急性心肌梗死患者氧化损伤及抗氧化酶活性

为了评价急性心肌梗死患者氧化损伤程度及与抗氧化酶活性的关系。采用鲁米诺依赖的中性粒细胞化学发光法 ,对 6 0例急性心肌梗死患者及 6 2例年龄和性别匹配的健康对照者 ,检测外周血中性粒细胞产生氧自由基的水平 ;采用化学定量法测定血脂质过氧化终末产物———丙二醛的浓度及超氧化物歧化酶、谷胱甘肽过氧化物酶、肌酸磷酸激酶的活性。结果发现 ,急性心肌梗死组中性粒细胞化学发光峰值、积分、吞噬指数、血浆丙二醛浓度较对照组明显升高 (P均 <0 .0 0 1) ;血浆超氧化物歧化酶和谷胱甘肽过氧化物酶活性较对照组均明显降低 (P均 <0 .0 0 1) ;中性粒细胞化学发光峰值与血浆丙二醛浓度及血清肌酸磷酸激酶活性存在明显的正相关 ,前者r=0 .5 8(F =148.9,P <0 .0 1,n =12 2 ) ,相关方程为Y =- 482 4.9+144 1.2X ;后者r=0 .47(F =6 8.9,P <0 .0 1,n =12 2 ) ) ,相关方程为Y =1190 .8+0 .730 4X。中性粒细胞化学发光峰值与血浆超氧化物歧化酶活性呈显著的负相关 ,其相关系数为r=- 0 .6 3 (F =193 .2 ,P <0 .0 1,n =12 2 ) ,相关方程为Y =82 30 .0 - 78.1X ,。此结果提示 ,急性心肌梗死患者体内存在着明显的氧化损伤 ,同时也导致体内抗氧化能力减弱 ,氧化损伤的程度可能与心肌梗死的范围有关。     

维生素C对急性心肌梗死患者氧化代谢的影响

为评价抗氧化剂维生素Ｃ对急性心肌梗死患者氧化代谢指标的影响。将３０例急性心肌梗死患者随机分成常规治疗疗组和维生素Ｃ治疗组,分别予以急性心肌梗死的常规治疗和急性心肌梗死的常规治疗基础上加用维生素Ｃ,每天２克,静脉滴注,共用７天。分别测定两组患者治疗前,治疗第３天及治疗第７天的中性粒细胞化学发光参数,血清肌酸磷酸激酶活性和血浆丙二醛浓度等氧化损伤指标,并测定血浆谷胱甘肽过氧化物酶和超氧化物歧化酶活性抗     

增龄对小鼠心肌氧自由基浓度、超氧化物歧化酶活性及丙二醛含量的影响

以心肌氧自由基(OFR)浓度、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量为指标,观察了增龄对心肌自由基反应的影响。结果表明:(1)心肌OFR浓度随增龄上升,至13、17月龄时达到显著水平(P<0.05):(2)心肌SOD活性随增龄下降,至13、17月龄时达到显著水平(P<0.05);(3)心肌MDA含量随增龄而增加,至13、17月龄时增加显著(P<0.05,P<0.01);(4)老年小鼠(17月龄)心肌SOD活性与OFR浓度呈高度显著的负相关关系(P<0.01),而MDA含量与OFR浓度呈显著的正相关关系(P<0.05)。上述结果表明,随增龄心肌自由基损伤性因素(OFR—MDA)增加,而保护性因素(SOD)减弱,这可能是老化心脏在结构、功能、代谢方面发生衰退的原因之一。     

