Delcroix M, Mélot C, Vermeulen F, Naeije R
Laboratory of Cardiovascular and Respiratory Physiology, Erasme University Hospital, Brussels, Belgium.
J Appl Physiol (1985). 1996 Apr;80(4):1240-8. doi: 10.1152/jappl.1996.80.4.1240.
Hypoxic pulmonary vasoconstriction (HPV) is inhibited in several models of acute lung injury. Whether HPV is preserved in pulmonary embolism is unknown. We investigated the effects of a reduction in the fraction of inspired O2 (FIO2) on pulmonary hemodynamics and gas exchange in anesthetized dogs before and after autologous blood clot pulmonary embolism. In a first group of 14 dogs, stimulus-response curves for HPV were constructed as pulmonary arterial pressure (Ppa) vs. FIO2 varied between 1.0 and 0.06 at a cardiac output (Q) kept constant at 3.5 l.min-1.m-2. Gas exchange was evaluated by using the multiple inert-gas elimination technique at FIO2 of 1.0, 0.4, and 0.1. Embolism decreased the relative magnitude of HPV, expressed as the gradient between Ppa and pulmonary arterial occluded pressure in hypoxia divided by (Ppa-pulmonary arterial occluded pressure) at FIO2 of 1.0, from 1.8 to 1.2 (P < 0.05). Retention minus excretion gradients for sulfur hexafluoride and ethane were increased by decreased FIO2 (P < 0.005 and P < 0.05, respectively) before but not after embolism. Hypoxia-induced deterioration in gas exchange before embolism was related to the amount of baseline very low ventilation-perfusion (VA/Q) ratios. Similar results were obtained in a second group of seven dogs with Q decreased to maintain Ppa at the same average value as before embolism. However, gas exchange was not affected by inspiratory hypoxia before as well as after embolism in this group, which presented with a lesser amount of baseline very low VA/Q. In both groups of dogs, increase in the FIO2 from 0.4 to 1.0 did not affect gas exchange. We conclude that 1) pulmonary embolism is associated with a partial inhibition of HPV, 2) HPV does not contribute to preserve gas exchange in pulmonary embolism, and 3) a strong HPV may deteriorate gas exchange in severe hypoxia in the presence of minor very low VA/Q inequality.
在几种急性肺损伤模型中，低氧性肺血管收缩（HPV）受到抑制。HPV在肺栓塞中是否得以保留尚不清楚。我们研究了在自体血凝块肺栓塞前后，吸入氧分数（FIO₂）降低对麻醉犬肺血流动力学和气体交换的影响。在第一组14只犬中，构建HPV的刺激-反应曲线，即在心输出量（Q）保持恒定为3.5 l·min⁻¹·m⁻²时，肺动脉压（Ppa）与FIO₂在1.0至0.06之间变化。在FIO₂为1.0、0.4和0.1时，使用多惰性气体清除技术评估气体交换。栓塞使HPV的相对幅度降低，以低氧时Ppa与肺动脉闭塞压之间的梯度除以FIO₂为1.0时的（Ppa - 肺动脉闭塞压）来表示，从1.8降至1.2（P < 0.05）。栓塞前，随着FIO₂降低，六氟化硫和乙烷的潴留减去排泄梯度增加（分别为P < 0.005和P < 0.05），但栓塞后无此现象。栓塞前低氧诱导的气体交换恶化与基线极低通气/灌注（VA/Q）比值的数量有关。在第二组7只犬中得到了类似结果，其中Q降低以维持Ppa与栓塞前相同的平均值。然而，该组栓塞前后吸气性低氧均未影响气体交换，其基线极低VA/Q的数量较少。在两组犬中，FIO₂从0.4增加到1.0均未影响气体交换。我们得出结论：1）肺栓塞与HPV的部分抑制有关；2）HPV在肺栓塞中对维持气体交换无作用；3）在存在轻微极低VA/Q不平等的情况下，强烈的HPV可能在严重低氧时使气体交换恶化。
