Ogburn P
Vet Clin North Am. 1976 May;6(2):287-95. doi: 10.1016/s0091-0279(76)50036-0.
Vasoactive agents may have vasoconstrictor, vasodilator, cardiac stimulatory, or combined effects on the cardiovascular system. The intensity or degree of therapeutic effect differs with each agent. Table 1 provides a relative ranking of each discussed compound's effect regarding its ability to produce one or more of the listed effects. The effects of vasoconstrictor drugs such as methoxamine, phenylephrine, and norepinephrine have been generally unfavorable in shock because of the inhibition of tissue perfusion which results from their use. Debate still exists, however, and these agents have been shown to provide some benefit in selected cases. The rationale that shock results at least in part because of intense vasoconstriction has led to the usage of vasodilators in therapy. Currently isoproterenol, a beta adrenergic stimulating agent, is being used to elicit vasodilation in lieu of alpha blockage because the alpha blocking drugs phenoxybenzamine and chlorpromazine have longer, more irreversible effects. The merit of isoproterenol has to be evaluated in light light of its cardiac stimulatory effect. With the current antishock drugs, those which possess cardiac stimulatory effects seem to be most effective with the exception of those with alpha stimulatory properties. The importance of cardiac stimulation in treating shock is related to the fact that in many forms of shock a decrease in cardiac function is evident. Drugs which effect increases in cardiac performance will increase cardiac output and tissue perfusion. The increased excitability of the heart caused by many of the drugs is a drawback, but compounds such as dopamine seem to have less excitatory effect than does isoproterenol. It may be that vasoconstriction, vasodilation, and cardiac stimulation are all contributory to the alleviation of shock. However, it is important to remember that the use of vasoactive agents must be reserved for those deteriorating shock states in which primary and secondary factors responsible for the initial state have been adequately controlled and only when appropriate methods for judging hemodynamic performance have been instituted.
血管活性药物可能对心血管系统产生血管收缩、血管舒张、心脏刺激或联合作用。每种药物的治疗效果强度或程度各不相同。表1提供了每种讨论化合物在产生一种或多种所列效应方面的相对排名。去氧肾上腺素、去甲肾上腺素等血管收缩药物在休克中的作用通常是不利的,因为使用它们会抑制组织灌注。然而,争论仍然存在,并且这些药物在某些特定情况下已显示出一些益处。休克至少部分是由于强烈的血管收缩导致的这一理论,促使血管舒张剂被用于治疗。目前,β肾上腺素能刺激剂异丙肾上腺素被用于引发血管舒张以替代α受体阻滞,因为α受体阻滞药物酚苄明和氯丙嗪具有更长、更不可逆的作用。必须根据其心脏刺激作用来评估异丙肾上腺素的优点。就目前的抗休克药物而言,除了具有α刺激特性的药物外,那些具有心脏刺激作用的药物似乎最有效。心脏刺激在治疗休克中的重要性与以下事实有关:在许多形式的休克中,心脏功能明显下降。能提高心脏性能的药物将增加心输出量和组织灌注。许多药物引起的心脏兴奋性增加是一个缺点,但多巴胺等化合物的兴奋作用似乎比异丙肾上腺素小。血管收缩、血管舒张和心脏刺激可能都有助于缓解休克。然而,重要的是要记住,血管活性药物的使用必须仅保留给那些病情恶化的休克状态,在这些状态下,导致初始状态的主要和次要因素已得到充分控制,并且只有在已经建立了判断血流动力学性能的适当方法时才能使用。