Smedegård G, Revenäs B, Lundberg C, Arfors K E
Acta Physiol Scand. 1981 Mar;111(3):239-47. doi: 10.1111/j.1748-1716.1981.tb06732.x.
Mechanisms inducing a low cardiac output (CO) state in IgE-mediated (cytotropic) anaphylactic shock in anesthetized Macaca irus monkeys were studied. 7 monkeys were sensitized by 2 i.v. injections of a human reaginic serum containing a high concentration of IgE antibodies against dog albumin. Anaphylactic shock was elicited 48 h after the last sensitization dose, by an i.v. injection of dog albumin. The severe anaphylactic shock which developed was characterized by an initial phase consisting of increased CO (+16%, mean value, 1 min after challenge), pulmonary hypertension and systemic vasodilatation followed by a phase consisting of decreased CO (-67%), a fall in mean arterial pressure from 113 to 45 mmHg, decreases in left and right arterial pressures (-5.3 and -3.2 mmHg, respectively) and increases in pulmonary vascular (+364%) and total peripheral (+30%) resistances. These changes were recorded 5 min after challenge and the values then remained essentially unaltered during the rest of the 30-min observation period. Pulmonary vascular resistance was only increased by 140% at the end of that period. Myocardial blood flow was maintained during shock at the expense of flow to other organs. However, initially there was a redistribution of blood flow within the left ventricular myocardium, resulting in a relative decrease in subendocardial flow. This finding was not related either to occasional S-T changes in the electrocardiograms or to the level of decreased CO. The oxygen supply to the myocardium was reduced in shock but the reduction was always smaller than the corresponding decrease in heart work. Two additional monkeys sensitized with an IgE fraction from the human serum showed a smaller amount of specific IgG in their serum prior to challenge than the other monkeys. The response to challenge was milder, but resembled the initial vasodilatory reaction in monkeys sensitized with serum. These data on cytotropic anaphylaxis in the monkey show that the main cause of decreased CO and thus of the shock state is a decreased venous return, primarily due to peripheral blood pooling and, to a smaller extent, extravasation of plasma. No appreciable involvement of the heart in the induction of shock was detected.
研究了在麻醉的猕猴中，IgE介导（亲细胞性）过敏性休克导致低心输出量（CO）状态的机制。7只猴子通过静脉注射2次含有高浓度抗犬白蛋白IgE抗体的人反应素血清进行致敏。在最后一次致敏剂量后48小时，通过静脉注射犬白蛋白引发过敏性休克。所发生的严重过敏性休克的特征是，初始阶段心输出量增加（激发后1分钟平均值增加16%）、肺动脉高压和全身血管扩张，随后是心输出量降低（降低67%）、平均动脉压从113 mmHg降至45 mmHg、左、右动脉压降低（分别降低5.3和3.2 mmHg）以及肺血管阻力（增加364%）和总外周阻力（增加30%）阶段。这些变化在激发后5分钟记录，然后在30分钟观察期的其余时间内基本保持不变。在该观察期末，肺血管阻力仅增加140%。休克期间心肌血流得以维持，但以其他器官的血流为代价。然而，最初左心室心肌内血流重新分布，导致心内膜下血流相对减少。这一发现与心电图偶尔出现的S-T段变化或心输出量降低的程度均无关。休克时心肌的氧供应减少，但减少幅度总是小于相应的心脏作功减少幅度。另外2只用人血清IgE组分致敏的猴子，在激发前血清中特异性IgG含量比其他猴子少。对激发的反应较轻微，但类似于用血清致敏的猴子的初始血管舒张反应。这些关于猕猴亲细胞性过敏反应的数据表明，心输出量降低从而导致休克状态的主要原因是静脉回流减少，主要是由于外周血液淤积，在较小程度上是由于血浆外渗。未检测到心脏在休克诱导中有明显参与。
