Chang H Y
Department of Internal Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Am J Physiol. 1997 May;272(5 Pt 2):H2173-9. doi: 10.1152/ajpheart.1997.272.5.H2173.
To determine the contribution of nitric oxide (NO) to the vasodilator response induced by salbutamol in diaphragmatic microcirculation, we studied a diaphragmatic preparation in anesthetized rats. With bicarbonate-buffered Ringer solution continuously suffusing the diaphragm, laser-Doppler flowmetry was used to record microvascular blood flow (QLDF). The drugs were applied to the surface of the diaphragm. Salbutamol (3.2 x 10(-7)-10(-4) M), isoproterenol (3.2 x 10(-8)-3.2 x 10(-6) M), and forskolin (3.2 x 10(-7)-10(-5) M) each elicited a concentration-dependent increase in QLDF. The vasodilator response induced by salbutamol (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was attenuated by a 15-min suffusion of N omega-nitro-L-arginine (L-NNA, 10(-4) M), and pretreatment with L-arginine (10(-2) M) could restore salbutamol-induced vasodilator responses. Salbutamol-induced vasodilation was also abolished by propranolol (10(-5) M). Similarly, the vasodilator response elicited by isoproterenol (3.2 x 10(-8), 10(-7), and 3.2 x 10(-7) M) and forskolin (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was inhibited by L-NNA (10(-4) M). In contrast, the vasodilator response induced by adenosine (10(-6), 10(-5), and 10(-4) M) was not affected by L-NNA (10(-4) M). These data indicate that in rat diaphragmatic microcirculation salbutamol-induced vasodilation may be partly mediated by beta-adrenoceptors on the endothelium. Moreover, these data suggest that an elevation of cyclic AMP in the endothelium may cause release of NO.
为了确定一氧化氮（NO）对沙丁胺醇诱导的膈肌微循环血管舒张反应的作用，我们研究了麻醉大鼠的膈肌标本。用碳酸氢盐缓冲的林格氏液持续灌注膈肌，采用激光多普勒血流仪记录微血管血流量（QLDF）。将药物应用于膈肌表面。沙丁胺醇（3.2×10⁻⁷ - 10⁻⁴ M）、异丙肾上腺素（3.2×10⁻⁸ - 3.2×10⁻⁶ M）和福斯可林（3.2×10⁻⁷ - 10⁻⁵ M）均引起QLDF浓度依赖性增加。Nω-硝基-L-精氨酸（L-NNA，10⁻⁴ M）灌注15分钟可减弱沙丁胺醇（3.2×10⁻⁷、10⁻⁶和3.2×10⁻⁶ M）诱导的血管舒张反应，而用L-精氨酸（10⁻² M）预处理可恢复沙丁胺醇诱导的血管舒张反应。普萘洛尔（10⁻⁵ M）也可消除沙丁胺醇诱导的血管舒张。同样，L-NNA（10⁻⁴ M）可抑制异丙肾上腺素（3.2×10⁻⁸、10⁻⁷和3.2×10⁻⁷ M）和福斯可林（3.2×10⁻⁷、10⁻⁶和3.2×10⁻⁶ M）引起的血管舒张反应。相比之下，腺苷（10⁻⁶、10⁻⁵和10⁻⁴ M）诱导的血管舒张反应不受L-NNA（10⁻⁴ M）影响。这些数据表明，在大鼠膈肌微循环中，沙丁胺醇诱导的血管舒张可能部分由内皮细胞上的β-肾上腺素能受体介导。此外，这些数据提示内皮细胞中环磷酸腺苷（cAMP）升高可能导致NO释放。
