正常心肌超声图像纹理分析初步探讨

目的 :探讨计算机图像纹理分析方法定量描述正常心肌超声图像纹理特征的价值。方法 :对 5 2例正常人进行常规经超声心动图检查 ,分别于收缩末期和舒张末期获取左心长轴观与乳头肌水平短轴观的二维超声图像 ,对获取图像的原始数据进行存贮供脱机分析。利用计算机图像纹理共生矩阵分析法提取 3个参量 :对比度 (CON)、二次角矩 (ASM )、熵 (ENT) ,对心肌二维图像的纹理特征进行定量分析。在同一观上 ,比较收缩末期与舒张末期同一参量的变化。同时 ,分别于收缩末期与舒张末期 ,对左心长轴与乳头肌水平短轴观上的同一参量进行比较。结果 :①分别在左心长轴与短轴观上 ,参量ENT收缩末期与舒张末期比较、②收缩末期左心长轴与短轴观的同一参量比较、③舒张末期两个观上同一参量比较 ,均差异有显著性意义 (P <0 .0 5 )。结论 :计算机图像纹理分析方法能对正常心肌的二维超声图像纹理特征进行定量描述。     

超声微泡造影观测钬激光心肌激光再血管化的实验研究

目的：应用经静脉注射造影剂心肌超声微泡造影探讨激光心肌再血管化的机制及对心肌缺血的治疗效果。方法：部分钳闭犬的冠状动脉前降支形成急性心肌缺血模型，用钬激光在缺血区进行心肌激光再血管化，并在缺血前、缺血后及激光打孔后取左室短轴切面进行超声微泡造影。结果：缺血后心肌超声微泡声学密度较缺血前明显降低（Ｐ＜０．００１），心肌激光再血管化后，缺血区超声微泡声学密度较缺血时明显升高（Ｐ＜０．００１），接近正常心肌超声微泡声学密度（Ｐ＞０．０５），激光再血管化区心肌超声微泡较正常心肌提前显像。结论：心肌激光再血管化可即刻明显缓解心肌缺血，使缺血区血流灌注明显改善。经静脉注射造影剂进行心肌超声微泡造影可作为观测和评价心肌激光再血管化的可靠手段，钬激光心肌再血管化的中远期效果尚待观察。     

缺血预处理对心肌梗死大鼠心肌肝细胞生长因子表达的影响

目的 通过观察大鼠心肌梗死和远距缺血预处理后缺血心肌中肝细胞生长因子(HGF)基因表达的变化,探讨HGF在远距缺血预处理中的作用.方法　实验分组:①急性心肌梗死组;②下肢缺血预适应组:夹闭双侧股动脉后再灌注,重复4次后结扎左前降支.③肾缺血预适应组:夹闭双侧肾动脉再灌注,重复3 次后结扎左前降支.④正常对照组.用evans-TTC染色法区分梗死区和缺血区心肌,切取梗死区心肌及缺血区心肌并称重.用RT-PCR法检测大鼠缺血区心肌HGF mRNA表达.结果 除了正常对照组外其他三组缺血程度无明显差异;而肾缺血预处理组心肌梗死程度(46.18%±6.15%)、下肢缺血预处理组梗死程度(46.92%±6.69%)较急性心肌梗死组(66.44%±13.68%)相比均降低约30%(P＜0.05).肾缺血预处理组及下肢缺血预处理组4、6、12 h HGF mRNA表达较急性心梗组各时间点降低(P＜0.01).结论 提示HGF可能是远距缺血预处理减少梗死区面积的机制之一.     

