Hamed A T, Ginos J Z, Ekas R D, Jandhyala B S, Lokhandwala M F
J Cardiovasc Pharmacol. 1983 Mar-Apr;5(2):207-12.
The present study was conducted to determine if selective prejunctional dopamine receptor agonists will be useful in improving renal hemodynamics in acute hemorrhagic shock in anesthetized mongrel dogs. Both bromocriptine and N-n-propyl-N-n-butyl dopamine (PBDA) effectively increased renal blood flow, due to a decrease in renal vascular resistance in intact anesthetized dogs. However, these two agents failed to increase renal blood flow after acute hemorrhage in the innervated or denervated kidneys. Dopamine was effective in increasing renal blood flow in both intact and hemorrhaged animals. However, this action of dopamine in hemorrhaged animals was associated with a significant increase in arterial blood pressure. These data could be explained based on the observations that the reduction in renal blood flow following hemorrhage was primarily due to a decrease in blood pressure as a result of the decrease in cardiac output and was not due to an increase in renal vascular resistance. Because elevation of sympathetic tone appeared to play little role, prejunctional inhibition by bromocriptine and/or PBDA of sympathetic nerve function was ineffective in altering renal vascular resistance. Dopamine was effective in increasing renal blood flow, not because of its pre- or postjunctional actions on dopamine receptors on renal nerves or vasculature, but because of its ability to increase cardiac output and arterial pressure. Based on the experimental model employed in these studies, it is concluded that agents such as PBDA and bromocriptine, which are considered to be selective prejunctional dopamine agonists, may not be clinically useful in improving renal circulation during hemorrhagic shock.
本研究旨在确定选择性突触前多巴胺受体激动剂是否有助于改善麻醉杂种犬急性失血性休克时的肾脏血流动力学。在完整的麻醉犬中，由于肾血管阻力降低，溴隐亭和N-正丙基-N-正丁基多巴胺（PBDA）均能有效增加肾血流量。然而，在神经支配或去神经支配的肾脏急性出血后，这两种药物未能增加肾血流量。多巴胺在完整动物和出血动物中均能有效增加肾血流量。然而，多巴胺在出血动物中的这种作用与动脉血压的显著升高有关。这些数据可以基于以下观察结果来解释：出血后肾血流量的减少主要是由于心输出量减少导致血压下降，而不是由于肾血管阻力增加。由于交感神经张力升高似乎作用不大，溴隐亭和/或PBDA对交感神经功能的突触前抑制在改变肾血管阻力方面无效。多巴胺能有效增加肾血流量，不是因为其对肾神经或血管上多巴胺受体的突触前或突触后作用，而是因为其增加心输出量和动脉血压的能力。基于这些研究中使用的实验模型，得出结论：被认为是选择性突触前多巴胺激动剂的PBDA和溴隐亭等药物在出血性休克期间改善肾循环可能在临床上并无用处。
