冠脉原位血栓大鼠血浆vWF水平的变化意义

目的 探讨冠脉原位血栓大鼠血浆血管性假血友病因子（vWF）水平的变化及意义。方法 将雄性SPF级SD大鼠78只,随机分为模型组（n=36）、假手术组（n=36）和正常对照组（n=6）,模型组与假手术组按术后1 h,1,7,14,21,28 d各分6只。模型组经主动脉根部注入月桂酸钠,假手术组注入生理盐水,正常对照组不做任何处理。将心肌切片经HE与纤维素快速染色后,观察冠脉微血管原位血栓的形成。用ELISA检测血浆中vWF的水平。用超声心动图检查心脏的结构与功能。结果 模型组大鼠心肌微血管中,可见血小板纤维蛋白血栓,有原位血栓形成的微血管数量显著增加（P<0.01）;血浆中vWF的水平明显升高(P<0.05);心脏扩大,心功能降低;而假手术组和正常对照组未见明显变化。 结论 冠脉微血管内皮细胞损伤释放的vWF可介导冠脉微血管内以血小板纤维蛋白沉积为主的原位血栓形成。     

缺血预处理时心肌细胞三磷酸腺苷含量和超微结构变化

采用生物发光技术，分别测定缺血预处理和对照组再灌注60min时心肌细胞三磷酸腺苷（ATP）含量，同时留取心肌标本行光镜和电镜观察，探讨缺血预处理保护心肌的作用机理。结果表明：①缺血预处理组心肌细胞ATP含量明显高于对照组，差异显著（P＜0．05）；②缺血预处理组光镜、电镜所见心肌损伤均明显比对照组轻。提示：缺血预处理可以减少心肌细胞能量消耗，保护线粒体的结构和功能，从而对缺血心肌具有一定保护作用。     

心肌组织TF表达对兔无复流作用的实验研究

目的：观察无复流区心肌组织因子（TF）mRNA表达,探讨心肌组织局部TF激活的外源凝血途径在兔实验性无复流（NR）中的作用。方法：将13只新西兰大白兔随机分为TF组（n=10）和对照组（n=3）：均予结扎回旋支（LCX）中段120min,再灌注60min,建立急性心肌梗死（AMI）后再灌注NR模型。在再灌注末,从左心房注入6％硫磺素S1ml／kg使复流区着色,NR区不着色;再于原位重新结扎LCX,TF组从左心房注入Evan’s蓝,使结扎区外着蓝色,缺血区不着蓝色,对照组不予Evan’s蓝。采用RT-PCR法检测TF组NR区、缺血区和正常区心肌组织TF mRNA表达;对照组光镜下观察不同心肌组织血栓形成和心肌损伤情况。结果：TF组NR区TF mRNA表达明显高于缺血区和正常区心肌组织（0．488±0．190对0．310±0．148对0．200±0．091,P〈0．05）,但缺血区和正常区心肌组织TFmRNA表达无统计学差异（P〉0．05）。对照组NR区心肌组织可见较多血栓形成,心肌损伤程度明显加重。结论：NR区心肌组织局部TF表达增强,并在NR发病过程中起到重要促进作用。     

三种停搏液心肌保护实验研究中心肌结构观察

目的　观察三种方法对体外循环犬心肌在缺血前、缺血中及再灌注后的心肌结构变化,以评价其心肌保护效果。方法　１５ 只犬随机分成３ 组（ ｎ＝ ５） 分别灌注三种停搏液。在心肌缺血前,缺血后１２０ ｍｉｎ 及再灌注３０ ｍｉｎ 于右心室相同部位取心肌作光镜及电镜观察。电镜采用线粒体计数作半定量分析。结果　３ 组在缺血前、中及再灌注后光镜结构无明显改变。电镜结构线粒体半定量分析显示在缺血１２０ ｍｉｎ 及再灌注３０ ｍｉｎ 冷血停搏液间断顺灌组及血利钾停搏液及双向性灌注组心肌线粒体损伤轻于冷晶体停搏液组（Ｐ＜０－０５）。前两组之间无显著差异（ Ｐ＞ ０－０５）。结论三种方法均能提供较好的心肌保护,血利钾停搏液及双向性灌注组心肌保护效果同等于冷血停搏液间断顺灌组,优于冷晶体停搏液间断顺灌组。     

