WEIL M H, SUDRANN R B, SHUBIN H
Calif Med. 1962 Feb;96(2):86-8.
Hemodynamic studies have demonstrated that the fall of blood pressure in shock caused by endotoxin in dogs does not result primarily from dilatation or "vasomotor collapse." Indeed, vasoconstriction is increased and may be excessive. Progression of shock has recently been blamed on such excessive vasoconstriction. For this reason the use of sympathomimetic drugs as vasopressor agents has been challenged and sympatholytic or adrenolytic agents have been recommended. In the present study, vasopressor and vasodilator drugs were used for the treatment of shock in dogs caused by endotoxin. Vasodilator drugs, when used after the onset of shock, hastened a fatal outcome but vasopressor agents were not detrimental when used in moderate doses. The effectiveness of the vasopressor agent is not necessarily due to a primary vasoconstrictor action on arteries and arterioles, as previously assumed.
血流动力学研究表明，内毒素所致犬类休克时的血压下降并非主要源于血管扩张或“血管运动性虚脱”。事实上，血管收缩增强，甚至可能过度。近来，休克的进展被归咎于这种过度的血管收缩。因此，将拟交感神经药物用作血管升压药受到了质疑，有人推荐使用抗交感神经或抗肾上腺素能药物。在本研究中，血管升压药和血管扩张药被用于治疗内毒素所致犬类休克。休克发作后使用血管扩张药会加速致命结局，但中等剂量使用血管升压药并无危害。血管升压药的有效性不一定如先前所认为的那样，主要归因于对动脉和小动脉的原发性血管收缩作用。