硫化氢对大鼠压力负荷性心力衰竭发展过程中氧化应激的影响

目的腹主动脉缩窄大鼠心力衰竭(心衰)模型通过腹腔给予硫化氢(H_2S)供体硫氢化钠(NaHS),观察压力负荷性心衰形成过程中H_2S对氧化应激状态的影响。方法 SD大鼠63只,随机分为对照组、心衰组、NaHS组,每组21只。各组均在第4、8、12周时,各取7只大鼠取血及心脏进行检测。结果心衰组4、8、12周血清H_2S含量、心肌H_2S合酶活性均较对照组明显降低,NaHS组4、8、12周血清H_2S含量较心衰组明显升高,心肌H_2S合酶活性较心衰组略有增高,但仍低于对照组。与对照组比较,心衰组4、8、12周血清MDA含量明显升高,超氧化物歧化酶(SOD)活性明显降低;与心衰组比较,NaHS组SOD活性上升,MDA含量下降,其中MDA含量在8、12周时下降明显,但仍明显高于对照组;SOD在12周时明显增高,但仍明显低于对照组。与心衰组比较,NaHS组4、8、12周血清氧化型低密度脂蛋白含量明显降低,但8、12周时仍明显高于对照组。结论外源性给予H_2S供体NaHS能改善压力负荷引起的心衰大鼠体内和心肌内的氧化应激状态,可能是H_2S心脏保护作用机制之一。     

缬沙坦对阿霉素致心肌损伤大鼠心肌结构改变的影响

目的研究缬沙坦对阿霉素(adriamycin,ADR)致大鼠心功能损伤及心肌结构改变的保护作用。方法大鼠腹腔注射ADR(20mg/kg)造成心脏损伤模型。观察缬沙坦对ADR致心肌损伤大鼠体重、左心室功能、血清超氧化物歧化酶(SOD)、肌酸激酶同工酶(CK-MB)和丙二醛(MDA)的变化。结果①ADR组大鼠血清CK-MB活性和MDA含量及左心室舒张末期压(LVEDP)较对照组明显增加;血清SOD、左心室收缩压(LVSP)、左心室等容收缩期压力变化速率最大值( dp/dtmax)显著降低;电镜下可见,ADR组大鼠心肌细胞严重损伤,心肌纤维溶解,肌质网扩张空泡化,线粒体水肿,嵴断裂。②缬沙坦 阿霉素组大鼠CK-MB活性和MDA含量及LVEDP显著降低;SOD和 dp/dtmax显著升高;电镜下可见,局灶性的心肌细胞肌浆溶解;散在性的心肌细胞空泡样变。结论缬沙坦可减轻自由基对心脏的损伤,改善ADR致心肌损伤的毒性反应,并能有效地防治心功能损伤。     

Persistence of oxidative stress after heart transplantation: a comparative study of patients with heart transplant versus chronic stable heart failure

INTRODUCTION AND OBJECTIVE: Chronic heart failure (CHF) is associated with oxidative stress. Heart transplantation, an important therapeutic alternative in these patients, could reduce oxidative stress by improving cardiac function. Our aim was to evaluate post-heart transplantation oxidative stress. PATIENTS AND METHOD: We studied three experimental groups: a) heart transplant recipients without evidence of rejection (n = 11); b) NYHA class III CHF patients (n = 19), and c) healthy control subjects (n = 14). Oxidative stress was assessed by measuring plasma malondialdehyde levels (MDA), and determining the enzymatic activities of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD). RESULTS: The demographic characteristics of the three groups were similar. Mean time from transplantation was 20.0 4.8 months. Mean MDA plasma levels in heart transplantation and CHF patients were significantly higher than in normal subjects (3.35 0.8; 3.27 1.7 y 0.9 0.3 microM, respectively). GSH-Px activity increased after transplantation compared to control subjects (0.40 0.06 and 0.33 0.05 U/g Hb, respectively), but not the CHF group. A significant decrease in SOD activity was found in the heart transplant vs. CHF group (0.44 0.1 vs. 0.87 0.6 U/mg Hb). There were no differences in CAT values between heart transplant and CHF patients. CONCLUSION: These findings demonstrated the presence of permanent oxidative stress in patients who have undergone heart transplantation, characterized by an increase in MDA and a decrease in SOD activity, despite an increase in GSH-Px activity.     

Release of endothelin from cultured bovine endothelial cells.

Recently discovered endothelin is a powerful vasoconstrictor of vascular smooth muscle in vitro, which also profoundly affects the mechanical function of the heart. An increased level of plasma endothelin in patients with acute myocardial infarction suggests the enhanced release of endothelin from vascular endothelium under pathophysiological conditions of the heart. The reperfusion of ischemic myocardium is associated with the activation of polymorphonuclear leukocytes (PMN) generating oxygen-derived free radicals (OFR), as well as, enhanced responsiveness of myocardial alpha 1-adrenergic receptor. Both OFR and catecholamines are implicated in the modulation of release of endothelium-derived peptides.     