缺血预适应后离体鼠心生理功能及形态学改变的实验观察

本实验旨在了解离体鼠心缺血预适应后心肌收缩功能和形态学的改变。方法：通过测定LVDP、dp／dt。RPP等心功能指标，以及形态学评级来评价单纯全心缺血30分钟并再灌注60分钟（B组，n=10）与缺血预适应（C组，n=11）对心肌收缩功能和心肌细胞超微结构的影响。结果：复灌30分钟时缺血预适应组的LVDP、dp／dt、RPP恢复百分率高于对照组（P＜0.05。电镜下心肌细胞的损伤评级缺血预适应组低于对照组（P＜0．05）．结论：缺血预适应能加强离体鼠心全心缺血后心肌收缩功能的恢复，减轻心肌细胞的损伤。     

心肌组织TF表达对兔无复流作用的实验研究

目的：观察无复流区心肌组织因子（TF）mRNA表达,探讨心肌组织局部TF激活的外源凝血途径在兔实验性无复流（NR）中的作用。方法：将13只新西兰大白兔随机分为TF组（n=10）和对照组（n=3）：均予结扎回旋支（LCX）中段120min,再灌注60min,建立急性心肌梗死（AMI）后再灌注NR模型。在再灌注末,从左心房注入6％硫磺素S1ml／kg使复流区着色,NR区不着色;再于原位重新结扎LCX,TF组从左心房注入Evan’s蓝,使结扎区外着蓝色,缺血区不着蓝色,对照组不予Evan’s蓝。采用RT-PCR法检测TF组NR区、缺血区和正常区心肌组织TF mRNA表达;对照组光镜下观察不同心肌组织血栓形成和心肌损伤情况。结果：TF组NR区TF mRNA表达明显高于缺血区和正常区心肌组织（0．488&#177;0．190对0．310&#177;0．148对0．200&#177;0．091,P〈0．05）,但缺血区和正常区心肌组织TFmRNA表达无统计学差异（P〉0．05）。对照组NR区心肌组织可见较多血栓形成,心肌损伤程度明显加重。结论：NR区心肌组织局部TF表达增强,并在NR发病过程中起到重要促进作用。     

经冠状动脉移植自体BM-MNCs治疗猪急性心肌梗死的作用

目的探讨冠状动脉内移植自体骨髓单个核细胞（BM—MNCs）治疗猪急性心肌梗死的有效性。方法实验动物分为冠脉内移植MNCs组（n=6）及冠脉对照组（n=5）。冠脉内移植BM—MNCs后4周观察移植细胞归巢情况、小血管密度、心功能变化。结果冠脉内MNCs移植后4周,心肌细胞间可见发蓝色荧光的移植细胞,散在分布,心肌细胞间有较多新生毛细血管并可见新生的心肌样细胞。移植组小血管密度、左室射血分数（LVEF）及短轴缩短率（FS）明显高于对照组（P〈0．01）,左室舒张末期内径（LVEDd）低于对照组（P〈0．05）。结论经冠脉移植的BM—MNCs可归巢到宿主心肌,有促进缺血心肌血管新生、改善左室收缩功能、减轻心室重构的作用。     

