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缺氧诱导高血压发生发展及消退过程中大鼠右心室乳头肌的形态计量学研究

Morphometry of right ventricular papillary muscle in rat during development and regression of hypoxia-induced hypertension.

作者信息

Hung K S, Pacheco H, Lessin D, Jordan K, Mattioli L

机构信息

Department of Anatomy, University of Kansas Medical Center, Kansas City 66103.

出版信息

Adv Exp Med Biol. 1988;227:337-46. doi: 10.1007/978-1-4684-5481-9_31.

DOI:10.1007/978-1-4684-5481-9_31
PMID:3381706
Abstract

Morphometric analyses of the right ventricular papillary muscle, as well as measurements of right ventricular pressure and weight, were carried out in the rat during the development and recovery of hypoxic pulmonary hypertension. Animals were divided into hypoxic and normobaric control groups. The hypoxic rats were placed in hypobaric chambers for 1, 2, and 3 wks; and after 3 wks exposure, subgroups of hypoxic rats were allowed to recover in normoxia for 1 to 9 wks. Hematocrit (HCT) and right ventricular systolic pressure (RVSP) were measured prior to sacrifice. The heart was perfused, and the right ventricle (RV) was separated from the left ventricle and septum (LV+S) and weighed. The papillary muscles were dissected and processed for ultrastructural morphometry. Results showed that HCT, RVSP, and RV weight increased in the rats during the hypoxic exposure and then gradually returned to control levels after 3 to 4 wks of normobaric recovery. The papillary muscle of the hypoxic rats showed increased volume density of interstitium, increased diameter and cross sectional area of the cardiac myocytes, reduced volume density of mitochondria, and reduced mitochondria to myofilament ratio. During normoxic recovery, these morphometric indices returned toward control values at various periods of time ranging from less than 3 wks to 9 wks. The results indicate that the adaptive ultrastructural changes of the papillary muscle in RV hypertrophy paralleled the RVSP changes, and also demonstrate the reversibility of these changes in ambient oxygen.

摘要

在低氧性肺动脉高压的发展和恢复过程中,对大鼠右心室乳头肌进行了形态计量学分析,并测量了右心室压力和重量。将动物分为低氧组和常压对照组。低氧大鼠置于低压舱中1、2和3周;在暴露3周后,将低氧大鼠亚组置于常氧环境中恢复1至9周。在处死前测量血细胞比容(HCT)和右心室收缩压(RVSP)。对心脏进行灌注,将右心室(RV)与左心室及室间隔(LV+S)分离并称重。解剖乳头肌并进行超微结构形态计量学处理。结果显示,在低氧暴露期间,大鼠的HCT、RVSP和RV重量增加,在常压恢复3至4周后逐渐恢复到对照水平。低氧大鼠的乳头肌间质体积密度增加,心肌细胞直径和横截面积增加,线粒体体积密度降低,线粒体与肌丝比例降低。在常氧恢复期间,这些形态计量学指标在不到3周至9周的不同时间段内恢复到对照值。结果表明,右心室肥大时乳头肌的适应性超微结构变化与RVSP变化平行,也证明了这些变化在环境氧中的可逆性。

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