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运动障碍心肌节段的氧需求

Oxygen requirements of the dyskinetic myocardial segment.

作者信息

Gayheart P A, Vinten-Johansen J, Johnston W E, Hester T O, Cordell A R

机构信息

Department of Physiology, Bowman Gray School of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.

出版信息

Am J Physiol. 1989 Oct;257(4 Pt 2):H1184-91. doi: 10.1152/ajpheart.1989.257.4.H1184.

Abstract

Oxygen requirements of a noncontracting myocardial segment subjected to passive systolic stretch (dyskinesis) have not been well described. The purpose of this study was to measure oxygen consumption (MVO2) of a myocardial segment made dyskinetic by intracoronary infusion of lidocaine. In 12 anesthetized open-chest dogs, segmental shortening was measured sonomicrometrically in regions perfused by the left anterior descending (LAD) and circumflex (Cfx) coronary arteries. MVO2 was measured by arterial-venous oxygen content differences and transmural blood flow. Dose-response curves to intracoronary lidocaine showed that complete dyskinesis was achieved by a 0.25-mg/ml dose of lidocaine, whereas the Cfx region maintained a constant level of segmental shortening. MVO2 of the LAD segment was similar to that of the Cfx segment under control conditions. With lidocaine-induced dyskinesis, MVO2 in the arrested segment was reduced by 33% (P less than 0.05), despite the loss of contractile function. When bulging was prevented by ventricular unloading, MVO2 in the arrested segment decreased to 2.65 ml O2.min-1.100 g-1 (i.e., basal oxygen requirements). In conclusion, MVO2 in a pharmacologically arrested myocardial segment undergoing systolic bulging is paradoxically high relative to both basal requirements and MVO2 in the normally contracting segment.

摘要

被动收缩期伸展(运动障碍)下非收缩心肌节段的氧需求尚未得到充分描述。本研究的目的是测量通过冠状动脉内注入利多卡因使心肌节段出现运动障碍时的耗氧量(MVO2)。在12只麻醉开胸犬中,用超声心动图测量左前降支(LAD)和回旋支(Cfx)冠状动脉灌注区域的节段缩短情况。通过动静脉氧含量差异和透壁血流量测量MVO2。冠状动脉内利多卡因的剂量反应曲线表明,0.25mg/ml剂量的利多卡因可导致完全运动障碍,而Cfx区域的节段缩短保持恒定水平。在对照条件下,LAD节段的MVO2与Cfx节段相似。利多卡因诱导运动障碍时,尽管收缩功能丧失,但停滞节段的MVO2降低了33%(P<0.05)。当通过心室卸载防止膨出时,停滞节段的MVO2降至2.65ml O2·min-1·100g-1(即基础氧需求)。总之,与基础需求和正常收缩节段的MVO2相比,药理学停滞且经历收缩期膨出的心肌节段的MVO2反常地高。

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