间隙连接通道蛋白不均一降解对心肌传导速度影响的研究

目的探讨急性短时间心肌缺血时连接蛋白43（Cx43）的降解对心肌电传导速度的影响。方法16只犬随机分为正常对照组（n=4）和缺血组（n=12），缺血组通过结扎冠状动脉1h造成急性心肌缺血，测定缺血区心肌电传导速度，应用激光共聚焦显微镜技术和荧光免疫组织化学方法对缺血心肌Cx43含量进行定量研究。结果（1）急性心肌缺血时Cx43迅速降解，心肌电传导速度明显下降；（2）缺血区各局部传导速度与该部位Cx43像素密度明显正相关；（3）出现持久传导阻滞的区域其Cx43降解程度均大于50％。结论急性短时间（1小时）缺血时Cx43的降解已经开始对心肌传导速度产生明显的影响作用，而局部心肌Cx43的严重降解将导致该区域出现持久传导阻滞。     

人参二醇组皂甙对实验犬心肌缺血再灌注损伤保护作用的研究

结扎犬左冠脉前降支９０ｍｉｎ，恢复再灌注２４０ｍｉｎ。将犬随机分为治疗组及对照组。缺血即刻、治疗组静点人参二醇组皂甙（ＰＤＳ）２５ｍｇ／ｋｇ，以生理盐水１００ｍｌ稀释，对照组静点生理盐水１００ｍｌ。观察血清肌酸磷酸激酶（ＣＰＫ）、血清过氧化脂质（ＬＰＯ）及心肌超氧化物歧化酶（ＳＯＤ）活力和ＬＰＯ含量的变化。结果表明，治疗组在缺血９０ｍｉｎ、再灌注１２０ｍｉｎ、２４０ｍｉｎ、血清ＣＰＫ值显著低于对照组（Ｐ＜０．０５），于再灌注２４０ｍｉｎ、血清及心肌ＬＰＯ含量显著低于对照组（Ｐ＜０．０５），心肌ＳＯＤ活力显著高于对照组（Ｐ＜０．０５）。提示ＰＤＳ对犬在体缺血再灌注损伤心脏具有保护作用，认为可能是通过提高心肌组织ＳＯＤ活力，加强氧自由基清除，减轻了细胞损伤。     

犬肢体缺血预处理对心肌的影响

目的：缺血预处理的机制尚不清楚，本文探讨了犬肢体缺血对心肌的保护作用。方法：２４只犬分为３组。股动脉预处理组（Ｆ组，８只）：阻断股动脉１０分钟再灌注２０分钟，反复３次；心肌预处理组（Ｈ组，８只）：结扎冠状动脉左前降支１０分钟，再灌注２０分钟，反复３次；对照组（Ｃ组，８只）：旷置９０分钟。各组均结扎冠状动脉左前降支４０分钟，再灌注１２０分钟。资料统计用ｔ检验和χ２分析。结果：Ｆ组及Ｈ组心肌梗死／心肌缺血范围（１７．１±４．９％，１０．３±２．８％）小于Ｃ组（４１．８±６．０％，Ｐ均＜０．０５）。室性心动过速和心室颤动的发生犬数在持续缺血期及再灌注期Ｆ组（２，２）和Ｈ组（１，２）低于Ｃ组（７，８，Ｐ均＜０．０５）。结论：犬肢体缺血预处理引起的全身性改变对心肌也有保护作用，为冠状动脉粥样硬化性心脏病（冠心病）的治疗提供了新的线索。     

Pharmacokinetic analysis of coronary venous retroinfusion: a comparison with anterograde coronary artery drug administration using metoprolol as a tracer.