Increased oxygen free radical activity in patients on cardiopulmonary bypass undergoing aortocoronary bypass surgery.

Cardiac dysfunction after cardiopulmonary bypass (CPB) has been reported by various investigators. Oxygen free radicals have been shown to depress cardiac function and contractility. To evaluate the possible role of oxygen free radicals (OFR) in post-pump cardiac dysfunction, measurements of cardiac function, OFR producing activity of polymorphonuclear (PMN) leukocytes (PMN chemiluminescence) and malondialdehyde (MDA), a lipid peroxidation product, in blood were made at induction of anesthesia (T1), before cross clamping of the aorta (T2), after closure of the chest (T3), and 24 hours postoperatively (T4) in 21 patients undergoing aortocoronary bypass surgery. The total OFR-derived chemiluminescence at T1, T2, T3, and T4 was 1590 +/- 156, 3169 +/- 338, 1972 +/- 214, and 2614 +/- 366 mv.min.10(6) PMN-1, respectively. Superoxide dismutase (SOD)-inhibitable chemiluminescence at T1, T2, T3, and T4 was 1214 +/- 129, 2674 +/- 328, 1752 +/- 215, and 2139 +/- 292 mv.min.10(6) PMN-1, respectively. Superoxide anion at T1, T2, T3, and T4 was 0.99 +/- 0.14, 1.30 +/- 0.17, 1.07 +/- 0.14, and 1.19 +/- 0.12 nmol.10(6) PMN-1.30 min-1, respectively. Blood MDA at T1, T2, T3, and T4 was 0.17 +/- 0.02, 0.25 +/- 0.03, 0.20 +/- 0.03, and 0.23 +/- 0.02 nmol/ml, respectively. OFR-derived and SOD inhibitable chemiluminescence, superoxide anion, and blood MDA increased significantly during CPB and postoperatively. There were decreases in the blood pressure and stroke volume, and increases in the central venous pressure, capillary wedge pressure, and heart rate during CPB and postoperatively. Cardiac output remained unchanged during this procedure. There was leukopenia during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen-derived free radicals induced cellular injury in superior mesenteric artery occlusion shock: protective effect of superoxide dismutase

This study was designed to investigate the beneficial effect of administration of exogenous superoxide dismutase (SOD) on the inhibition of lipid peroxidation and cellular protection during superior mesenteric artery occlusion shock in rats. Wistar rats were anesthetized with sodium pentobarbital (30 mg/kg body weight), and the superior mesenteric artery occlusion shock model was induced by clamping the superior mesenteric artery for a 60-min period and then releasing the arterial clamp. The following parameters were determined: 1) average arterial blood pressure; 2) survival rate and mean survival time (MST); 3) activities of plasma lysosomal enzymes beta-glucuronidase (beta-G) and acid phosphatase (ACP); and 4) the contents of malondialdehyde (MDA) in visceral tissues. The SOD group received 15,000 U/kg body weight SOD intra-arterially 15 min before release of the clamp. The saline group received intra-arterially a corresponding volume of saline given to the SOD group. The superior mesenteric artery of rats in the control group was not clamped. In the saline group, the contents of MDA presented significant increases (P less than 0.05) in bowel and heart tissues at 1 hr after release of the clamp and showed more significant increases (P less than 0.01-0.05) in bowel, heart, liver, and lung tissues at 2 hr after release of the clamp, when compared with control values. However, the contents of MDA in bowel and heart tissues in the SOD group showed significant decreases (P less than 0.05) compared with values in the saline group and had insignificant changes (P greater than 0.05) compared with control values at 1 hr after release of the clamp. The contents of MDA in bowel, heart, and lung tissues in the SOD group were still lower than those in the saline group (P less than 0.05) at 2 hr after release of the clamp, although they were higher than those in the control group (P less than 0.05). The activities of plasma lysosomal enzymes in the SOD group were much lower than those in the saline group at 1 and 2 hr after release of the clamp. The mean survival time of shocked animals was prolonged when treated with SOD. These results suggested that administration of exogenous SOD may protect cells against lipid peroxidation injury mediated by oxygen-derived free radicals, depress the release of lysosomal enzymes, and prolong the mean survival time of shocked animals.     

