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首页> 外文期刊>American Journal of Physiology >Susceptibility to systolic dysfunction in the myocardium from chronically infarcted spontaneously hypertensive rats
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Susceptibility to systolic dysfunction in the myocardium from chronically infarcted spontaneously hypertensive rats

机译：慢性自发性高血压大鼠心肌收缩功能障碍的敏感性

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First published November 9, 2007; doi:10.1152/ajpheart.01024.2007.-We explored whether the hypertensive heart is susceptible to myocardial dysfunction in viable nonin-farcted tissue post-myocardial infarction (MI), the potential mechanisms thereof, and the impact of these changes on pump function. Six to seven months after the ligation of the left anterior descending coronary artery, left ventricular (LV) myocardial systolic function, as assessed from the percent shortening of the noninfarcted lateral wall segmental length determined over a range of filling pressures (ultrasonic transducers placed in the lateral wall in anaesthetized, open-chest, ventilated rats) and the percent thickening of the posterior wall (echocardiography), was reduced in infarcted spontaneous hypertensive rats (SHR-MI) (P < 0.05) but not in normotensive Wistar-Kyoto (WKY-MI) animals compared with corresponding controls [SHR-sham operations (Sham) and WKY-Sham]. This change in the regional myocardial function in SHR-MI, but not in WKY-MI, occurred despite a similar degree of LV dilatation (increased LV end-diastolic dimensions and volume intercept of the LV end-diastolic pressure-volume relation) in SHR-MI and WKY-MI rats and a lack of difference in LV relative wall thinning, LV wall stress, apoptosis [terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling (TUNEL)], or necrosis (pathological score) between SHR-MI and WKY-MI rats. Although the change in regional myocardial function in the SHR-MI group was not associated with a greater reduction in baseline global LV chamber systolic function [end-systolic elastance (LV E_(es)) and endocardial fractional shortening determined in the absence of an adrenergic stimulus], in the presence of an isoproterenol challenge, noninfarct-zone LV systolic myocardial dysfunction manifested in a significant reduction in LV E_(es) in SHR-MI compared with WKY-MI and SHR and WKY-Sham rats (P < 0.04). In conclusion, these data suggest that with chronic MI, the hypertensive heart is susceptible to the development of myocardial dysfunction, a change that cannot be attributed to excessive chamber dilatation, apoptosis, or necrosis, but which in turn contributes toward a reduced cardiac adrenergic inotropic reserve.
机译：首次发布于2007年11月9日; doi：10.1152 / ajpheart.01024.2007.-我们探讨了高血压心脏是否容易在心肌梗塞后可行的非梗塞组织中发生心肌功能障碍，其潜在机制以及这些变化对泵功能的影响。结扎左冠状动脉前降支后六至七个月，根据在一定充盈压范围内确定的非梗塞性侧壁节段长度的缩短百分比，评估左心室（LV）心肌收缩功能（超声换能器置于梗死的自发性高血压大鼠（SHR-MI）（P <0.05）降低了麻醉的开胸通气大鼠的侧壁和后壁增厚的百分比（超声心动图），但血压正常的Wistar-Kyoto（WKY）并未降低-MI）动物与相应的对照[SHR假手术（Sham）和WKY-Sham]进行比较。尽管SHR中的LV扩张程度相似（LV舒张末期尺寸增大和LV舒张末期压力-容积关系的体积截距增加），但SHR-MI而非WKY-MI的局部心肌功能发生了这种变化-MI和WKY-MI大鼠，并且SHR-MI与LV相对壁变薄，LV壁应力，凋亡[末端脱氧核苷酸转移酶生物素-dUTP缺口末端标记（TUNEL）]或坏死（病理评分）缺乏差异WKY-MI大鼠。尽管SHR-MI组的局部心肌功能改变与基线总体LV室收缩功能[收缩末期弹性（LV E_（es））和在没有肾上腺素缺乏症的情况下确定的心内膜分数缩短]的更大降低没有相关性刺激]，在存在异丙肾上腺素挑战的情况下，与WKY-MI和SHR和WKY-Sham大鼠相比，SHR-MI的非梗塞区LV收缩期心肌功能异常表现为LV E_（es）显着降低（P <0.04） 。总之，这些数据表明，对于慢性心肌梗死，高血压心脏易患心肌功能障碍，这种变化不能归因于过度的房室扩张，细胞凋亡或坏死，但反过来又有助于降低心脏的肾上腺功能性正性肌力保留。

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