Goadby P
J Pharm Pharmacol. 1975 Apr;27(4):254-61. doi: 10.1111/j.2042-7158.1975.tb10695.x.
The study was undertaken to discover whether the catecholamines released as a result of the stress and hypoxia of anaphylaxis were responsible for the concomitant loss of lipid from the lung. A method is described whereby the respiratory rate and volume and heart-rate of conscious sensitized guinea-pig were measured and the electrocardiogram recorded during anaphylaxis induced by aerosolized antigen. After 7 days or more, some animals were anaesthetized with pentobarbitone and respiration was artificially maintained at the level recorded in the conscious state, whilst the quantity of catecholamines liberated during anaphylaxis was assayed using an extra-corporeal blood circulation to superfuse smooth muscle preparations. In other animals of the same group, it was shown that intravenous infusion of adrenaline in a similar quantity to that detected in the circulation following anaphylaxis (0.3 mug min-(-1) for 40 min) caused losses of triglyceride and partial glycerides from the lungs. Thus, the loss of choline-containing phospholipid was attributed to the direct effects of the anaphylactic reaction on the lung tissue.
开展这项研究是为了探究因过敏反应的应激和缺氧而释放的儿茶酚胺是否是导致肺部脂质同时流失的原因。本文描述了一种方法，通过该方法可以测量清醒致敏豚鼠在雾化抗原诱导的过敏反应期间的呼吸频率、呼吸量和心率，并记录心电图。7天或更长时间后，一些动物用戊巴比妥麻醉，并将呼吸人工维持在清醒状态下记录的水平，同时使用体外血液循环来灌注平滑肌制剂，以测定过敏反应期间释放的儿茶酚胺量。在同一组的其他动物中，研究表明，静脉输注与过敏反应后循环中检测到的量相似的肾上腺素（0.3微克·分钟⁻¹，持续40分钟）会导致肺部甘油三酯和部分甘油酯的流失。因此，含胆碱磷脂的流失归因于过敏反应对肺组织的直接影响。