急性心肌梗死大鼠心脏一氧化氮合酶表达的改变

目的 通过建立大鼠心肌梗死模型，观察急性心肌梗死对大鼠心脏内皮型一氧化氮合酶mRNA和诱导型一氧化氮合酶蛋白表达的影响。方法48只健康成年SD大鼠（体重200～250g）随机分为假手术组和缺血组，取1、2、8和24h四个不同时间点观察。采用开胸结扎冠状动脉左前降支建立心肌缺血模型，逆转录聚合酶链反应检测大鼠心肌梗死后1、2及24h三个时段缺血心肌内皮型一氧化氮合酶mRNA的表达；免疫组织化学染色检测冠状动脉结扎后8h缺血心肌诱导型一氧化氮合酶蛋白的表达。结果冠状动脉结扎后2h，缺血组大鼠缺血心肌组织内皮型一氧化氮合酶mRNA表达下降（P〈0．05），并持续至结扎后24h；结扎后24h组内皮型一氧化氮mRNA的表达与结扎后2h组相比无显著性差异（P〉0．05）。冠状动脉结扎后8h，梗死区存活心肌组织细胞诱导型一氧化氮合酶蛋白大量表达，而假手术组未见诱导型一氧化氮合酶蛋白表达。结论正常大鼠心肌组织有内皮型一氧化氮合酶基因表达，无诱导型一氧化氮合酶蛋白表达。在心肌梗死早期缺血心肌内皮型一氧化氮合酶mRNA表达减少。心肌急性缺血刺激早期诱导大鼠缺血心肌组织诱导型一氧化氮合酶蛋白大量表达。     

应变率显像对犬急性心肌缺血的评价

目的 :探讨急性缺血心肌的应变和应变率参数变化特征 ,并筛选最佳参数。方法 :12只健康杂种犬 ,分别于冠状动脉 (冠脉 )闭塞前、结扎后 15min(I15)采集图像。分别比较缺血节段 (IS)和非缺血节段 (NS)在冠脉结扎前后的参数变化 ,并对IS和NS在I15时的参数进行比较。结果 :IS的I15时与基础状态相比收缩期峰值应变率 (SSR)、舒张早期应变率 (ESR)、收缩期应变 (εS)均明显降低 (均P <0 .0 5 ) ,IS等容舒张期应变率 (IVRSR)、等容舒张期应变率与收缩期应变率之比 (IVRSR/SSR)、收缩后应变 (εPSS)在I15时明显增大 ,其中IVRSR/SSR变化最显著。NS在冠脉结扎前后各参数无明显差异。结论 :应变和应变率显像能显示急性心肌缺血各心肌节段的变化特征 ,IVRSR/SSR是反映心肌缺血的重要参数。     

Apelin-13对急性缺血诱导的大鼠心肌细胞凋亡的影响

目的研究Apelin在大鼠急性心肌缺血时的变化及外源性给予Apelin-13对大鼠急性心肌缺血损伤的保护机制。方法采用酶联免疫吸附法测定大鼠前降支结扎30、60和120min时心肌组织及血浆Apelin含量;并通过结扎大鼠前降支120min建立急性心肌缺血模型,于缺血前5min经尾静脉分别注射10、100μg/kgApelin-13,观察Apelin-13对心脏功能、心肌细胞凋亡及Bcl-2、Bax和Caspase-3表达的影响。结果心肌缺血30～60min时,大鼠心肌组织Apelin含量逐渐增高,而缺血120min时Apelin含量降至正常水平以下,血浆中Apelin含量在缺血120min内呈逐渐增高趋势。缺血前给予100μg/kgApelin-13能改善心脏功能,减少心肌细胞凋亡,抑制促凋亡基因Bax和Caspase-3的表达,并提高抗凋亡基因Bcl-2的表达。结论在心肌缺血早期心肌组织Apelin含量代偿性增高,长时间缺血时含量下降;外源性Apelin-13在急性心肌缺血中的保护作用与抑制心肌细胞凋亡有关。     

对体外反搏提高切应力抑制血管紧张素转换酶的探讨

目的　通过观察体外反搏对心肌缺血犬血管切应力和局部血管紧张素转换酶的影响 ,探讨其保护缺血心肌的机制。方法　采用冠状动脉结扎法复制犬急性心肌缺血模型 ,外加体外反搏治疗 ,观测缺血及反搏过程中头背干动脉切应力与缺血心肌、主动脉局部ANGⅡ水平、ACE活性的改变 ,分析主动脉ACE活性与头背干动脉切应力之间的关系。结果　反搏能提高缺血降低的切应力使之达正常水平 ;还能抑制缺血激活的缺血心肌与主动脉ACE活性、ANGⅡ水平 ,其中主动脉ACE活性达正常水平 ;主动脉ACE活性与头背干动脉切应力有相关关系。结论　体外反搏能抑制心血管局部肾素 血管紧张素系统 ,提高切应力 ,且二者有相关关系 ,这可能是体外反搏保护缺血心肌的作用机制之一     