依达拉奉治疗病毒性心肌炎心力衰竭的研究

目的 研究依达拉奉治疗病毒性心肌炎心力衰竭的效果及其抗氧自由基的作用.方法 病毒性心肌炎患者41例随机分为两组.观察组给予依达拉奉治疗,对照组给予辅酶Q10治疗,观察用药前后患者心功能分级(NYHA分级),左室射血分数(LVEF)和脑利钠肽(BNP)指标变化.通过检测治疗前后血清超氧化物歧化酶(SOD)、丙二醛(MDA)了解依达拉奉的抗氧化作用.结果 治疗后观察组NYHA分级(2.1±0.2)级,较对照组(2.3±0.3)级下降(P<0.05),LVEF(40.3±4.3)%较对照组(37.9±5.9)%上升(P<0.05),BNP(741±33)ng/L较对照组(1 273±38)ng/L下降(P<0.01).依达拉奉组患者SOD活性上升高于对照组(P<0.01); MDA下降高于对照组(P<0.05).结论 依达拉奉治疗病毒性心肌炎心力衰竭临床疗效满意.     

Hemodynamic changes and renal plasma flow in early heart failure: implications for renin,aldosterone, norepinephrine,atrial natriuretic peptide and prostacyclin

Summary Vasoconstrictory and vasodilatory hormone systems may be important in the regulation of peripheral vascular resistance and renal hemodynamics in the carly phase of heart failure. The activity of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous activity, and, as possible counterregulating systems, the activity of prostacyclin and atrial natriuretic peptide (ANP) were studied in 6 conscious dogs during the first 4 days of congestive heart failure in relation to hemodynamic changes and renal plasma flow. Congestive heart failure was induced by rapid right ventricular pacing, which caused a considerable decrease of cardiac output (–38%; p<0.05), oxygen saturation of the mixed venous blood (–13%; p<0.05), and mean arterial pressure (–24 mm Hg; p<0.05) on the 4th day. Mean pulmonary arterial pressure and mean pulmonary capillary wedge pressure increased (+4 mm Hg; p<0.05 and +7 mm Hg, respectively; p<0.05). Renal plasma flow was slightly reduced (N.S.), renal vascular resistance did not change. Peripheral vascular resistance showed a significant increase only on the 1st day. Sympathetic nervous activity was stimulated (from 175±31 pg/ml to 391±100 pg/ml; p<0.05), while plasma renin concentration was significantly suppressed on the 4th day (from 3.3±0.4 ngAI/ml/h to 1.9±0.5 ngAI/ml/h; p<0.05), and plasma aldosterone levels were decreased (from 108±12 pg/ml to 76±12 pg/ml; p<0.05). ANP increased 3-fold (p<0.05) and 6-keto-prostaglandin F1 alpha increased in 4 out of 6 dogs. Since ANP is known to inhibit renin release and aldosteronc production, the suppressed RAAS may be an effect of the highly elevated plasma levels of ANP in the early phase of heart failure. The depressor systems such as ANP and prostacyclin may balance the stimulated sympathetic system, resulting in no change of renal blood flow and renal vascular resistance and preventing a considerable increase of peripheral vascular resistance.Supported by the Deutsche Forschungsgemeinschaft     

Can fructose 1–6 diphosphate (FDP) be an additive to ECC during cardiac surgery?

Extracorporeal circulation (ECC) is the basic support system for patients undergoing cardiac surgery, during which oxygen free radicals (OFR) are generated and involved in ischemic reperfusion injury. This study was done to investigate the protective function of fructose 1–6 diphosphate (FDP) with fresh human red blood cells (RBCs) as a model in vitro and presumably during ECC and cardiac surgery. RBCs were exposed to OFR and mechanical trauma, and then FDP was incubated to RBCs alone and then to RBCs plus OFR. Malondialdehyde (MDA) and red cell filtration rate (RFR) were measured. There was a significant decrease of MDA in RBCs exposed to FDP plus OFR (p<0.01,p<0.001) and an increase of RFR (p<0.05,p<0.001) when compared with RBCs alone or with OFR. A negative correlation was found between MDA and RFR. These results suggest that the protective action of FDP is promising as an additive during ECC in man so as to improve the blood cell rheology and the microcirculation in cardiac surgery with ECC.     

