Prostaglandin F2α Improves Oxygen Tension and Reduces Venous Admixture during One‐lung Ventilation in Anesthetized Paralyzed Dogs
Prostaglandin F2α Improves Oxygen Tension and Reduces Venous Admixture during One‐lung Ventilation in Anesthetized Paralyzed Dogs
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前列腺素 F2α 改善麻醉瘫痪狗单肺通气期间的氧张力并减少静脉混合
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发表时间：
1985
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通讯作者：
P. Lawin
中科院分区：
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作者：
R. Scherer;G. Vigfússon;E. Hultsch;H. Aken;P. Lawin
作者研究了前列腺素F2α输注于急性肺不张狗肺动脉的作用。7只犬用吡吡酯和戊巴比妥麻醉，并用Kottmeier犬支气管内管插管。通过留置导管测量心输出量、肺动脉、毛细血管楔和全身动脉压。双肺66% O2通气，Pao2为327±15 mmHg (mean±SD)，静脉混合液（Q±sp/Q1）为11±3%。单肺不张使Pao2降低至91±12 mmHg，使Q±sp/Qt升高至40±4%。前列腺素F2α分别以0.4、0.6、1.2和1.8 μg±kg−1·min−1的剂量通过第二肺动脉导管注入肺不张肺动脉。当剂量为1.2 μg·kg−1·min−1时，Q·sp/Qt呈剂量依赖性降低至至少25±4%，Pao2升高至168±25 mmHg，这可能是由于肺不电性血管收缩增强，血流向通气肺分流增加所致。输注1.8 μg·kg−1·min−1可使Pao2降低至156±32 mmHg，使Q±sp/Qt升高至32±9%。观察到前列腺素F2α的全身作用增加，推测与前列腺素脱氢酶饱和导致双肺血管收缩，从而减少向通气肺的血流转移有关。
The authors investigated the effect of prostaglandin F2α infused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, Pao2 was 327±15 mmHg (mean±SD) and venous admixture (Q±sp/Q1) was 11±3%. One-lung atelectasis reduced Pao2 to 91±12 mmHg and increased Q±sp/Qt to 40±4%. Prostaglandin F2α in doses of 0.4, 0.6, 1.2, and 1.8 μg ± kg−1 · min−1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 μg · kg−1 · min−1 there was a dose-dependent reduction in Q·sp/Qt to a minimum of 25±4% and an increase in Pao2 to 168±25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 μg · kg−1 · min−1 decreased Pao2 to 156±32 mmHg and increased Q±sp/Qt to 32±9%. Increased systemic effects of prostaglandin F2α were observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.