。结论 MSC通过促进MI大鼠梗死区胶原蛋白修复性合成,减少非梗死区胶原蛋白沉积,从而抑制心室重构,改善心脏功能。