Effects of platelet-activating factor on cardiovascular function,oxygen free radical status,and blood chemistry

Platelet-activating factor (PAF) is released in numerous clinical situations. PAF primes or directly activates polymorphonuclear (PMN) leukocytes, which results in release of oxyradicals (O ₂ ^– , H₂O₂, .OH) and hypochlorous acid (HOCl). The authors investigated the effects of PAF (1 µg/kg IV) in the absence and in the presence of antioxidants (superoxide dismutase [SOD], catalase [CAT], dimethylthiourea [DMTU]) and methionine, a quencher of HOCl, on cardiac function and contractility; blood lactate, gases, and pH levels; serum creatine kinase activity (CK); chemiluminescent activity of PMN leukocytes; and cardiac tissue malondialdehyde (MDA) in anesthetized dogs. Hemodynamic measurements and collection of blood samples for various biochemical measurements were made before and at various intervals up to two hours after PAF administration in the presence and absence of various antioxidants.PAF produced a decrease in indices of cardiac function and contractility and an increase in systemic and pulmonary vascular resistance. There were decreases in the blood pH and PMN leukocyte chemiluminescence and increases in blood lactate, serum CK activity, and tissue MDA content. SOD plus catalase or DMTU plus methionine reduced the effects of PAF on cardiac function and contractility, blood lactate and pH, serum CK, and cardiac tissue MDA. The antioxidants only partially antagonized the deleterious effects of PAF. The combination of SOD + CAT was superior to that of DMTU + methionine in reducing the deleterious effects of PAF.These results suggest that PAF-induced depression of cardiac function and contractility, and the increase in systemic and pulmonary vascular resistance, may be partly mediated by the release of oxyradicals and HOCl from PMN leukocytes. Antioxidants may be beneficial in reducing the deleterious effects of PAF on the cardiovascular system.     

成年糖尿病大鼠重要器官组织SOD、MDA含量变化

目的研究成年糖尿病大鼠重要器官组织超氧化物歧化酶(SOD)、丙二醛(MDA)含量变化。方法测定对照组(C)、胰岛素治疗糖尿病组(ID)、糖尿病组(D)大鼠重要器官组织SOD活力、MDA含量。结果大鼠心、肝、肺、脾、胰组织D组与C组比较,SOD活力下降(P<0.05、P<0.01),肝、脾、胰组织ID组与C组比较,SOD活力下降(P<0.05),肺D组与ID组比较,ID组SOD活力提高(P<0.05),肾组织SOD活力无变化;D组心、肺、胰、脾组织中MDA含量升高,与C组比较,有显著差异(P<0.05,P<0.01);ID组心、胰、脾组织MDA含量与C组比较有显著差异(P<0.05,P<0.01),心、脾组织MDA含量ID组与D组比较,有显著差异(P<0.05,P<0.01),肝、肾组织MDA含量无变化。结论糖尿病大鼠重要器官组织抗氧化酶水平低下,经胰岛素治疗后,有提高趋势。     

冠心病介入术后氧自由基的生成及其对脂质过氧化和纤溶的影响

目的:探讨冠心病介入治疗术后氧自由基的生成及其对患者体内脂质过氧化和纤溶状况的影响。方法:48例接受经皮冠脉介入治疗(PCI)术的冠心病患者分别于术前,术后即刻、30 min、1 h、24 h和一周采用ELISA法测定血浆中丙二醛、D-二聚体、血管假性血友病因子相关抗原(vWF Ag)浓度。结果:PCI术后短时间内(0～24 h)血浆中丙二醛、D-二聚体,vWFAg水平均明显升高(P<0．05)。结论:PCI术后短时间内即有大量的氧自由基生成,凝血系统的激活和继发性纤溶功能亢进。     

