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心肌收缩力和心室收缩期硬度与冠状动脉灌注相关的变化。

Coronary perfusion related changes in myocardial contractile force and systolic ventricular stiffness.

作者信息

Iwamoto T, Bai X J, Downey H F

机构信息

Department of Physiology, University of North Texas Health Science Center at Fort Worth 76107-2699.

出版信息

Cardiovasc Res. 1994 Sep;28(9):1331-6. doi: 10.1093/cvr/28.9.1331.

Abstract

OBJECTIVE

The mechanism by which changes in coronary perfusion alter myocardial oxygen consumption (MVO2; Gregg phenomenon) is controversial. This study examined the effect of coronary perfusion on myocardial contractile force and systolic ventricular stiffness in the intact, ejecting heart.

METHODS

During selective perfusion of the left anterior descending coronary artery, coronary blood flow was changed with or without concurrent changes in coronary perfusion pressure in 19 alpha chloralose anaesthetised dogs. Regional myocardial segment length (end diastolic length; end systolic length) and developed force were measured with piezoelectric crystals and with a miniature force transducer, respectively. MVO2 was calculated from coronary flow and arteriovenous O2 difference. The slope of the force-length curve during ejection period (delta F/delta SL) was used as an index of systolic myocardial stiffness.

RESULTS

When coronary perfusion pressure was varied from 60 to 180 mm Hg (protocol 1, n = 11), maximum developed force (Fmax), delta F/delta SL, and MVO2 increased with perfusion pressure while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. When coronary blood flow was increased at constant perfusion pressure by infusion of either a low dose or a high dose adenosine (protocol 2, n = 8), Fmax, delta F/delta SL, and MVO2 increased while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. MVO2 and delta F/delta SL increased more steeply with flow in protocol 1.

CONCLUSIONS

(1) Increased coronary blood flow enhances myocardial contractile force, systolic ventricular stiffness, and MVO2 in the intact, ejecting heart. (2) Coronary blood flow induced changes in myocardial contractile force and systolic ventricular stiffness, but not end diastolic length, are probably responsible for coronary blood flow related changes in MVO2.

摘要

目的

冠状动脉灌注变化改变心肌耗氧量(MVO2;格雷格现象)的机制存在争议。本研究在完整的射血心脏中,考察了冠状动脉灌注对心肌收缩力和心室收缩期硬度的影响。

方法

在对19只α-氯醛糖麻醉犬的左前降支冠状动脉进行选择性灌注期间,改变冠状动脉血流,同时改变或不改变冠状动脉灌注压。分别用压电晶体和微型力传感器测量局部心肌节段长度(舒张末期长度;收缩末期长度)和产生的力。根据冠状动脉血流和动静脉氧分压差计算MVO2。射血期力-长度曲线的斜率(δF/δSL)用作收缩期心肌硬度的指标。

结果

当冠状动脉灌注压从60 mmHg变化至180 mmHg时(方案1,n = 11),最大产生力(Fmax)、δF/δSL和MVO2随灌注压增加,而舒张末期长度、节段缩短和其他血流动力学变量保持不变。当在恒定灌注压下通过输注低剂量或高剂量腺苷增加冠状动脉血流时(方案2,n = 8),Fmax、δF/δSL和MVO2增加,而舒张末期长度、节段缩短和其他血流动力学变量保持不变。在方案1中,MVO2和δF/δSL随血流增加更为陡峭。

结论

(1)冠状动脉血流增加可增强完整射血心脏的心肌收缩力、心室收缩期硬度和MVO2。(2)冠状动脉血流引起的心肌收缩力和心室收缩期硬度变化,而非舒张末期长度变化,可能是MVO2与冠状动脉血流相关变化的原因。

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