Carlyle P F, Cohn J N
Department of Medicine, University of Minnesota Medical School, Minneapolis.
Am Heart J. 1990 Sep;120(3):619-24. doi: 10.1016/0002-8703(90)90020-x.
In seven dogs with long-standing left ventricular dysfunction induced 16 weeks earlier by repetitive transmyocardial direct current (DC) shock, the acute hemodynamic effect of the alpha 1-adrenoceptor antagonist urapidil was studied. Left ventricular end-diastolic pressure (LVEDP) was significantly increased from preshock levels at the time of study and cardiac output was reduced. Plasma norepinephrine was significantly increased from control levels and was not altered by urapidil infusion. The mean arterial pressure fell in response to alpha 1-blockade from 111 to 85 mm Hg, the LVEDP fell from 16 to 9 mm Hg, and cardiac output increased from 2.90 to 3.70 L/min (all p less than 0.01). Regional blood flows measured by microsphere injection revealed an increase in blood flow to skeletal muscle, which had not been significantly decreased by the left ventricular dysfunction in this model, and further decreases in splanchnic flow, which was already depressed compared with that in normal dogs. Therefore acute alpha-adrenoceptor blockade improves central hemodynamics in experimental heart failure but does not normalize the resting blood flow maldistribution in this model.
在7只16周前因反复经心肌直流电（DC）休克诱导出现长期左心室功能障碍的犬中，研究了α1肾上腺素能受体拮抗剂乌拉地尔的急性血流动力学效应。研究时左心室舒张末期压力（LVEDP）较休克前水平显著升高，心输出量降低。血浆去甲肾上腺素较对照水平显著升高，且未因输注乌拉地尔而改变。平均动脉压因α1受体阻断从111 mmHg降至85 mmHg，LVEDP从16 mmHg降至9 mmHg，心输出量从2.90 L/min增加至3.70 L/min（均p<0.01）。通过微球注射测量的局部血流显示，骨骼肌血流增加，在该模型中左心室功能障碍并未使其显著降低，而内脏血流进一步减少，与正常犬相比其已经降低。因此，急性α肾上腺素能受体阻断可改善实验性心力衰竭的中心血流动力学，但不能使该模型中静息血流分布不均恢复正常。
