Lin H L, Katele K V, Grimm A F
Circ Res. 1977 Dec;41(6):830-6. doi: 10.1161/01.res.41.6.830.
We studied hearts in which hypertrophy was caused by both pressure and volume overload. Pressure hypertrophy was induced by an aortic constriction; volume hypertrophy was induced by an iron-copper deficiency (anemia). The ventricular weight was increased by 34% in the pressure-hypertrophied hearts at the end of 6 weeks. The ventricular weight was increased by 54% in the volume-hypertrophied hearts at the end of 3 months. A potassium arrest-formalin fixation technique was used to produce a "diastole-like" ventricle. In the pressure-hypertrophied ventricle, the ventricular wall thickness and external radii were significantly increased, whereas the valve-to-apex distance and internal radii remained unchanged. We also found that in the volume-hypertrophied ventricle there was an increase in the valve-to-apex distance, external radii, internal radii, and wall thickness. Although external and internal dimensions increased, the ventricular shape did not change significantly in the volume-hypertrophied ventricle.
我们研究了因压力负荷和容量负荷均导致肥厚的心脏。压力性肥厚通过主动脉缩窄诱导产生;容量性肥厚通过铁铜缺乏(贫血)诱导产生。6周结束时,压力性肥厚心脏的心室重量增加了34%。3个月末,容量性肥厚心脏的心室重量增加了54%。采用钾停搏-甲醛固定技术制作“舒张样”心室。在压力性肥厚心室中,心室壁厚度和外径显著增加,而瓣膜至心尖距离和内径保持不变。我们还发现,在容量性肥厚心室中,瓣膜至心尖距离、外径、内径和壁厚度均增加。尽管外部和内部尺寸增加,但容量性肥厚心室的心室形状无显著变化。