Plasma and myocardial tissue concentrations of metoprolol were studied in ischemic and nonischemic areas of 22 pigs after 90 (n = 19) and 16 (n = 3) min of left anterior descending coronary artery occlusion. Group A (n = 6) received simultaneous intravenous metoprolol (0.2 mg/kg body weight) and tritium-labeled (3H)-metoprolol (0.2 mg/kg) retrogradely into the coronary vein. In group B (n = 5), metoprolol and 3H-metoprolol were administered in the same way, but at half the volume to study the influence of derived coronary venous pressure on the myocardial concentration of drug. In group C (n = 3), metoprolol was given retrogradely and saline solution was infused into the left anterior descending artery before induced death to wash out metoprolol from the coronary veins. To rule out a possible influence of the development of myocardial necrosis on drug distribution, metoprolol was retroinfused after 1 min of arterial occlusion in three pigs (group D). In group E (n = 5), metoprolol (0.2 mg/kg) was infused anterogradely into the left anterior descending artery. Peak plasma concentration was significantly higher after intravenous infusion of metoprolol (1,188 +/- 503 nmol/liter) than after coronary venous infusion (417 +/- 155 nmol/liter; p less than 0.001). In groups A and B, the nonischemic myocardial concentration of metoprolol was 250 to 300 pmol/g, whether the drug was infused intravenously or into the coronary vein. Coronary venous retroinfusion, however, resulted in a substantial accumulation of metoprolol in the ischemic myocardium. In group A pigs, subendocardial myocardial concentration was 16,800 +/- 7,774, mid-myocardial 39,590 +/- 18,043 and subepicardial 57,143 +/- 29,030 pmol/g (mean +/- SE). The ischemic myocardial concentration in pigs from group B was somewhat less pronounced, probably secondary to a lower coronary venous pressure (15 +/- 3 mm Hg) with the lower volume of infusion (6.1 +/- 0.3 ml) in group B compared with 32 +/- 5 mm Hg with a 14 +/- 1 ml infusion in group A. Coronary artery anterograde administration resulted in myocardial ischemic and nonischemic zone drug concentrations similar to those observed after retroinfusion into the coronary vein. With both modes of administration, there was a transmyocardial gradient from a somewhat lower drug concentration in the subendocardium, toward an increasing level in the mid-myocardium, to the highest concentration in the subepicardial zone of the ischemic myocardium. Coronary venous retroinfusion resulted in pronounced drug accumulation in the ischemic myocardium. The derived coronary venous pressure during infusion influenced the concentration of drug.(ABSTRACT TRUNCATED AT 400 WORDS)     

葛根素抗心肌缺血及其机理的实验研究

自的：探讨葛根素对心肌梗死（MI）犬心的保护作用及其机理。方法：12只犬随机分成葛根素处理组（G组）和对照组（C组），建立急性MI模型，分别给予葛根素和生理盐水，共21d，冠状动脉（冠脉）结扎前、后不同时间点行冠脉造影，术前及术后第22天查11项血液流变学指标，测量梗死面积及心肌血管面密度。结果：①G组梗死面积明显小于C组。②冠脉结扎后2h和22dG组侧支血管明显多于C组。③在MI急性期，血小板聚集性和血粘度较梗死前明显塔高，而葛根素能阻止上述改变。④G组缺血区和梗死区心肌毛细血管和供血血管面密度较C组明显增加。结论：葛根素能促进大冠脉侧支循环的开放和形成，抑制MI后血小板聚集和降低血粘度，改善微循环，对缺血心肌具有保护作用。     

Effects of residual coronary stenosis on myocardial salvage after reperfusion in dogs

In order to study the effects of residual stenosis on myocardial salvage, we created 99% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n = 8), the artery was occluded for 1h before being fully reperfused. In Group B (n = 9), the artery was occluded for 1h, then subjected to 6h of 99% stenosis without contrast washout delay. In Group C (n = 8), the artery was occluded for 1h, followed by 1 week of 99% stenosis without contrast washout delay. In Group D (n = 10), again the artery was occluded for 1h, then subjected to 6h of 99% stenosis with contrast washout delay. In Group E (n = 8), the artery was occluded for 7h, then fully reperfused for 1 week. Finally, in Group F (n = 8), the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8 +/- 12.5% that of non-infarcted myocardium. Myocardial CK in Group B (46.5 +/- 7.4%) was little different but in Group C it dropped to 26.6 +/- 8.4%, suggesting that 99% residual stenosis is not deleterious if it is continued for 6h or less but that it will result in considerable depletion of myocardial CK, it is is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3 +/- 3.7%, little different from that for either Group E (13.3 +/- 2.6%) or Group F (9.3 +/- 3.3%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dependency of location of salvageable myocardium on type of intervention