缺血后适应对兔心肌急性缺血再灌注损伤的影响及其机制的研究

目的通过建立兔心肌急性缺血再灌注模型来研究缺血后适应对心脏的保护作用,同时对其机制进行探讨,从而为临床上运用缺血后适应提供理论基础。方法 60只新西兰大白兔随机分为对照组、缺血后适应组、缺血后适应+PD98059组、缺血后适应+LY294002组和假手术组,每组12只。对照组结扎左前降支30 min后立即恢复心肌灌注,持续达180 min。缺血后适应组结扎左前降支30 min后,实施间断性心肌灌注,方案为:再灌注30 s,再次结扎该血管30秒(重复4次),然后恢复心肌灌注180 min。缺血后适应+PD98059组仍结扎左前降支30 min,但在静脉推注PD98059 10 min后实施间断性心肌灌注,方案同缺血再灌注组。缺血后适应+LY294002组亦结扎左前降支30 min,在静脉推注LY294002 10 min后后实施间断性心肌灌注,方案同缺血再灌注组。结扎血管采用"二线二结"法。假手术组仅将线从左前降支周围心肌中穿过,但并不结扎。实验中持续心电监护并于术前、结扎后10 min和再灌注后120 min描记Ⅱ导心电图。实施缺血再灌注各组分别于结扎前和再灌注后60 min从股静脉取血1 mL,假手术组于穿线前和穿线后60 min同样途径取静脉血1 mL,运用ELISA法测定血清肌钙蛋白浓度。再灌注结束后取心肌行相关检查。其中每组中6只兔运用2,3,5-氯化三苯基四氮唑染色测定各组心肌坏死面积,另外六只兔取心肌运用光学显微镜和透射式电子显微镜行组织形态学检查,并提取蛋白,通过Western Blot检测Bad、Akt、P-Akt、ERK1/2和P-ERK1/2蛋白表达。结果 (1)各组兔术前性别、体重和心率无明显差异(P>0.05)。心肌缺血后心率有增快趋势,但与术前比亦无明显差异(P>0.05)。(2)血管结扎后四组心电图均可见Ⅱ导联ST段弓背上抬,再灌注后120 min四组心电图均可见ST段回落。对照组、缺血后适应+PD98059组再灌注后分别有8只和6只兔ST段下降50%,而缺血后适?     

急性缺血与L-精氨酸干预对大鼠心肌组织一氧化氮合酶基因表达的影响

目的观察急性心肌缺血状态下大鼠心脏内皮型和诱生型两种一氧化氮合酶表达和左旋精氨酸（L-Arg）对大鼠心脏组织内生型一氧化氮合酶（eNOS）基因表达的影响。方法60只健康成年SD大鼠随机分为假手术组、缺血组两组。分别取1、2、8、24h四个不同时间点。采用开胸结扎冠状动脉左前降支的方法建立心肌缺血模型,用逆转录聚合酶链式反应（RT-PCR）检测大鼠心梗后不同时间点及L-Arg（30mg&#183;kg-1&#183;次^-1&#215;3）给药后缺血心肌eNOSmRNA表达;免疫组织化学方法检测冠脉结扎后8h缺血心肌诱生型一氧化氮合酶（iNOS）蛋白。结果①冠脉结扎后2h缺血组大鼠缺血心肌组织eNOSmRNA表达下降（P〈0.05）,并持续至结扎后24h;梗死后24h组eNOS mRNA表达与结扎后2h组相比无显著性差异（P〉0.05）。②与生理盐水组相比,L-Arg静脉注射可增加冠脉结扎后大鼠缺血心肌组织细胞eNOS mRNA表达（P〈0.05）。③冠脉结扎后8h,梗死及周围区存活心肌组织细胞出现大量iNOS蛋白表达,而假手术组未见iNOS蛋白表达。结论①正常心肌组织有eNOS基因表达,无iNOS蛋白表达;心肌急性缺血刺激早期诱导大鼠缺血心肌细胞iNOS蛋白大量表达。②在心梗早期缺血心肌组织细胞eNOS基因表达减少。③L-Arg静脉用药可增加急性心肌梗死大鼠缺血心肌组织细胞eNOS mRNA表达。     

