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伴有左心室肥厚的清醒犬在心房起搏期间的收缩和舒张功能障碍

Systolic and diastolic dysfunction during atrial pacing in conscious dogs with left ventricular hypertrophy.

作者信息

Fujii A M, Gelpi R J, Mirsky I, Vatner S F

机构信息

Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts.

出版信息

Circ Res. 1988 Mar;62(3):462-70. doi: 10.1161/01.res.62.3.462.

DOI:10.1161/01.res.62.3.462
PMID:2963705
Abstract

To determine the extent to which the hypertrophied left ventricle responds to the chronotropic stress induced by graded atrial pacing rates, we studied conscious, chronically instrumented dogs with severe compensated pressure overload left ventricular (LV) hypertrophy induced by aortic banding in puppies 8-10 weeks of age. At 1-2 years, dogs with severe LV hypertrophy (LV free wall/body wt ratio 6.8 +/- 0.6 g/kg) and sham-operated littermates (LV free wall/body wt ratio 4.0 +/- 0.3 g/kg) were instrumented with ultrasonic dimension crystals to measure LV short axis internal diameter and wall thickness, miniature LV pressure transducers, and aortic and LV catheters. During atrial pacing (240 beats/min) in eight control dogs, LV pressure did not change from 119 +/- 2 mm Hg, and mean velocity of circumferential fiber shortening (VCF) did not change from 1.25 +/- 0.09/sec. In seven dogs with LV hypertrophy, atrial pacing (240 beats/min) decreased systolic LV function; that is, LV systolic pressure decreased (p less than 0.01) by 65 +/- 12 from 254 +/- 14 mm Hg, and VCF decreased (p less than 0.01) by 0.19 +/- 0.03 from 0.97 +/- 0.15/sec. Diastolic dysfunction was also observed in the dogs with LV hypertrophy. In the control dogs during atrial pacing (240 beats/min), LV end-diastolic pressure decreased (p less than 0.01) by 8 +/- 1 from 9 +/- 1 mm Hg, end-diastolic stress decreased (p less than 0.01) by 18 +/- 2 from 22 +/- 2 g/cm2, and the radial myocardial stiffness constant did not change from 5.6 +/- 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了确定肥厚的左心室对分级心房起搏频率诱导的变时性应激的反应程度,我们研究了8 - 10周龄幼犬经主动脉缩窄诱导产生严重代偿性压力超负荷左心室(LV)肥厚的清醒、长期植入仪器的犬。1 - 2岁时,对严重左心室肥厚的犬(左心室游离壁/体重比为6.8±0.6 g/kg)和假手术的同窝犬(左心室游离壁/体重比为4.0±0.3 g/kg)植入超声尺寸晶体以测量左心室短轴内径和壁厚、微型左心室压力传感器以及主动脉和左心室导管。在8只对照犬心房起搏(240次/分钟)期间,左心室压力从119±2 mmHg未发生变化,圆周纤维缩短平均速度(VCF)从1.25±0.09/秒未发生变化。在7只左心室肥厚的犬中,心房起搏(240次/分钟)降低了左心室收缩功能;即左心室收缩压从254±14 mmHg降低(p<0.01)65±12,VCF从0.97±0.15/秒降低(p<0.01)0.19±0.03。左心室肥厚的犬也观察到舒张功能障碍。在对照犬心房起搏(240次/分钟)期间,左心室舒张末期压力从9±1 mmHg降低(p<0.01)8±1,舒张末期应力从22±2 g/cm²降低(p<0.01)18±2,径向心肌硬度常数从5.6±1.0未发生变化。(摘要截取自250字)

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2
Decreased Gs alpha mRNA levels accompany the fall in Gs and adenylyl cyclase activities in compensated left ventricular hypertrophy. In heart failure, only the impairment in adenylyl cyclase activation progresses.在代偿性左心室肥厚中,Gsα信使核糖核酸水平降低伴随着Gs和腺苷酸环化酶活性的下降。在心力衰竭时,只有腺苷酸环化酶激活受损会继续发展。
J Clin Invest. 1991 Jan;87(1):293-8. doi: 10.1172/JCI114985.
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Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure.
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