The purposes of this study were (1) to determine the location of the salvageable border zone in relation to the ischemic coronary bed, and (2) to determine whether the location of salvaged tissue differs depending on the mechanism of salvage and the type of intervention. Forty-four open chest dogs were subjected to either 6 hours of occlusion of the left anterior descending coronary artery or 4 hours of occlusion of this artery followed by 2 hours of reperfusion. Dogs with 6 hours of occlusion received either saline solution (Group I, n = 9), ibuprofen, 12.5 mg/kg body weight, (Group II, n = 7), flurbiprofen, 1 mg/kg (Group III, n = 10), or L-hydroxyphenyl-glycine, 10 mg/kg (Group IV, n = 8) intravenously 30 minutes and 3 hours after coronary occlusion. Dogs in Group V (n = 10) were subjected to 4 hours of coronary occlusion followed by 2 hours of reperfusion, but received no drugs. Although from 17 to 42 percent of the myocardium at risk did not become infarcted in Groups II through V compared with only 6 percent in Group I, the location of salvaged tissue was different in dogs receiving reperfusion (Group V) from that of dogs receiving drug interventions (Groups II, III and IV). In Group V, the salvaged tissue was primarily subepicardial with virtually no lateral zone of salvaged tissue (ratio of salvaged subepicardium to salvaged subendocardium 14.8 ± 1.9 to 1). In Groups II, III and IV, there was a portion of the myocardium at risk at both lateral margins that did not become infarcted, as well as a portion of subepicardial tissue (ratio of subepicardium to subendocardium salvaged 3.3 ± 0.4 in Group II, 2.5 ± 0.1 in Group III and 2.0 ± 0.2 in Group IV).Thus, infarct size reduction by ibuprofen, flurbiprofen and L-hydroxy-phenylglycine is accompanied by lateral and subepicardial zones of salvage, whereas tissue salvaged by reperfusion is located primarily in the subepicardium. These observations should help to resolve the controversy regarding the existence and location of the various zones of ischemic myocardium that can be salvaged by drugs or reperfusion.     

冠心病患者纤溶活性、血小板功能及内皮素在运动前后的变化及其临床意义

目的研究冠心病患者在运动前后纤溶活性、血小板活化状态及血管内皮功能的变化。方法根据冠状动脉造影结果，选择冠心病患者（ＣＨＤ组）３７例，分为单支及多支病变组；另选健康人２７例为对照组（Ｃ组）。采用次极量运动试验观察上述部分指标在运动前后的变化。结果（１）运动前，组织型纤溶酶原激活剂（ｔＰＡ）、纤溶酶原激活剂抑制因子１（ＰＡＩ１）活性、血浆５羟色胺（５ＨＴ）水平及血小板５ＨＴ２Ａ受体密度，ＣＨＤ组均高于Ｃ组（Ｐ＜０．０５）；血浆内皮素（ＥＴ）１浓度两组差异无显著性（Ｐ＞０．０５）。（２）运动后，ＣＨＤ组ｔＰＡ活性下降（Ｐ＜０．０５），ＰＡＩ１活性上升（Ｐ＜０．０２５）；血浆５ＨＴ水平及血小板５ＨＴ２Ａ受体密度增加（Ｐ＜０．０５）；血浆ＥＴ１浓度上升，与Ｃ组比较差异有显著性（Ｐ＜０．０５）。上述各指标的增高，多支病变组较单支病变组明显（Ｐ＜０．０１～０．００５）。（３）运动前仅ＰＡＩ１活性与心肌缺血面积呈正相关（ｒ＝０．４５２，Ｐ＜０．００５）。结论冠心病患者纤溶活性下降，血小板激活，血管内皮受损，使冠心病患者易发生冠状动脉痉挛及血栓形成。次极量运动使之进一步加重而易诱发冠心病事件。     

