Background Recent research suggests that β2-adrenergic agonists increase alveolar fluid clearance （AFC） under physiologic and pathologic conditions. It is unknown whether β3-adrenergic agonists also increase AFC u...Background Recent research suggests that β2-adrenergic agonists increase alveolar fluid clearance （AFC） under physiologic and pathologic conditions. It is unknown whether β3-adrenergic agonists also increase AFC under pathologic conditions. The aim of this study was to investigate the effect of β3-adrenergic agonists on AFC following hypoxic lung injury and the mechanisms involved. Methods Hypoxic rats were exposed to 10% oxygen. BRL-37344 （133-adrenergic agonist） or CGP-12177 （selective β3-adrenergic agonist） alone or combined with β receptor antagonists, sodium channel blockers, or Na＋/＋^-ATPase blockers were perfused into the alveolar space of rats exposed to 10% oxygen for 48 hours. Total lung water content （TLW） and AFC were measured. Results AFC did not change for the first 24 hours but then decreased after 48-hour exposure to 10% oxygen. The perfusion of BRL-37344 or CGP-12177 significantly increased AFC in normal and hypoxic rats. The AFC-stimulating effect of CGP-12177 was lowered with amiloride （a Na＋ channel blocker） and ouabain （a Na~/K^-ATPase inhibitor） by 37% and 49%, respectively. Colchicine significantly inhibited the effect of CGP-12177. Conclusions These findings suggest that β3-adrenergic agonists can increase AFC during hypoxic lung injury in rats and accelerate the amelioration of pulmonary edema.展开更多
文摘Background Recent research suggests that β2-adrenergic agonists increase alveolar fluid clearance （AFC） under physiologic and pathologic conditions. It is unknown whether β3-adrenergic agonists also increase AFC under pathologic conditions. The aim of this study was to investigate the effect of β3-adrenergic agonists on AFC following hypoxic lung injury and the mechanisms involved. Methods Hypoxic rats were exposed to 10% oxygen. BRL-37344 （133-adrenergic agonist） or CGP-12177 （selective β3-adrenergic agonist） alone or combined with β receptor antagonists, sodium channel blockers, or Na＋/＋^-ATPase blockers were perfused into the alveolar space of rats exposed to 10% oxygen for 48 hours. Total lung water content （TLW） and AFC were measured. Results AFC did not change for the first 24 hours but then decreased after 48-hour exposure to 10% oxygen. The perfusion of BRL-37344 or CGP-12177 significantly increased AFC in normal and hypoxic rats. The AFC-stimulating effect of CGP-12177 was lowered with amiloride （a Na＋ channel blocker） and ouabain （a Na~/K^-ATPase inhibitor） by 37% and 49%, respectively. Colchicine significantly inhibited the effect of CGP-12177. Conclusions These findings suggest that β3-adrenergic agonists can increase AFC during hypoxic lung injury in rats and accelerate the amelioration of pulmonary edema.
