Prolonged isoproterenol infusion impairs the ability of beta(2)-agonists to increase alveolar liquid clearance.
Prolonged isoproterenol infusion impairs the ability of beta(2)-agonists to increase alveolar liquid clearance.
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延长异丙肾上腺素输注会损害 β(2) 激动剂增加肺泡液体清除率的能力。
DOI：
10.1152/ajplung.00381.2001
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发表时间：
2002
期刊：
影响因子：
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通讯作者：
Maron,MichaelB
中科院分区：
文献类型：
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作者：
Morgan,EricE;Hodnichak,CherylM;Stader,SonyaM;Maender,KayC;Boja,JohnW;Folkesson,HansG;Maron,MichaelB
L666-L674, 2002年。首次发表于2001年12月14日；10.1152 / ajplung。00381.2001.我们确定大鼠长期输注异丙肾上腺素（Iso）是否会损害2-肾上腺素能激动剂特布他林增加肺泡液体清除率（ALC）的能力。我们使用皮下植入的微渗透泵给大鼠注射Iso（剂量为4、40或400 gkg 1 h 1）或对照物（0.001 N HCl） 48 h。在此之后，麻醉大鼠，在基线条件下和给药特布他林后测定ALC（通过向肺中注入含白蛋白的乳酸林格液后的质量平衡）。基线和特布他利未刺激大鼠ALC平均分别为19.6 1.2%（SE）和44.7 1.5%/h。特布他林增加ALC的能力在400 gkg 1 h 1 Iso时被消除，在40 gkg 1 h 1 Iso时被抑制26%，而在4 gkg 1 h 1 Iso时不受影响。40和400 gkg 1 h 1输注速率降低了新分离的大鼠肺泡上皮II型（ATII）细胞的-肾上腺素能受体（AR）密度。这些数据表明，长时间暴露于激动剂会损害2-激动剂刺激ALC和产生ATII细胞AR下调的能力。肺液平衡；肺水肿;肾上腺素能受体;以上;差别受体对这些肺泡上皮II型细胞
L666–L674, 2002. First published December 14, 2001; 10.1152/ajplung. 00381.2001.—We determined if prolonged isoproterenol (Iso) infusion in rats impaired the ability of the2-adrenergic agonist terbutaline to increase alveolar liquid clearance (ALC). We infused rats with Iso (at rates of 4, 40, or 400 gkg 1 h 1) or vehicle (0.001 N HCl) for 48 h using subcutaneously implanted miniosmotic pumps. After this time, the rats were anesthetized, and ALC was determined (by mass-balance after instillation of Ringer lactate containing albumin into the lungs) under baseline conditions and after terbutaline administration. Baseline and terbutalinestimulated ALC in vehicle-infused rats averaged, respectively, 19.6 1.2%(SE) and 44.7 1.5%/h. The ability of terbutaline to increase ALC was eliminated at 400 gkg 1 h 1 Iso, inhibited by 26% at 40 gkg 1 h 1 Iso, and was not affected by 4 gkg 1 h 1 Iso.-adrenergic receptor (AR) density of freshly isolated alveolar epithelial type II (ATII) cells from Iso-infused rats was reduced by the 40 and 400 gkg 1 h 1 infusion rates. These data demonstrate that prolonged exposure to-agonists can impair the ability of2-agonists to stimulate ALC and produce ATII cell AR downregulation. lung fluid balance; pulmonary edema;-adrenergic receptor; receptor downregulation; alveolar epithelial type II cell