Johnson D H, Hurst T S, Mayers I
Department of Anaesthesia, University of Saskatchewan, Saskatoon, Canada.
Anesth Analg. 1991 Apr;72(4):440-8. doi: 10.1213/00000539-199104000-00005.
We studied the interactions of atelectasis and halothane on hypoxic pulmonary vasoconstriction using an isolated canine lobe. We divided pulmonary vascular resistance into arterial, venous, and middle segmental resistances by a vascular occlusion technique. We found that middle segmental resistance significantly increased (P less than 0.05) from 0.016 +/- 0.007 cm H2O.mL-1.min-1 during normoxic ventilation to 0.06 +/- 0.007 cm H2O.mL-1.min-1 during hypoxic ventilation. We then produced sublobar atelectasis by introducing 4.5-mm steel ball bearings into the lobar bronchus, which resulted in a significant increase (P less than 0.05) of middle segmental resistance to 0.046 +/- 0.014 cm H2O.mL-1.min-1 during normoxic ventilation and a further significant increase (P less than 0.05) to 0.084 +/- 0.02 cm H2O.mL-1.min-1 during hypoxic ventilation. Ventilation with 2.0% halothane but not 0.5% halothane prevented the increases in middle segmental resistance observed with either atelectasis or hypoxic ventilation. Values of arterial and venous segmental resistances were not similarly affected. We conclude that sublobar atelectasis increases pulmonary vascular resistance by stimulating hypoxic pulmonary vasoconstriction. Both halothane and hypoxia primarily act upon the middle vascular segment, but their effects are in opposite directions and, in the former instance, are concentration-dependent.
我们使用离体犬肺叶研究了肺不张与氟烷对低氧性肺血管收缩的相互作用。我们采用血管闭塞技术将肺血管阻力分为动脉、静脉和中间节段阻力。我们发现，中间节段阻力在常氧通气时从0.016±0.007 cm H₂O·mL⁻¹·min⁻¹显著增加（P＜0.05）至低氧通气时的0.06±0.007 cm H₂O·mL⁻¹·min⁻¹。然后，我们通过向肺叶支气管内引入4.5毫米钢珠造成肺叶下不张，这导致中间节段阻力在常氧通气时显著增加（P＜0.05）至0.046±0.014 cm H₂O·mL⁻¹·min⁻¹，在低氧通气时进一步显著增加（P＜0.05）至0.084±0.02 cm H₂O·mL⁻¹·min⁻¹。用2.0%氟烷通气而非0.5%氟烷通气可防止肺不张或低氧通气时观察到的中间节段阻力增加。动脉和静脉节段阻力值未受到类似影响。我们得出结论，肺叶下不张通过刺激低氧性肺血管收缩增加肺血管阻力。氟烷和低氧均主要作用于中间血管节段，但它们的作用方向相反，且在前者情况下，作用呈浓度依赖性。