直接心肌植入VEGF_(165)基因的实验研究

目的 :评估VEGF1 6 5基因直接心肌内注射促进心肌血运重建的疗效。方法 :中国实验小型猪 11只 ,体重 (2 9 3± 4 3)kg。在左冠状动脉回旋支 (LCX)近心端放置Ameroid收缩环。术后 6周行冠脉造影示LCX狭窄 >95 %为慢性心肌缺血模型形成。将选用模型随机分为治疗组 (n =6 )和对照组 (n =5 )。治疗组将VEGF1 6 5质粒注射到左室侧壁 10处有标记的心肌中层。对照组只注射空白质粒。治疗前和治疗 6周后 ,采用体表超声心动图观察静息与小剂量多巴酚丁胺负荷 (LDDSE)状态下左心室壁运动及功能 (LVEF、RT、MVCF、WMSI) ,通过2 0 1 TI SPECT观察心肌灌注改变。处死动物后进行心肌血管密度和VEGF基因mRNA表达测定。结果 :治疗 6周后 ,在静息与LDDSE(10 μg min kg)状态下 ,A组RT和WMSI较治疗前显著改善 ,侧壁灌注缺损明显缩小 ,B组改善不明显。A组每个视野的血管面积、血管周长及血管数目均较B组多。A组 2 3例局部心肌VEGF基因mRNA的表达明显 ,B组 3 3例均无表达。结论 :直接心肌内注射VEGF1 6 5基因可促进慢性缺血心肌的血管再生 ,改善局部心肌灌注和室壁运动。     

麝香保心丸对心力衰竭大鼠内皮素1和肾上腺髓质素水平的影响

目的探讨麝香保心丸对心肌梗死后慢性心力衰竭大鼠血浆内皮素1(ET-1)和肾上腺髓质素(ADM)水平的影响。方法 80只Wistar大鼠随机分为正常对照组(A组,10只)、假手术组(B组,10只)、其余60只制作心力衰竭模型,将制模成功35只大鼠又分对照组(C组,9只)、麝香保心丸小剂量组(D组,9只)、麝香保心丸大剂量组(E组,9只)和阳性药物对照组(F组,8只),采用灌胃法给药。超声心动图检测用药前后大鼠心脏功能,放射免疫法检测ET-1、ADM水平。结果 A组与B组用药前LVEF、左心室舒张末内径(LVEDD)、左心室收缩末内径(LVESD)无显著差异。与B组用药前比较,C组、D组、E组、F组大鼠LVEF明显降低,LVEDD、LVESD明显增加(P0.01);与C组用药后比较,E组大鼠LVEF明显升高,LVEDD、LVESD明显减小(P0.05),D组、F组LVESD明显减小(P0.05);与B组比较,C组大鼠ET-1、ADM水平明显升高(P0.05,P0.01);与C组比较,D组、E组、F组大鼠ET-1水平明显降低(P0.05,P0.01),E组ADM水平明显降低(P0.01)。结论麝香保心丸可能通过改善心肌血供,进而抑制慢性心力衰竭时神经内分泌系统的激活,并起到了有效治疗作用。     

The effects of cytochrome C on the extent of myocardial infarction and regional function of the ischemic myocardium

