Näslund U, Häggmark S, Johansson G, Pennert K, Reiz S, Marklund S L
University Hospital, Umeå, Sweden.
Cardiovasc Res. 1992 Feb;26(2):170-8. doi: 10.1093/cvr/26.2.170.
The aim was to study the effects on myocardial infarct size of reperfusion alone or of CuZn superoxide dismutase (SOD) as an adjunct to reperfusion.
Occlusion was induced in closed chest, pentobarbitone anaesthetised, mechanically ventilated pigs by injection of a 2 mm ball into a preselected coronary artery. Reperfusion was achieved by retraction of the ball via an attached filament. Twenty nine placebo treated and 25 SOD treated animals were subjected to 30 (n = 21), 60 (n = 21), and 90 (n = 12) min of coronary occlusion followed by reperfusion to 24 h; a control group of 24 pigs was subjected to a sustained occlusion for 24 h. Infarct size was assessed by tetrazolium staining and plasma creatine kinase (CK), aspartate aminotransferase (ASAT), and lactate dehydrogenase (LD). In the CuZn SOD group, 200 mg bovine CuZn SOD was given as a bolus intravenously immediately before reperfusion followed by a continuous infusion (100 mg) for 60 min. The size of the ischaemic myocardium at risk was measured from post mortem autoradiograms.
Infarct size as percent of myocardium at risk was 46.0(SD 15.5)%, 80.1(9.9)%, and 88.9(5.0)% respectively in placebo animals with 30, 60, and 90 min occlusion, and 94.2(5.1)% in pigs with 24 h sustained occlusion. Compared to 24 h sustained occlusion, limitation of infarct size by reperfusion was only demonstrated in the 30 (p less than 0.001) and 60 min groups (p less than 0.001). Plasma values of CK, ASAT, and LD at 90 min post-reperfusion correlated closely with infarct size as assessed by tetrazolium staining and were related to occlusion duration. No myocardial salvage, as assessed by plasma ASAT, CK, or LD, was shown in the SOD treated groups.
Early reperfusion resulted in myocardial salvage as assessed by tetrazolium staining and peak ASAT, CK, and LD at 90 min after the reperfusion. No limitation of infarct size by SOD could be demonstrated from analyses of plasma CK, ASAT, or LD.
研究单纯再灌注或铜锌超氧化物歧化酶（SOD）作为再灌注辅助手段对心肌梗死面积的影响。
在戊巴比妥麻醉、机械通气的闭胸猪中，通过向预先选定的冠状动脉内注射一个2毫米的球囊诱导闭塞。通过连接的细丝回缩球囊实现再灌注。29只接受安慰剂治疗和25只接受SOD治疗的动物分别经历30分钟（n = 21）、60分钟（n = 21）和90分钟（n = 12）的冠状动脉闭塞，随后再灌注至24小时；24只猪的对照组持续闭塞24小时。通过四氮唑染色以及血浆肌酸激酶（CK）、天冬氨酸转氨酶（ASAT）和乳酸脱氢酶（LD）评估梗死面积。在铜锌SOD组中，在再灌注前立即静脉推注200毫克牛铜锌SOD，随后持续输注（100毫克）60分钟。从死后放射自显影片测量有风险的缺血心肌面积。
在闭塞30分钟、60分钟和90分钟的安慰剂动物中，梗死面积占危险心肌的百分比分别为46.0（标准差15.5）%、80.1（9.9）%和88.9（5.0）%，在持续闭塞24小时的猪中为94.2（5.1）%。与持续闭塞24小时相比，仅在30分钟组（p < 0.001）和60分钟组（p < 0.001）中显示再灌注对梗死面积的限制。再灌注后90分钟时血浆CK、ASAT和LD值与通过四氮唑染色评估的梗死面积密切相关，且与闭塞持续时间有关。在接受SOD治疗的组中，通过血浆ASAT、CK或LD评估未显示心肌挽救。
通过四氮唑染色以及再灌注后90分钟时的ASAT、CK和LD峰值评估，早期再灌注可实现心肌挽救。从血浆CK、ASAT或LD分析中未显示SOD对梗死面积的限制。
