Zhang Y, Lautt W W
Department of Pharmacology & Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Br J Pharmacol. 1992 Apr;105(4):765-7. doi: 10.1111/j.1476-5381.1992.tb09052.x.
A haemorrhage model was used to impose severe metabolic stress in anaesthetized cats by removing blood (15.3 ml min-1) to attain an arterial pressure of ca. 50 mmHg for a 2 h period. Adenosine levels in central venous blood rose by 5 min, reached a peak of about 3.5 times control levels by 15 min and then returned to the basal level (1 microM) by 60 min. However, the adenosine concentration in arterial blood remained unchanged for the entire 2 h period of hypotension. These data demonstrate that haemorrhage results in rapid adenosine release, but the released adenosine is not able to serve a role as a systemic circulating vasodilator even in this severe model.
采用出血模型,通过放血(15.3毫升/分钟)使麻醉猫承受严重的代谢应激,持续2小时以达到约50 mmHg的动脉压。中心静脉血中的腺苷水平在5分钟时升高,15分钟时达到约对照水平3.5倍的峰值,然后在60分钟时恢复到基础水平(1微摩尔)。然而,在低血压的整个2小时期间,动脉血中的腺苷浓度保持不变。这些数据表明,出血导致腺苷快速释放,但即使在这个严重的模型中,释放的腺苷也不能作为全身循环血管舒张剂发挥作用。