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醋酸脱氧皮质酮-盐性高血压大鼠的心脏收缩储备和冠状动脉血流储备

Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats.

作者信息

Yamamoto J, Tsuchiya M, Saito M, Ikeda M

出版信息

Hypertension. 1985 Jul-Aug;7(4):569-77. doi: 10.1161/01.hyp.7.4.569.

DOI:10.1161/01.hyp.7.4.569
PMID:3159665
Abstract

Cardiac contractility and coronary flow were compared in conscious rats with established deoxycorticosterone acetate-salt hypertension and in those with sham treatment. The hypertensive rats showed a 32% increase in left ventricular/body weight ratio at 9 weeks of treatment and 42% at 18 weeks of treatment. Resting peak rate of change of pressure (dp/dt) was unchanged at 9 weeks and increased at 18 weeks in hypertensive rats, while isoproterenol-stimulated maximal, propranolol-induced minimal, and Ca2+-stimulated maximal peak dp/dt were greater at 18 weeks. These data indicate the preservation of contractile function. At 18 weeks, the beta-adrenergic receptor-mediated contractile reserve, estimated from isoproterenol-stimulated maximal and resting peak dp/dt, was reduced but the propranolol-induced decrease in peak dp/dt was increased in hypertensive rats compared with sham-treated rats. Thus, at this stage, a greater portion of the total contractile capacity appeared to be mobilized with prolongation of hypertension and progression of left ventricular hypertrophy. No differences were observed in left ventricular and right ventricular coronary flow (microspheres) and left ventricular inner/outer flow ratio at rest and with dipyridamole-induced maximal coronary dilatation, at 9 and 18 weeks. There were no alterations in left or right ventricular coronary flow reserves, as estimated from resting and dipyridamole-induced values. The minimal coronary vascular resistance (normalized for gram of tissue) of both the left and right ventricles was increased at either stage, which suggests the occurrence of structural coronary vascular changes. Thus, basal coronary flow and a coronary flow reserve were uncompromised despite evidence of structural coronary vascular alterations in these hypertensive rats.

摘要

对患有已确诊的醋酸脱氧皮质酮 - 盐性高血压的清醒大鼠和接受假手术治疗的大鼠的心脏收缩力和冠状动脉血流进行了比较。在治疗9周时,高血压大鼠的左心室/体重比增加了32%,在治疗18周时增加了42%。高血压大鼠静息时压力变化的峰值速率(dp/dt)在9周时未改变,在18周时增加,而异丙肾上腺素刺激的最大、普萘洛尔诱导的最小以及Ca2+刺激的最大峰值dp/dt在18周时更大。这些数据表明收缩功能得以保留。在18周时,根据异丙肾上腺素刺激的最大和静息峰值dp/dt估计,β - 肾上腺素能受体介导的收缩储备减少,但与假手术治疗的大鼠相比,高血压大鼠中普萘洛尔诱导的dp/dt峰值降低增加。因此,在这个阶段,随着高血压的延长和左心室肥厚的进展,似乎动员了更大比例的总收缩能力。在9周和18周时,静息和双嘧达莫诱导的最大冠状动脉扩张时,左心室和右心室冠状动脉血流(微球)以及左心室内/外血流比值均未观察到差异。根据静息和双嘧达莫诱导的值估计,左心室或右心室冠状动脉血流储备没有改变。左心室和右心室的最小冠状动脉血管阻力(按每克组织标准化)在任一阶段均增加,这表明发生了结构性冠状动脉血管变化。因此,尽管这些高血压大鼠存在结构性冠状动脉血管改变的证据,但基础冠状动脉血流和冠状动脉血流储备并未受到损害。

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