目的:探讨应用亚硫酸钠(sodium sulfite,Na2SO3)快速去氧制备低氧性肺血管收缩(hypoxia pul-monary vasoconstriction,HPV)离体模型所需低氧性Krebs-Henseleit(KH)溶液的可行性。方法:在暴露于空气的开放环境中将不同剂量Na2SO3加至0.5 L温度为37℃的KH溶液中,用i-STAT便携式临床分析仪检测加样1min后溶液pH值、氧分压(PO2)、二氧化碳分压(PCO2)和钠离子(Na+)浓度的变化;选择适合HPV模型条件的Na2SO3剂量溶入0.5 L KH液后,检测此低氧溶液在1、10、20、30、60和90 min时上述指标的变化。结果:大于0.2g(包括0.2 g)Na2SO3加至0.5 L KH液中可降低KH液的PO2(P<0.01),且随着剂量的增加,PO2降低。其中,1.5 g Na2SO3剂量可使0.5 L KH液达到HPV模型所需的低氧状态PO2(20～40 mmHg)并维持此低氧状态至少90min,溶液pH值、PCO2和Na+浓度均处于正常范围。结论:应用Na2SO3可制备HPV离体模型所需的低氧溶液,方法简单,快速可行,状态稳定,无需密闭。
The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential in pulmonary arteries smooth muscle cells (PASMCs), so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction (HPV). Inhibition the function of channels by specific antagons, Antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, the O2 sensitivity of cloned K+ channels expressed in heterologous expression systems and gene targeting to knockout specific K+ channels have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive K+ channels. Although the mechanism of K+ channel inhibition by hypoxia is unknown, it appears that K+ α -subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or α-subunit. This review summarizes the role of K+ channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K+ channel subunits involved in this response, and the possible mechanisms of K+ channel regulation by hypoxia. [