Relationship of Oxidative Stress and Fibrinolysis in Diabetes Mellitus

This study attempted to verify the existence of a relationship between oxidative stress documented by malondialdehyde (MDA) and superoxide dismutase (SOD) and fibrinolysis analysed by tissue plasminogen activator (tPA) and its inhibitor (PAI-1) in diabetes mellitus. Forty-seven patients with Type 1 (n = 27) and Type 2 (n = 20) diabetes were examined together with 20 non-diabetic controls. The following were analysed: plasma MDA concentration, SOD activity in erythrocytes, tPA activity and antigen, PAI-1 activity and antigen, fasting blood glucose, fructosamine, glycated haemoglobin (HbA_lc), and urine albumin. SOD activity was decreased in patients with diabetes. This contrasted with an increased plasma MDA concentration especially in Type 2 diabetes as compared with Type 1 or healthy persons (p < 0.001). tPA activity was increased in both groups of patients with diabetes as compared to healthy persons (p < 0.001), PAI-1 activity was higher in Type 2 diabetes with vascular changes than in the remaining subgroups (p < 0.001). Multivariate analysis revealed a significant positive relationship between plasma MDA concentrations and PAI-1 antigen (r = 0.53, p < 0.001) and a negative relationship between SOD and tPA activities (r = −0.53, p < 0.01). We conclude that oxidative stress may modulate fibrinolytic properties in diabetes mellitus.     

Response of atrial natriuretic factor to acute and chronic increases of atrial pressures in experimental heart failure in dogs. Role of changes in heart rate, atrial dimension, and cardiac tissue concentration.

BACKGROUND. This study evaluated the role of changes in heart rate, atrial pressure, volume, and cardiac tissue atrial natriuretic factor (ANF) concentration in the modulation of plasma ANF concentration in a model of pacing-induced heart failure. METHODS AND RESULTS. The effects of acute right ventricular pacing (250 beats/min), acute volume expansion (35 ml/min), and volume expansion after 1 week of right ventricular pacing on plasma ANF concentration were compared in eight dogs (group 1). As shown during right ventricular pacing previously, volume expansion produced significant increases in cardiac filling pressures and left atrial volume. Right ventricular pacing and volume expansion produced similar increments in plasma ANF concentration: from 32 +/- 12 to 168 +/- 153 pg/ml (p less than 0.05) and from 32 +/- 9 to 137 +/- 113 pg/ml (p less than 0.05), respectively. When pacing was initiated after volume expansion, plasma ANF concentration increased further to 462 +/- 295 pg/ml (p less than 0.05) despite little change in filling pressures and left atrial volume. With repeated volume expansion after 1 week of pacing, there were no significant further increases in left atrial volume and plasma ANF concentrations (from 332 +/- 121 to 407 +/- 113 pg/ml) despite significant increases in filling pressures. Atrial and ventricular tissue samples were also obtained from 21 dogs paced to severe heart failure (group 2) and from 14 normal dogs (controls). In all groups, atrial ANF was higher than ventricular ANF concentration. At 1 week (group 1), left atrial appendage ANF concentration (6.2 +/- 2.5 versus 16.1 +/- 10.3 ng/mg) was reduced, whereas left ventricular free wall ANF concentration (0.62 +/- 0.31 versus 0.24 +/- 0.16 pg/mg) was increased compared with that of controls (both p less than 0.001). At severe heart failure (group 2), atrial ANF remained low, whereas ventricular ANF concentration was similar to that of the controls. CONCLUSIONS. These data indicate that in pacing-induced heart failure, changes in heart rate, atrial pressure, and volume all contribute to the increased plasma ANF concentration. However, by 1 week (early heart failure), ANF release is attenuated, perhaps because of the inability of the atria to be stretched further and because of reduced atrial ANF concentration. In addition, the ventricle may be an additional source of ANF.     

