Minardo J D, Tuli M M, Mock B H, Weiner R E, Pride H P, Wellman H N, Zipes D P
Department of Medicine, Indiana University School of Medicine, Indianapolis.
Circulation. 1988 Oct;78(4):1008-19. doi: 10.1161/01.cir.78.4.1008.
Epicardial phenol application or transmural myocardial infarction in dogs produces sympathetic denervation of myocardium apical to the site of the intervention. Because efferent denervation is probably postganglionic, reinnervation most likely occurs but has not been shown. We investigated whether 123I-labeled metaiodobenzylguanidine (MIBG), a norepinephrine analogue taken up by sympathetic nerve terminals, could provide a scintigraphic image that would detect apical sympathetic denervation and possible reinnervation. Dogs underwent MIBG scintigraphic imaging at various times after phenol application or transmural myocardial infarction. The results of MIBG scintigraphy were correlated with electrophysiological responses obtained during ansae subclaviae and norepinephrine stimulation to establish the presence of neural denervation and reinnervation. Apical defects in the MIBG scan, which were associated with either normal perfusion by thallium or a smaller-sized defect, were found consistently in dogs that had apical sympathetic innervation. MIBG scintigraphic images returned to normal after 14 weeks (mean) at a time when reinnervation was shown to have occurred. Thus, the results of MIBG scintigraphy correlated accurately with the presence of denervation and reinnervation established by neuroelectrophysiological testing. Supersensitive refractory period shortening in response to norepinephrine infusion was present after denervation and persisted for more than 3 weeks after scintigraphic and electrophysiological evidence of reinnervation. Conclusions are that 1) MIBG can be used noninvasively to determine the presence of regional myocardial efferent sympathetic denervation and subsequent reinnervation, 2) reinnervation occurs after phenol application or transmural myocardial infarction, and 3) denervation supersensitivity persists even after reinnervation occurs.
在犬类中,心外膜应用苯酚或透壁性心肌梗死会导致干预部位尖端心肌的交感神经去神经支配。由于传出神经去神经支配可能是节后性的,重新神经支配很可能发生,但尚未得到证实。我们研究了123I标记的间碘苄胍(MIBG),一种被交感神经末梢摄取的去甲肾上腺素类似物,是否能提供一种闪烁图像,以检测尖端交感神经去神经支配和可能的重新神经支配。犬在苯酚应用或透壁性心肌梗死后的不同时间接受MIBG闪烁成像。MIBG闪烁扫描的结果与在锁骨下袢和去甲肾上腺素刺激期间获得的电生理反应相关,以确定神经去神经支配和重新神经支配的存在。在有尖端交感神经支配的犬中, consistently发现MIBG扫描中的尖端缺损,这些缺损与铊的正常灌注或较小尺寸的缺损相关。在显示重新神经支配发生的14周(平均)后,MIBG闪烁图像恢复正常。因此,MIBG闪烁扫描的结果与神经电生理测试确定的去神经支配和重新神经支配的存在准确相关。去神经支配后,对去甲肾上腺素输注的超敏不应期缩短,并在闪烁扫描和电生理证据显示重新神经支配后持续超过3周。结论是:1)MIBG可用于无创性地确定局部心肌传出交感神经去神经支配和随后的重新神经支配的存在;2)在苯酚应用或透壁性心肌梗死后会发生重新神经支配;3)即使在重新神经支配发生后,去神经支配超敏反应仍持续存在。