Allan G, Cambridge D, Lee-Tsang-Tan L, Van Way C W, Whiting M V
Br J Pharmacol. 1986 Sep;89(1):149-55. doi: 10.1111/j.1476-5381.1986.tb11130.x.
Haemorrhagic shock was induced in anaesthetized, open-chest dogs by controlled arterial bleeding, sufficient to reduce and maintain mean arterial blood pressure at 40 mmHg for 30 min. The blood volume was then restored to the pre-shock level by rapid, intravenous reinfusion of the blood shed during the shock period. Haemorrhagic shock produced significant haemodynamic changes, characterized by a marked depression of myocardial function. Cardiac output (1226 +/- 57 ml min-1), peak aortic blood flow (6030 +/- 383 ml min-1) and maximum rate of rise of left ventricular pressure (2708 +/- 264 mmHg s-1) were all reduced by more than 50%. The haemodynamic profile was markedly improved by reinfusion of shed blood but this improvement was not sustained. There was a gradual decline such that 50% of the untreated animals suffered complete circulatory collapse and death between 60 and 120 min following reinfusion. Neither haemorrhagic shock, nor reinfusion of shed blood produced any consistent or significant changes in the myocardial adenine nucleotide pool. The ATP, ADP and AMP levels were, respectively, 25.9 +/- 4.2; 15.6 +/- 1.0; 4.3 +/- 1.9 nmol g-1 protein, before haemorrhagic shock; 21.6 +/- 3.4; 21.5 +/- 2.5; 10.2 +/- 2.7 nmol g-1 protein, after 30 min haemorrhagic shock; and 29.9 +/- 3.9; 16.5 +/- 1.2; 4.2 +/- 1.1 nmol g-1 protein, 60 min following reinfusion of shed blood. Pretreatment with allopurinol (50.0 mg kg-1 i.v.), 60 min before inducing haemorrhagic shock, had no significant effect upon the haemodynamic response to shock, but did prevent the gradual decline seen following reinfusion in the untreated animals. All of the allopurinol-treated animals displayed significantly better haemodynamic profiles than the untreated animals, furthermore, there was a 100% survival rate in this group. 5 Allopurinol had no significant effect upon the myocardial adenine nucleotide pool either during haemorrhagic shock or following reinfusion of shed blood.
在麻醉的开胸犬身上，通过控制性动脉出血诱导出血性休克，使平均动脉血压降低并维持在40 mmHg达30分钟。然后通过快速静脉输注休克期流失的血液，将血容量恢复到休克前水平。出血性休克导致了显著的血流动力学变化，其特征是心肌功能明显抑制。心输出量（1226±57 ml·min⁻¹）、主动脉血流峰值（6030±383 ml·min⁻¹）和左心室压力最大上升速率（2708±264 mmHg·s⁻¹）均降低了50%以上。回输流失血液后，血流动力学状况明显改善，但这种改善并未持续。出现逐渐下降，以至于50%未经治疗的动物在回输后60至120分钟内发生完全循环衰竭和死亡。出血性休克和回输流失血液均未使心肌腺嘌呤核苷酸池产生任何一致或显著的变化。出血性休克前，ATP、ADP和AMP水平分别为25.9±4.2；15.6±1.0；4.3±1.9 nmol·g⁻¹蛋白质；出血性休克30分钟后分别为21.6±3.4；21.5±2.5；10.2±2.7 nmol·g⁻¹蛋白质；回输流失血液60分钟后分别为29.9±3.9；16.5±1.2；4.2±1.1 nmol·g⁻¹蛋白质。在诱导出血性休克前60分钟，用别嘌呤醇（50.0 mg·kg⁻¹静脉注射）预处理对休克的血流动力学反应没有显著影响，但确实防止了未经治疗的动物回输后出现的逐渐下降。所有用别嘌呤醇治疗的动物的血流动力学状况均明显优于未经治疗的动物，此外，该组的存活率为100%。别嘌呤醇在出血性休克期间或回输流失血液后对心肌腺嘌呤核苷酸池均无显著影响。