单硝酸异山梨酯对慢性心力衰竭小鼠心功能的影响及作用机理

目的探讨单硝酸异山梨酯(ISMN)对慢性心衰(CHF)小鼠心功能的影响及其可能的作用机理。方法100只C57BL/6J品系雄性小鼠随机分为假手术组、模型组、ISMN低剂量组、中剂量组和高剂量组。构建CHF小鼠模型后,ISMN低剂量组、中剂量组和高剂量组小鼠每天分别给予50 mg、200 mg、400 mg的ISMN灌胃,假手术组和模型组小鼠给予等体积的生理盐水灌胃,持续给药6周。采用多普勒超声心电图检测各组小鼠心功能指标LVESD、LVEDD、LVEF、LVFS的变化;采用HE染色检查小鼠心肌组织病理学改变;采用全自动血液流变测试仪检测小鼠全血高切粘度、全血低切粘度、血浆粘度和红细胞聚集指数;采用NOS、SOD、MDA和GSH-Px检测试剂盒测定小鼠血清NOS、SOD、MDA和GSHPx水平。结果模型组小鼠LVESD和LVEDD较假手术组显著升高,LVEF和LVFS则显著降低;与模型组比较,ISMN各剂量组小鼠LVESD和LVEDD呈剂量依赖性下降,LVEF和LVFS呈剂量依赖性上调,差异有统计学意义(P<0.05);HE染色显示,与假手术组比较,模型组小鼠心肌细胞肥大且呈局灶性坏死,肌纤维间隙增加,并伴有大量炎性细胞浸润;与模型组比较,ISMN各剂量组小鼠心肌细胞肥大和坏死程度依次降低,肌纤维排列趋向规整,炎性浸润程度明显降低,且呈显著的剂量依赖性,差异有统计学意义(P<0.05);模型组小鼠全血高切粘度、全血低切粘度、血浆粘度、红细胞聚集指数、MDA血清含量较假手术组显著升高,SOD、GSH-Px和NOS的血清含量则显著下降;与模型组比较,ISMN各剂量组小鼠全血高切粘度、全血低切粘度、血浆粘度、红细胞聚集指数、MDA血清含量均呈剂量依赖性下降,SOD、GSH-Px和NOS血清含量则呈剂量依赖性升高,差异均有统计学意义(P<0.05)。结论ISMN可通过抑制细胞氧化应激和炎性反应水平,改善CHF小鼠微循环障碍和心功能损伤,值得临床中大力推广。     

cAMP反应元件结合蛋白在高糖所致内皮细胞损伤中的作用

目的探讨cAMP反应元件结合蛋白(CREB)在高糖致内皮细胞损伤中的作用。方法建立高糖诱导的血管内皮细胞损伤模型,将内皮细胞ECV304分为对照组、高糖组、转染PCI组、转染PCI+高糖组、转染PCI-CREB组和转染PCI-CREB+高糖组,采用MTT法检测细胞存活率,流式细胞仪检测细胞凋亡率,硫代巴比妥酸法检测丙二醛(MDA)含量,黄嘌呤氧化酶法检测细胞超氧化物歧化酶(SOD)活性。结果转染PCI-CREB组和转染PCI组内皮细胞存活率、SOD活性、MDA含量和细胞凋亡率与对照组相比差异无统计学意义(P>0.05);与对照组相比,高糖组内皮细胞存活率和SOD活性明显下降,而MDA含量和细胞凋亡率明显增加(P<0.05);转染PCI+高糖组内皮细胞存活率、SOD活性、MDA含量和细胞凋亡率与高糖组相比差异无统计学意义(P>0.05);与高糖组相比,转染PCI-CREB+高糖组细胞存活率和SOD活性明显高于高糖组(P<0.05),而MDA含量和细胞凋亡率明显低于高糖组(P<0.05)。结论过表达CREB对高糖诱导的内皮细胞损伤具有保护作用。     

连续灌注不停跳心脏移植对供心的保护作用

目的 通过建立大鼠同种异位供心停跳心脏移植模型与连续血液灌注供心不停跳心脏移植模型,探讨连续灌注不停跳心脏移植对供心的影响.方法 建立大鼠同种异位连续灌注心脏不停跳心脏移植模型（不停跳移植组）和改良Heron法建立大鼠异位心脏移植模型（停跳移植组）.移植成功后2h检测受体外周血肌酸激酶同工酶（CK-MB）和心肌肌钙蛋白I（cTnI）含量,测定供心心肌脂质过氧化终产物丙二醛（MDA）、过氧化物歧化酶（SOD）含量,电镜观察心肌结构变化,并观察心肌凋亡情况.结果 连续灌注心脏不停跳移植组受体外周血CK-MB及cTnI含量低于停跳移植组,差异有统计学意义（P＜0.05）.与停跳移植组比较,不停跳移植组心肌MDA含量相对较少,SOD含量相对较多,心肌细胞凋亡指数较小,差异均有统计学意义（P＜0.05）.不停跳移植组心肌线粒体等结构损伤相对较轻.结论 心脏不停跳技术能有效减轻心脏移植供心的脂质过氧化反应,保护心肌线粒体,抑制心肌细胞凋亡,可减轻心脏移植供心的再灌注损伤.