Zhang Z B, Wang C B, Qian J Q
Department of Pharmacology, Tongji Medical University, Wuhan, China.
Zhongguo Yao Li Xue Bao. 1998 Jan;19(1):54-7.
To investigate the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride (DDPH) on cardiac systolic and diastolic function, lactate dehydrogenase (LDH) activity, and LDH isoenzymes in rats with cardiac hypertrophy.
The cardiac hypertrophy of rats was induced by partly occluding abdominal aorta. The rats were given i.g. DDPH for 8 wk 4 wk after operation, and isolated working heart was made.
Eight wk later, in model group, left ventricle systolic pressure (LVSP), LV + dp/dtmax, -dp/dtmax and aorta pressure (AP) decreased by 20.2%, 20.0%, 41.4%, and 13.6%, respectively. Left ventricle ending diastolic pressure (LVEDP) increased by 173.9%. The hemodynamic study showed that flowing liquid of aorta (AF) and coronary (CF) and cardiac output (CO) decreased by 49.4%, 41.2%, and 48.9%, respectively. After the rats were given i.g. DDPH, the all above-mentioned parameters recovered to different degrees. Under condition of cardiac hypertrophy, LDH isoenzymes and subunits changed significantly. Isoenzymes LDH3, LDH4, and LDH5, especially LDH5 increased, LDH1 decreased, subunit M in hypertrophied heart increased 1.69 times than that in normal heart. DDPH could decrease subunit M and increase subunit H.
DDPH can increase cardiac function, coronary flow and reverse changes of LDH isoenzymes in rats with cardiac hypertrophy.
研究1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙氨基)丙烷盐酸盐(DDPH)对心肌肥厚大鼠心脏收缩和舒张功能、乳酸脱氢酶(LDH)活性及LDH同工酶的影响。
采用部分结扎腹主动脉法诱导大鼠心肌肥厚。术后4周开始灌胃给予DDPH,连续8周,然后制备离体工作心脏。
8周后,模型组左心室收缩压(LVSP)、左心室压力上升最大速率(LV + dp/dtmax)、左心室压力下降最大速率(-dp/dtmax)及主动脉压力(AP)分别下降20.2%、20.0%、41.4%和13.6%,左心室舒张末压(LVEDP)升高173.9%。血流动力学研究显示,主动脉血流量(AF)、冠状动脉血流量(CF)及心输出量(CO)分别下降49.4%、41.2%和48.9%。大鼠灌胃给予DDPH后,上述各项指标均有不同程度恢复。在心肌肥厚状态下,LDH同工酶及其亚基发生明显改变,LDH3、LDH4和LDH5同工酶尤其是LDH5升高,LDH1降低,肥厚心肌中亚基M比正常心肌增加1.69倍。DDPH可降低亚基M并增加亚基H。
DDPH可改善心肌肥厚大鼠的心功能、增加冠脉流量并逆转LDH同工酶的改变。