Robertson B E, Paterson D J, Peers C, Nye P C
University Laboratory of Physiology, Oxford.
Q J Exp Physiol. 1989 Nov;74(6):959-62. doi: 10.1113/expphysiol.1989.sp003369.
We have investigated the effects of tolbutamide on the hypoxic vasoconstriction of isolated, perfused rat lungs. We did this because lowered ATP may link hypoxia and constriction, and tolbutamide mimics the effects of ATP in other tissues by blocking ATP-sensitive potassium (ATP-K) channels. Pulmonary vasoconstriction, induced by lowering the oxygen of the gas ventilating the lungs from 95 to 2%, was always reduced or abolished by tolbutamide (1.7 x 10(-4)-8.5 x 10(-3) M). High concentrations (greater than or equal to 10(-3) M) of diazoxide, a drug that opens ATP-K channels, dramatically constricted the pulmonary vasculature and this effect was also reversed by tolbutamide. The opening of ATP-K channels may therefore underlie hypoxic pulmonary vasoconstriction.
我们研究了甲苯磺丁脲对离体灌注大鼠肺脏缺氧性血管收缩的影响。我们之所以这样做，是因为ATP水平降低可能将缺氧与血管收缩联系起来，并且甲苯磺丁脲通过阻断ATP敏感性钾（ATP-K）通道，在其他组织中模拟ATP的作用。通过将通气气体中的氧气从95%降至2%诱导的肺血管收缩，总是会被甲苯磺丁脲（1.7×10⁻⁴ - 8.5×10⁻³ M）降低或消除。高浓度（大于或等于10⁻³ M）的二氮嗪是一种可打开ATP-K通道的药物，它会显著收缩肺血管，而这种作用也会被甲苯磺丁脲逆转。因此，ATP-K通道的开放可能是缺氧性肺血管收缩的基础。
