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大鼠腹主动脉部分狭窄５周后，形成实验性左室肥厚（ＬＶＨ）模型，ＬＶＨ组左室重较伪手术组增加了９１％（Ｐ＜０．０１），分别给予ｍ－Ｎｉｆ与Ｎｉｆ１０ｍｇ·ｋｇ￣（－１），ｉｇ４周后，左室湿重分别比肥厚组减少２５％±９％和１６％±９％，ＬＶＨ组的左室顺应性明显降低，僵硬度系数显著升高。ＬＶＨ组ＤＨＰ受体总量较伪手术组显著增加，两药物组则较ＬＶＨ组分别降低了２８．３％±４．９％和２４．８％±１０．４％。结果提示ｍ－Ｎｉｆ和Ｎｉｆ均能显著降低ＬＶＨ大鼠左室心肌ＤＨＰ受体总数，预防压力超负荷所致的左室肥厚。
After 5 weeks of partial stenosis of the abdominal aorta in rats, experimental LVH model was established. The left ventricular mass of LVH group increased by 91% (P <0.01) compared with that of the sham-operated group, and the levels of m-Nif and Nif10mg · Kg ~ (-1). After 4 weeks, the left ventricular wet weight decreased by 25% ± 9% and 16% ± 9% respectively in the hypertrophic group. LVH compliance decreased significantly and the stiffness coefficient increased significantly. The total amount of DHP receptor in LVH group was significantly higher than that in sham-operation group, while the two drug groups decreased by 28.3% ± 4.9% and 24.8% ± 10.4% respectively compared with LVH group. The results suggest that both m-Nif and Nif can significantly reduce the total number of left ventricular DHP receptors in LVH rats and prevent left ventricular hypertrophy induced by pressure overload.