The effects of cytochrome C, an electron carrier in the process of oxidative phosphorylation, on infarct size and regional left ventricular function after a coronary artery occlusion were investigated. Thus, in 30 dogs, 1 minute after left anterior descending coronary artery occlusion, 99mTc-labeled albumin microspheres (8 mCi) were injected into the left atrium for subsequent assessment of the hypoperfused zone, that is, the area at risk of infarction. Fifteen minutes after coronary artery occlusion, dogs were randomized into a control group (n = 15) and a cytochrome C-treated group (n = 15). The latter immediately received cytochrome C, 2.5 mg/kg intravenously. Six hours after coronary artery occlusion the dogs were sacrificed and their left ventricles were cut into 3 mm thick slices. Infarct size was determined by triphenyltetrazolium chloride staining and measured by planimetry. The same slices were then submitted to autoradiography and the hypoperfused zone was then measured by planimetry. The hypoperfused zone was 22 +/- 2% and 23 +/- 2% of the left ventricle in the control and treated groups, respectively (NS), indicating that the extent of myocardium at risk before treatment was similar. The extent of the hypoperfused zone which evolved to necrosis was 90 +/- 3% in the control group but only 50 +/- 7% in the treated group (p less than 0.001). Myocardial salvage in the treated group was paralleled by improvement in systolic wall thickness of the ischemic segment as measured by two-dimensional echocardiography. Thus, cytochrome C reduced the extent of myocardial necrosis by 44% and improved systolic function of the ischemic myocardium.     

Pharmacokinetic analysis of coronary sinus retroinfusion in pigs

Summary Myocardial availability of drug, using metoprolol as a tracer, in acutely ischemic myocardium in the area of the left circumflex (LCX) coronary artery was compared following standard intravenous (IV) administration and after coronary sinus retroinfusion. Seven open-chest farm pigs were subjected to a 21-minute occlusion of the LCX coronary artery. All animals received simultaneous IV tritium-labeled metoprolol (0.2 mg/kg) and unlabeled metoprolol (0.2 mg/kg) retrogradely into the coronary sinus. The drug administration was starded after 1 minute of coronary artery occlusion and continued for 5 minutes. Intravenously administered metoprolol resulted in a higher peak plasma concentration of metoprolol (382±52 nmol/l) than coronary sinus retroinfusion (276±47 nmol/l). The nonischemic myocardial metoprolol concentration was of similar magnitude (393–454 pmol/g), whether infused IV or into the coronary sinus. Coronary sinus retroinfusion, however, resulted in a substantial accumulation of metoprolol in the ischemic myocardium (2887–5863 pmol/g). Coronary sinus retroinfusion resulted in a pronounced and specific accumulation in the ischemic myocardium in the territory of the LCX coronary artery.     

Experimental study on myocardial salvage by coronary thrombolysis and mechanical recanalization

Salvage of the ischemic myocardium by coronary thrombolysis and mechanical recanalization (simulated angioplasty) was studied in a canine experimental model of acute myocardial infarction induced by coronary occlusive thrombus at the left anterior descending coronary artery. Forty-four open-chest dogs divided into three groups were studied. Group I (n = 15, control group) was observed for 6 hours following the onset of infarct. In group II (n = 14, thrombolysis group), thrombolysis was obtained by intravenous administration of urokinase 2 hours after the onset of infarct. In group III (n = 15, mechanical recanalization group), simulated angioplasty was performed 2 hours after infarct. Coronary reperfusion was continued for 4 hours in groups II and III. The areas of left ventricular risk and infarct were measured by double staining methods with Evans blue dye and triphenyl tetrazolium hydrochloride. There were no significant differences in control blood flow and risk area in the three groups. Myocardial infarct area/risk area was 65 +/- 3% in group I, 45 +/- 1% in group II, and 35 +/- 2% in group III (group I vs II, p less than 0.001; group II vs III, p less than 0.001). Restored coronary blood flow in the left anterior descending artery was 8 +/- 1 ml/min in group II and 14 +/- 1 ml/min in group III (p less than 0.001). The data suggest that coronary mechanical recanalization is more effective than thrombolysis in salvaging the ischemic myocardium in the early phase of myocardial infarction, most probably because coronary blood flow is better restored by mechanical recanalization.