Sakio H, Iwase Y, Okuda C
Second Department of Anesthesiology, Dokkyo University School of Medicine, Tochigi.
Masui. 1990 Sep;39(9):1142-7.
We studied the effects of angiotensin II (A-II) antagonist, propranolol and prostaglandin F2 alpha (PGF2 alpha) on arterial hypoxemia after injecting autologous muscle to induce massive pulmonary embolism. Twenty-four anesthetized paralyzed dogs were divided into four groups; control, intravenous A-II antagonist (1-sarcosine, 8-isoleucine A-II) infusion at 5 micrograms.kg-1.min-1, intravenous propranolol injection at 1.5-2.0 mg, and intravenous PGF2 alpha infusion at 1 microgram.kg-1.min-1. With FIO2 of 0.33, the administration of A-II antagonist produced an increase in arterial PO2 from 134 +/- 16 (mean +/- SE) to 155 +/- 11 mmHg during infusion, and to 160 +/- 9 mmHg 30 min after infusion. Simultaneous hemodynamic measurements demonstrated no significant changes in arterial blood pressure and heart rate, but a slight increase in cardiac output was observed. On the other hand, propranolol and PGF2 alpha did not reverse the pulmonary oxygenation. Cardiac output decreased after propranolol, and alveolar dead space and pulmonary artery pressure increased further after PGF2 alpha. We conclude that A-II antagonist may be effective in the treatment of massive pulmonary embolism, possibly by improving the ventilation-perfusion relationship. The exact mechanism of the effect of A-II antagonist has not been clarified.
我们研究了血管紧张素II（A-II）拮抗剂、普萘洛尔和前列腺素F2α（PGF2α）对注射自体肌肉诱导大量肺栓塞后动脉低氧血症的影响。将24只麻醉致瘫的犬分为四组：对照组、以5微克·千克⁻¹·分钟⁻¹的速度静脉输注A-II拮抗剂（1-肌氨酸，8-异亮氨酸A-II）、静脉注射1.5 - 2.0毫克普萘洛尔以及以1微克·千克⁻¹·分钟⁻¹的速度静脉输注PGF2α。在吸入氧分数（FIO2）为0.33时，输注A-II拮抗剂期间动脉血氧分压（PO2）从134±16（均值±标准误）毫米汞柱升至155±11毫米汞柱，输注后30分钟升至160±9毫米汞柱。同时进行的血流动力学测量显示动脉血压和心率无显著变化，但心输出量略有增加。另一方面，普萘洛尔和PGF2α并未改善肺氧合。普萘洛尔注射后心输出量下降，PGF2α注射后肺泡死腔和肺动脉压进一步升高。我们得出结论，A-II拮抗剂可能对大量肺栓塞有效，可能是通过改善通气-灌注关系。A-II拮抗剂作用的确切机制尚未阐明。