益心胶囊对家兔急性心肌缺血模型血浆及心肌组织内皮素含量的影响

目的 :通过观察益心胶囊对家兔急性心肌缺血模型血浆及心肌组织内皮素含量的影响 ,探讨其防治心肌缺血的确切作用机制。方法 :将 2 0只雄性家兔随机分为 4组 ,每组 5只 ,即模型组、假手术组、益心胶囊组、通心络组 ,以结扎家兔左冠状动脉前降支复制成急性心肌缺血模型。结果 :与模型组相比 ,益心胶囊可明显降低急性心肌缺血家兔血浆及心肌组织内皮素的含量 (P <0 .0 5 ) ,其作用与通心络胶囊大致相当 (P >0 .0 5 )。结论 :益心胶囊对心肌缺血具有一定的防治作用 ,可通过保护缺血心肌血管内皮细胞 ,降低内皮素的生成和释放 ,从而改善内皮细胞功能障碍 ,这可能是益心胶囊防治心肌缺血损伤作用机制之一。     

Differential effects of nitroprusside on ischemic and nonischemic myocardial segments demonstrated by computer-assisted two dimensional echocardiography

Two dimensional echocardiographic analysis of global and regional left ventricular function was applied in seven closed chest dogs to study the effects of nitroprusslde In ischemic heart failure. Simultaneous hemodynamic and two dimensional echocardiographic measurements were obtained sequentially: (1) in the control period, (2) after proximal occlusion of the left anterior descending coronary artery, (3) after volume loading, which increased left ventricular end-diastollc pressure to 30.3 ± 9.1 mm Hg (mean ± siandard deviation), (4) during nltroprusside infusion at 33.8 ± 29.4 jug/min and (5) after discontinuation of infusion of nitroprusside. A Simpson reconstruction using five echocardiographic short axis cross sections was used for assessment of left ventricular volumes. Regional function in short axis cross sections at different levels of the left ventricle was expressed as sectional systolic fractional area of change. Furthermore, each short axis section was subdivided into eight 45 ° segments and segmental fractional area change was automatically calculated by computer.Nitroprusside reduced global end-diastolic and end-systolic volumes (p <0.05) and increased ejection fraction (p <0.05). Differential responses to nitroprusside were observed with two dimensional echocardiography in various zones of the left ventricle. Thus, in the mitral valve level cross section above the site of coronary occlusion, normal contraction prevailed in all segments. In the mid papillary muscle level section, nitroprusside significantly enhanced function of segments that were within the left anterior descending arterial supply zone. In contrast, segments in the severely ischemic dysfunctioning zone at the low papillary muscle level did not respond to the vasodilator. These differential responses to nitroprusside in profoundly ischemic, marginally ischémie and nonlschemic myocardium were readily demonstrated with two dimensional echocardiography standardized for quantitative assessment of ventricular sequence.     

A murine model of ischemic cardiomyopathy induced by repetitive ischemia and reperfusion

BACKGROUND: Repetitive brief myocardial ischemia has been implicated in the pathogenesis of the ventricular dysfunction associated with ischemic cardiomyopathy and myocardial hibernation. In this study we examine the effects of repetitive ischemia and reperfusion (I/R) on murine myocardium. METHODS: C57/BL6 mice underwent daily 15 min left anterior descending coronary occlusions followed by reperfusion. After 3, 5, 7, 14, 21 and 28 days, echocardiographic studies were performed, and hearts of I/R and sham-operated animals were processed for histological examination. RESULTS: Histological studies showed no evidence of myocardial necrosis in the ischemic region. Quantitative assessment of collagen revealed a marked persistent interstitial deposition of collagen after seven days I/R in the anterior left ventricular wall (sham 4.6 +/- 2.0 %, I/R 21.5 +/- 6.5 %, p < 0.05). Echocardiographic studies showed persistent regional anterior wall dysfunction in I/R animals. Histological evaluation showed absence of neovessel formation. After discontinuation of the I/R protocol, fibrosis and regional ventricular dysfunction decreased within 60 days. CONCLUSIONS: Repetitive brief murine myocardial I/R induces reversible fibrotic remodeling and ventricular dysfunction, without myocardial infarction and necrosis, and may play a role in the pathogenesis of ischemic cardiomyopathy and myocardial hibernation.     

