Gorodetskaya E A, Dugin S F, Medvedev O S, Allabergenova A E
Institute of Experimental Cardiology, Cardiology Research Center of the USSR, Moscow.
J Pharmacol Methods. 1990 Aug;24(1):43-51. doi: 10.1016/0160-5402(90)90048-p.
Changes in left ventricle (LV) function, systemic, and regional hemodynamics as a result of coronary artery embolization by 15 microns microspheres were studied in rats. Selective coronary embolization was produced by injection of microspheres during ascending aorta occlusion animals by using an "L"-shaped wire in closed chest animals. Maximal developed LV systolic pressure (LVSPmax) was determined during ascending aorta occlusion. Coronary embolization evoked reductions in LVSPmax and +dP/dtmax and then decreased in basal LVSP, dP/dtmax, dP/dtmax/P, with a parallel increase in LV end-diastolic pressure (LVEDP). The number of microspheres accumulating in the heart following coronary embolization was about 40% of the total amount of the injected microspheres (300,000-400,000). In conscious rats 48 hr after coronary vessel embolization (in LV myocardium 100,003 +/- 4,334 microspheres per gram) the cardiac index, mean arterial pressure, -dP/dtmax and stroke volume were reduced by 35.6%, 20%, 17.2%, and 26.7%, respectively, when compared with sham-operated rats. LVEDP was increased by 40%, when compared with sham-operated rats. These results show that in this rat model of coronary vessel embolization heart failure develops. The model created may be used for the studies of pathophysiology of acute heart failure as well as for screening new compounds potentially effective in heart failure.
研究了大鼠因15微米微球导致冠状动脉栓塞后左心室（LV）功能、全身及局部血流动力学的变化。在开胸动物中，通过使用“L”形金属丝在升主动脉闭塞时注射微球来实现选择性冠状动脉栓塞。在升主动脉闭塞期间测定最大左心室收缩压（LVSPmax）。冠状动脉栓塞导致LVSPmax和 +dP/dtmax降低，随后基础左心室收缩压、dP/dtmax、dP/dtmax/P降低，同时左心室舒张末期压力（LVEDP）平行升高。冠状动脉栓塞后心脏中积聚的微球数量约为注射微球总量（300,000 - 400,000）的40%。在冠状动脉血管栓塞48小时后的清醒大鼠中（左心室心肌每克有100,003 ± 4,334个微球），与假手术大鼠相比，心脏指数、平均动脉压、 -dP/dtmax和每搏输出量分别降低了35.6%、20%、17.2%和26.7%。与假手术大鼠相比，LVEDP升高了40%。这些结果表明，在这种大鼠冠状动脉血管栓塞模型中会发生心力衰竭。所建立的模型可用于急性心力衰竭病理生理学研究以及筛选对心力衰竭可能有效的新化合物。
