Krebs M O, Boemke W, Simon S, Wenz M, Kaczmarczyk G
Experimental Anesthesia, Clinic of Anesthesiology and Operative Intensive Care Medicine, 13353 Berlin, Germany.
J Appl Physiol (1985). 1999 Jun;86(6):1914-9. doi: 10.1152/jappl.1999.86.6.1914.
Acute hypoxic pulmonary vasoconstriction (HPV) may be mediated by vasoactive peptides. We studied eight conscious, chronically tracheostomized dogs kept on a standardized dietary sodium intake. Normoxia (40 min) was followed by hypoxia (40 min, breathing 10% oxygen, arterial oxygen pressures 36 +/- 1 Torr) during both control (Con) and losartan experiments (Los; iv infusion of 100 microg. min-1. kg-1 losartan). During hypoxia, minute ventilation (by 0.9 l/min in Con, by 1.3 l/min in Los), cardiac output (by 0.36 l/min in Con, by 0.30 l/min in Los), heart rate (by 11 beats/min in Con, by 30 beats/min in Los), pulmonary artery pressure (by 9 mmHg in both protocols), and pulmonary vascular resistance (by 280 and 254 dyn. s. cm-5 in Con and Los, respectively) increased. Mean arterial pressure and systemic vascular resistance did not change. In Con, PRA decreased from 4.2 +/- 0.7 to 2.5 +/- 0.5 ng ANG I. ml-1. h-1, and plasma ANG II decreased from 11.9 +/- 3.0 to 8.2 +/- 2.1 pg/ml. The renin-angiotensin system is inhibited during acute hypoxia despite sympathetic activation. Under these conditions, ANG II AT1-receptor antagonism does not attenuate HPV.
急性低氧性肺血管收缩(HPV)可能由血管活性肽介导。我们研究了八只清醒的、长期气管切开的狗,它们保持标准化的饮食钠摄入量。在对照(Con)实验和氯沙坦实验(Los;静脉输注100μg·min⁻¹·kg⁻¹氯沙坦)中,先进行40分钟的常氧状态,然后进行40分钟的低氧状态(呼吸10%氧气,动脉血氧分压36±1 Torr)。在低氧期间,分钟通气量(Con组增加0.9 l/min,Los组增加1.3 l/min)、心输出量(Con组增加0.36 l/min,Los组增加0.30 l/min)、心率(Con组增加11次/分钟,Los组增加30次/分钟)、肺动脉压(两个方案中均增加9 mmHg)和肺血管阻力(Con组和Los组分别增加280和254 dyn·s·cm⁻⁵)均升高。平均动脉压和全身血管阻力未改变。在Con组中,肾素活性(PRA)从4.2±0.7降至2.5±0.5 ng ANG I·ml⁻¹·h⁻¹,血浆血管紧张素II(ANG II)从11.9±3.0降至8.2±2.1 pg/ml。尽管交感神经激活,但在急性低氧期间肾素 - 血管紧张素系统受到抑制。在这些条件下,ANG II AT1受体拮抗作用不会减弱HPV。