Endogenous nitric oxide and myocardial adaptation to ischemia

Ischemic myocardium does not inevitably undergo necrosis but rather can survive through downregulation of contractile function, ie, "hibernate." To study the role of endogenous NO in this adaptation, 41 enflurane-anesthetized swine were subjected to 90 minutes of moderate left anterior descending coronary artery hypoperfusion and assigned to placebo (P), to 30 mg/kg N(G)-nitro-L-arginine (L-NNA) IV to inhibit NO synthase, or to aortic constriction (AO) to match the increased left ventricular pressure observed with L-NNA. During normoperfusion, a regional myocardial external work index (WI, mm Hg. mm, sonomicrometry and micromanometry) was reduced with L-NNA (from 326+/-27 [SEM] to 250+/-19, P<0.05) but increased with AO (from 321+/-16 to 363+/-19, P<0.05 versus L-NNA). At 10 minutes of ischemia, WI was lower with L-NNA (109+/-10, P<0.05) than P (180+/-22) and AO (170+/-11) and did not change further at 85 minutes of ischemia. Relationships between WI and transmural myocardial blood flow and oxygen consumption were shifted rightward by L-NNA versus P and AO at both 10 and 85 minutes of ischemia. The maximal increment in calcium-activated external work was not different during normoperfusion among groups but was decreased during ischemia with L-NNA. L-NNA transiently increased myocardial contractile calcium sensitivity along with systemic pressure but reduced it during ongoing ischemia. The free-energy change of ATP hydrolysis after an early ischemic decrease recovered toward baseline values in all groups, and necrosis was absent after 2 (triphenyltetrazolium chloride staining) or 8 (histology) hours of reperfusion. Thus, endogenous NO contributes to hibernation by reducing oxygen consumption and preserving calcium sensitivity and contractile function without an energy cost during ischemia.     

Partial coronary stenosis is sufficient and complete reperfusion is mandatory for preconditioning the canine heart.

Repeated brief episodes of total coronary artery occlusion (i.e., severe ischemia), each separated by brief periods of reperfusion, reduce infarct size after a subsequent sustained ischemia. The importance of the intensity of ischemia during these coronary artery occlusions and the role of the following transient reflow are poorly understood. Therefore, our objective was to determine whether moderate preconditioning ischemia induced by partial coronary artery stenosis (reducing coronary flow to approximately 50% of its baseline values), with or without a brief period of total reperfusion, could precondition the canine myocardium. Dogs were randomized to receive one of three preconditioning "treatments": the R(-) group underwent 15 minutes of partial coronary stenosis without subsequent brief reperfusion (n = 8); the R(+) group underwent 15 minutes of partial coronary stenosis followed by 10 minutes of full reflow (n = 8); and the control group underwent no intervention (n = 8). All dogs then underwent 1 hour of total coronary artery occlusion and 4.5 hours of reperfusion. Both treated groups were equally and moderately ischemic during partial stenosis: myocardial blood flow in the inner two thirds of the left ventricular wall averaged 0.25 +/- 0.05 and 0.31 +/- 0.07 ml/min per gram in the R(-) and R(+) groups, respectively (p = NS). Furthermore, all three groups were equally and severely ischemic during sustained total occlusion: myocardial blood flow in the inner two thirds of the left ventricular wall averaged 0.06 +/- 0.05, 0.05 +/- 0.03, and 0.07 +/- 0.03 ml/min/g in control, R(-), and R(+) groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

缺血预适应对糖尿病大鼠再灌注心肌的保护作用

目的　通过建立大鼠缺血预适应 (IP)模型 ,探讨IP对缺血 再灌注 (I/P)糖尿病大鼠心肌的保护作用。方法　在SD大鼠腹腔内注射链佐星 (6 0mg/kg)制造糖尿病大鼠模型。 2d后 ,随机时刻测定血糖 ,将血糖≥ 11.1mmol/L定为糖尿病大鼠 2 2只 ,另外 2 2只血糖正常鼠为非糖尿病鼠。 2周后 ,麻醉大鼠 ,结扎和放松冠状动脉左前降支(LAD)复制IP和I/P模型。将 44只大鼠分为IP糖尿病大鼠组 (DIP组 )、IP非糖尿病大鼠组 (NDIP组 )、非IP糖尿病大鼠组 (DNIP组 )和非IP非糖尿病大鼠组 (NDNIP组 )各 11只。记录II导联心电图。取心脏切片染色 ,计算心肌缺血范围和心肌坏死范围。结果　各组间心肌缺血范围无显著差异 (P >0 .0 5 )。DIP组心肌坏死范围较DNIP组明显减小 (P <0 .0 1)。DNIP组室性心律失常增多 ,尤其心室颤动较其他各组显著增多 (P <0 .0 1)。结论　缺血预适应可以减轻糖尿病大鼠随后较长时间缺血 再灌注对心肌的严重损害 ,能减少心肌坏死范围和降低心室颤动的发生率。     

