Mody F V, Buxton D B, Araujo L I, Fishbein M E, Selin C E, Schelbert H R, Schwaiger M
Department of Radiological Sciences, University of California, Los Angeles School of Medicine.
J Am Coll Cardiol. 1993 Jan;21(1):233-9. doi: 10.1016/0735-1097(93)90742-j.
The relation of myocardial blood flow and indium-111 (111In) antimyosin antibody uptake was studied by inducing myocardial infarction in 18 dogs, 8 with closed chest left anterior descending artery balloon occlusion for 3 h followed by reperfusion (group A) and 10 dogs with open chest left anterior descending artery ligation (without reperfusion, group B).
The relation of antimyosin uptake to myocardial injury has been documented. However, its relation to tracer delivery by myocardial blood flow has not been studied and has been assumed to be independent.
Indium-111 antimyosin antibody, 2 mCi, was injected 20 min after reperfusion and 3 h after coronary artery ligation in groups A and B, respectively. Regional blood flows were determined by radiolabeled microspheres during occlusion and 24 h later in both groups. On day 2, dogs were killed after risk zone delineation with gentian violet. The heart was excised and stained with triphenyltetrazolium chloride solution and graded for increasing severity of tissue injury based on extent of staining. Microsphere activity and 111In antimyosin activity were measured in control tissue (grade 1), noninfarct tissue at risk (grade 2), mixed tissue (grade 3), infarct tissue (grade 4) and hemorrhagic infarct tissue (grade 5, present only in group A dogs). Count activity was normalized to that of the mean value in control tissue (grade 1) and expressed as a ratio of activity.
Indium-111 antimyosin activity was high in triphenyltetrazolium chloride grade 4 tissue in both groups but was attenuated in grade 4 tissue in group B dogs (10.6 +/- 5.1 vs. 5.0 +/- 4.5; p < 0.05 group A vs. group B), which had lower blood flow on day 2 (0.51 +/- 0.36 vs. 0.23 vs. 0.22; p < 0.01). Normalizing 111In antimyosin activity for blood flow on day 2 resulted in equivalent 111In antimyosin uptake for infarct tissue (32.6 +/- 21.6 vs. 36.6 +/- 29.8 for group A vs. group B; p = NS).
Thus, 111In antimyosin uptake is a specific marker of necrotic tissue with a high signal ratio in reperfused tissue. However, its uptake is dependent on residual blood flow in the infarct territory. Indium-111 antimyosin could potentially serve as a suitable tracer for infarct sizing if myocardial blood flow in the same region were factored simultaneously.
通过对18只犬诱导心肌梗死来研究心肌血流与铟 - 111(¹¹¹In)抗肌凝蛋白抗体摄取之间的关系,其中8只犬采用开胸左前降支动脉球囊闭塞3小时后再灌注(A组),10只犬采用开胸左前降支动脉结扎(无再灌注,B组)。
抗肌凝蛋白摄取与心肌损伤的关系已有文献记载。然而,其与心肌血流示踪剂输送的关系尚未研究,且一直被认为是独立的。
A组和B组分别在再灌注20分钟后及冠状动脉结扎3小时后注射2毫居里的铟 - 111抗肌凝蛋白抗体。两组均在闭塞期间及24小时后通过放射性微球测定局部血流。在第2天,用龙胆紫划定危险区后处死犬。切除心脏,用氯化三苯基四氮唑溶液染色,并根据染色范围对组织损伤严重程度增加进行分级。在对照组织(1级)、有风险的非梗死组织(2级)、混合组织(3级)、梗死组织(4级)和出血性梗死组织(5级,仅在A组犬中出现)中测量微球活性和¹¹¹In抗肌凝蛋白活性。计数活性以对照组织(1级)的平均值进行标准化,并表示为活性比值。
两组中氯化三苯基四氮唑4级组织中的铟 - 111抗肌凝蛋白活性均较高,但B组犬的4级组织中活性减弱(10.6±5.1对5.0±4.5;A组与B组比较,p<0.05),B组在第2天的血流较低(0.51±0.36对0.23±0.22;p<0.01)。将第2天的血流对¹¹¹In抗肌凝蛋白活性进行标准化后,梗死组织的¹¹¹In抗肌凝蛋白摄取相当(A组对B组为32.6±21.6对36.6±29.8;p=无显著性差异)。
因此,¹¹¹In抗肌凝蛋白摄取是坏死组织的特异性标志物,在再灌注组织中信号比高。然而,其摄取取决于梗死区域的残余血流。如果同时考虑同一区域的心肌血流,铟 - 111抗肌凝蛋白可能潜在地用作梗死面积测定的合适示踪剂。