Maron M B
Am J Physiol. 1985 Feb;248(2 Pt 2):H225-31. doi: 10.1152/ajpheart.1985.248.2.H225.
The purpose of this study was to determine if aspirin, in doses that elevate plasma salicylate concentrations to values reported in patients with salicylate-induced pulmonary edema, produce pulmonary vasoconstriction in a canine, isolated perfused left lower lung lobe (LLL) preparation. In 10 LLL's, aspirin (avg 97.8 mg/dl plasma) caused LLL arterial pressure to rise from 9.1 +/- 0.3 to 23.0 +/- 1.8 (SE) Torr. In contrast, no vascular pressure changes were observed in placebo-treated control LLL's. Sodium meclofenamate and indomethacin, structurally dissimilar cyclooxygenase inhibitors, elicited similar responses to aspirin, suggesting that a mechanism involving products of prostaglandin cyclooxygenase was involved in producing the vasoconstriction. The double-occlusion technique was used to localize the sites of the vasoconstriction. The results suggested that all three drugs caused both lobar arterial and venous tone to increase. Although high doses of aspirin produced pulmonary vasoconstriction in the isolated, perfused LLL, the aspirin-treated LLL's gained less weight and extravascular water than the control lobes.
本研究的目的是确定阿司匹林剂量升高血浆水杨酸浓度至水杨酸诱导的肺水肿患者报告的水平时,是否会在犬类离体灌注左下肺叶(LLL)制备物中引起肺血管收缩。在10个LLL中,阿司匹林(平均血浆浓度97.8mg/dl)使LLL动脉压从9.1±0.3升至23.0±1.8(SE)托。相比之下,安慰剂处理的对照LLL未观察到血管压力变化。甲氯芬那酸钠和吲哚美辛,结构不同的环氧化酶抑制剂,对阿司匹林产生类似反应,表明涉及前列腺素环氧化酶产物的机制参与了血管收缩的产生。采用双闭塞技术定位血管收缩部位。结果表明,所有三种药物均导致叶动脉和静脉张力增加。尽管高剂量阿司匹林在离体灌注的LLL中产生肺血管收缩,但与对照叶相比,阿司匹林处理的LLL重量增加和血管外水分增加较少。