Effect of hyaluronidase during the early phase of acute myocardial ischemia: An ultrastructural and morphometric analysis

Hyaluronidase has been shown to reduce the size of experimental myocardial infarcts and to prevent the reduction in collateral coronary blood flow that normally occurs 15 minutes to 6 hours after coronary occlusion. To study the mechanism of action of this agent further, its effects on cardiac ultrastructure during the early phases of myocardial ischemia in the rat were examined. The left coronary artery was ligated for 1 or 3 hours in untreated and hyaluronidase-treated rats and tissue was sampled for electron microscopy. Morphometric analysis, using light microscopy on 1 μ thick specimens of tissue taken from comparable anatomic sites of the ischemic anterior left ventricular wall 3 hours after occlusion, showed that in the untreated rats 80 ± 7 percent (mean ± standard error) of myocardial cells and 48 ± 8 percent of vessels had morphologic evidence of ischemic damage, whereas in treated rats 50 ± 10 percent of myocardial cells (P < 0.05) and 24 ± 6 percent (P < 0.05) of vessels had ischemic changes. Ultrastructural studies of untreated ischemic tissue at 1 hour showed absence of glycogen, nuclear chromatin clumping, intermyofibrillar edema, I bands, intramitochondrial dense bodies and edema, endothelial blebs, gaps and swelling and decreased pinocytotic vesicles, red cell sludging and microscopic foci of hemorrhage. At 3 hours myocardial cell and vascular damage were more severe. In treated animals, more myocardial and endothelial cells from the ischemic anterior ventricular wall appeared normal on electron microscopy at both times. In these animals, myocardial cells that showed ischemic damage had nuclear, mitochondrial and myofibrillar morphologic features similar to those of untreated rats, but more glycogen granules were present than in the untreated group. Hyaluronidase may protect ischemic myocardium by preserving glycogen, and its preservation of collateral flow may be related to its reduction of ischemic damage in the microvasculature.     

Role of leukocytes in coronary vascular endothelial injury due to ischemia and reperfusion

A possible cause of the coronary endothelial injury that occurs with ischemia and reperfusion is the local accumulation of leukocytes during these events. To investigate the role of leukocytes in coronary endothelial injury, we tested the effect of leukocyte removal by filtering on coronary endothelial function in a canine model of regional myocardial ischemia and reperfusion. Blood was supplied to the left anterior descending and circumflex arteries of anesthetized dogs via an extracorporeal circulation. A 60-minute left anterior descending occlusion was followed by 120 minutes of reperfusion either with (n = 6) or without (n = 6) leukocyte filters in the extracorporeal circuit. Regional myocardial blood flow was measured with radiolabeled microspheres. Radiolabeled autologous transferrin (113mIn) and erythrocytes (99mTc) were given intravenously during reperfusion for assessment of microvascular permeability. Left anterior descending and circumflex coronary artery rings were assessed in vitro for endothelium-dependent dilation to acetylcholine, ADP, and thrombin. In unfiltered dogs, ischemia and reperfusion increased the protein leak index of ischemic myocardium 2.3-fold compared with that of nonischemic myocardium (2.3 +/- 0.5 to 5.2 +/- 1.6, p less than 0.05). In filtered dogs, there was no difference in the protein leak index of nonischemic versus ischemic myocardium (1.5 +/- 0.4 versus 1.9 +/- 0.5, p = NS). There was impaired left anterior descending coronary artery relaxation (versus circumflex) in response to endothelium-dependent vasodilators in vitro. However, relaxation was not consistently improved by leukocyte filtering. We conclude that leukocytes are responsible for the endothelial injury secondary to ischemia and reperfusion in the coronary microvasculature but have little or no effect on the endothelial injury in epicardial coronary arteries.     

