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梗死心肌和存活心肌的血流:维拉帕米对急性缺血犬心脏作用的意义。

Blood flow to infarct and surviving myocardium: implications regarding the action of verapamil on the acutely ischemic dog heart.

作者信息

Davenport N, Goldstein R E, Bolli R, Epstein S E

出版信息

J Am Coll Cardiol. 1984 Apr;3(4):956-65. doi: 10.1016/s0735-1097(84)80354-x.

Abstract

After coronary occlusion, myocardium originally supplied by the occluded vessel ultimately separates into infarct and surviving muscle. To clarify this process, evolution of collateral blood flow to infarct and to surviving myocardium was retrospectively analyzed after permanent left anterior descending occlusion in 24 closed chest dogs. Microspheres were injected before occlusion and 5 and 20 minutes and 4 hours after occlusion. Ten minutes after occlusion, dogs received either verapamil, 0.4 mg/kg, followed by 0.6 mg/kg per hour for 6 hours (n = 10) or equivalent saline solution (n = 14). These dogs were sacrificed 3 days later, the distribution of the occluded artery was defined by dye perfusion and infarcted myocardium was determined by triphenyltetrazolium staining of heart slices. Surviving muscle within the distribution of the occluded artery was divided into medial regions adjacent to the infarct (medial adjacent) and remote from the infarct (medial remote) and lateral regions adjacent to infarct (lateral adjacent) and remote from the infarct (lateral remote). In both control and verapamil groups, collateral flows in all regions increased significantly by 140 to 400% over 4 hours. However, the relative magnitude of collateral flow to different regions showed a consistent order: infarct less than medial adjacent less than medial remote less than lateral remote. There were no significant differences in regionally matched flows or size of infarction between control and verapamil-treated groups. Collateral perfusion begins to show distinctive patterns of change in infarct and surviving muscle very soon after coronary occlusion. Collateral flow within subdivisions of the occluded coronary artery bed increases as distance from the infarct increases, with lateral segments having higher flows than medial segments. This relation persists during the first 4 hours after occlusion. In this study, verapamil neither increased collateral flow to the occluded bed nor altered minimal flow requirements for myocardial survival.

摘要

冠状动脉闭塞后,原本由闭塞血管供血的心肌最终会分离为梗死心肌和存活心肌。为阐明这一过程,对24只开胸犬进行永久性左前降支闭塞后,回顾性分析梗死心肌和存活心肌侧支血流的演变情况。在闭塞前、闭塞后5分钟、20分钟和4小时注射微球。闭塞10分钟后,犬只接受维拉帕米,剂量为0.4mg/kg,随后每小时0.6mg/kg,持续6小时(n = 10)或等量生理盐水(n = 14)。3天后处死这些犬只,通过染料灌注确定闭塞动脉的分布,通过对心脏切片进行三苯基四氮唑染色确定梗死心肌。将闭塞动脉分布范围内的存活心肌分为梗死灶附近的内侧区域(内侧邻接区)和远离梗死灶的内侧区域(内侧远隔区)以及梗死灶附近的外侧区域(外侧邻接区)和远离梗死灶的外侧区域(外侧远隔区)。在对照组和维拉帕米组中,所有区域的侧支血流在4小时内均显著增加了140%至400%。然而,不同区域侧支血流的相对大小呈现出一致的顺序:梗死灶<内侧邻接区<内侧远隔区<外侧远隔区。对照组和维拉帕米治疗组在区域匹配血流或梗死面积方面无显著差异。冠状动脉闭塞后不久,侧支灌注就在梗死心肌和存活心肌中开始呈现出独特的变化模式。闭塞冠状动脉床各亚区内的侧支血流随着与梗死灶距离的增加而增加,外侧段的血流高于内侧段。这种关系在闭塞后的最初4小时内持续存在。在本研究中,维拉帕米既未增加闭塞床的侧支血流,也未改变心肌存活所需的最小血流量。

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