Marino T A, Brody E, Lauva I K, Kent R L, Cooper G
Anat Rec. 1986 Feb;214(2):141-7. doi: 10.1002/ar.1092140206.
The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophing in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.
本定量结构研究的目的是确定在压力超负荷心肌中观察到的组织学改变在去除压力超负荷刺激后是否如体外收缩功能一样恢复正常。研究了三个实验组,每组四只猫:一组通过肺动脉束带造成压力超负荷,一组经历了相同时长的压力超负荷然后去除该压力超负荷,以及一组假手术对照组。每次手术后7至10周,仅在肺动脉束带组右心室压力升高。仅在压力超负荷组右心室/体重比显著增加。三组在处死时的体重、左心室/体重比和右心室舒张末期压力无显著差异。右心室心肌因压力超负荷而肥厚时显著的组织学变化是心肌细胞体积密度降低和乳头肌结缔组织增加。当去除压力超负荷时这些变化逆转。本研究表明,当去除压力超负荷时,心肌结构随功能恢复正常而恢复正常。鉴于心肌细胞和结缔组织成分的比例对心脏收缩和舒张功能至关重要,这些数据支持以下假说,即这些结构的异常比例为猫右心室压力超负荷肥大中观察到的至少一些功能异常提供了潜在的形态学基础。