环氧化酶抑制剂干预心肌缺血损伤的实验研究

目的 :评价环氧化酶抑制剂对心肌缺血损伤 （AIM）的保护作用。方法 :将成年家兔 （1.8～ 2 .5 kg） 2 4只随机分为正常对照组 （A组 ） ,单纯心肌缺血组 （B组 ） ,心肌缺血加迪克乐克组 （C组 ） ,建立 AIM模型 ,给予相应的干预 ,术后 6 h观察血液学指标 ,缺血心肌的 HE染色及 COX- 2的多克隆抗体免疫组织化学染色进行病理观察。结果 :缺血心肌中 COX- 2高度表达 ,血液学指标示术后 6 h白细胞计数在 B、C组间有明显差异 （P<0 .0 5 ） ,i NOS测定值在A、B组有显著差异 （P<0 .0 5 ） ,MDA、SOD含量在 A、B组间有显著性差异 （P<0 .0 5 ） ,C组应用非选择性环氧化酶抑制剂 ,在术后 6 h白细胞计数升高程度与 A、B组均有显著性差异 （P<0 .0 5 ） ,i NOS测定值与 B组无显著差异（P>0 .0 5 ） ,MDA、SOD含量与 B组差异显著 （P<0 .0 5 ）。结论 :缺血心肌存在显著的炎症活动 ,环氧化酶抑制剂对实验性心肌缺血损伤有保护作用。     

Myocardial segment motion during regional ischemia--regional contraction and relaxation

Several aspects of regional ischemic myocardial function determined by segment motion are discussed, based on our studies. Although global left ventricular function decreased progressively as the global severity of myocardial ischemia increased, there are several possible factors which may modify this relationship. As for the site of the ischemic area, occlusion of the left anterior descending artery resulted in a greater decrease in the left ventricular ejection fraction than occlusion of the left circumflex artery. Interaction between the ischemic myocardium and the non-ischemic myocardium may be a multifactorial phenomenon rather than simple tandem stretching. The segment length motion during acute ischemia appears to be complicated. The segment motion of the severe ischemic myocardium during systole and diastole was explained for the most part by a uniform tension-length curve which was independent of changes in the loading condition. This non-linear elastic property was fundamental to the production of segment motion asynchrony. The wall motion of the hypokinetic segment might be explained by a combination of the active change in myocardial stiffness and the non-linear elastic property of the myocardium.     

Beneficial metabolic effects of methylprednisolone sodium succinate in acute myocardial ischemia.

The metabolic and hemodynamic effects of methylprednisolone sodium succinate (40 mg/kg body weight) after acute myocardial ischemia were determined in 24 heparinized mongrel dogs. Myocardial ischemia was produced by ligation of the left anterior descending coronary artery. Catheters in the coronary sinus and the vein draining the left anterior descending coronary arterial area were used to collect blood samples from nonischemic and ischemic myocardium. Lactate, pyruvate, glucose, free fatty acids and oxygen were measured in arterial and venous blood from ischemic and nonischemic areas before and 3, 30 and 60 minutes after myocardial ischemia in animals with (Group II) and without (Group I) steroid treatment. In both Groups I and II glucose, lactate, free fatty acids, oxygen and coronary blood flow in nonischemic areas were not significantly changed, whereas glucose uptake in ischemic areas was significantly increased with myocardial ischemia and remained elevated. In Group I lactate uptake in ischemic areas became negative after coronary arterial ligation and remained so; in Group II, it increased after 30 (70%) and 60 (111%) minutes. Free fatty acid uptake in ischemic areas was reduced after myocardial ischemia in Group I, but in Group II it increased after 30 (224%) and 60 minutes (173%), and there was a concomitant increase in oxygen uptake. Pyruvate uptake in nonischemic areas decreased after 60 minutes in Group I, whereas it was reduced after 30 (68%) and 60 minutes (513%) in Group II. The changes were similar in ischemic myocardium. There were no significant changes in hemodynamic indexes. Coronary blood flow in ischemic areas decreased in Group I after myocardial ischemia and further after 30 and 60 minutes, but in Group II it increased after 30 (82%) and 60 minutes (53%). The data indicate that administration of methylprednisolone results in improved collateral blood flow into the infarcted area and a significantly improved metabolic response of ischemic myocardium. The glucocorticoid may also have a direct benefical effect on carbohydrate metabolism and cause the increased pyruvate neccesary to maintain the generation of energy-producing substrates. The results also suggest that methylprednisolone increases cell survival time and results in greater salvage of ischemic myocardium.