Pulmonary vasoconstrictor response to acute decrease in blood P50.
Pulmonary vasoconstrictor response to acute decrease in blood P50.
复制标题
肺血管收缩剂对血液 P50 急剧下降的反应。
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
C. Soulard
中科院分区：
文献类型：
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作者：
B. Teisseire;C. Soulard
触发缺氧性肺血管收缩的氧传感器可能不仅对肺泡缺氧敏感，而且对混合静脉血中的缺氧也敏感。血液贡献的具体测试将是降低混合静脉PO 2（PvO 2），这可以通过增加血红蛋白-O2亲和力来实现。当我们用氰酸盐处理的红细胞[在50%血红蛋白饱和度（P50）= 21 Torr时的PO 2]或Créteil红细胞（P50 = 13.1 Torr）交换输血大鼠时，我们将PvO 2分别从39 +/- 5降低到25 +/- 4和14 +/- 4 Torr，而不改变动脉血气或血红蛋白浓度。右心室收缩压从32 +/- 2 Torr增加到36 +/- 3 Torr（使用氰酸盐红细胞）和44 +/- 5 Torr（使用Créteil红细胞）。心输出量无变化。对照交换输血与正常大鼠或2，3-二磷酸甘油酸丰富的人红细胞对PvO 2或右心室压力没有影响。肺泡缺氧加高O2亲和力血液引起的右心室收缩压增加更大比任何刺激单独。我们得出的结论是，PvO 2是大鼠肺血管张力的重要决定因素。
The O2 sensor that triggers hypoxic pulmonary vasoconstriction may be sensitive not only to alveolar hypoxia but also to hypoxia in mixed venous blood. A specific test of the blood contribution would be to lower mixed venous PO2 (PvO2), which can be accomplished by increasing hemoglobin-O2 affinity. When we exchanged transfused rats with cyanate-treated erythrocytes [PO2 at 50% hemoglobin saturation (P50) = 21 Torr] or with Créteil erythrocytes (P50 = 13.1 Torr), we lowered PvO2 from 39 +/- 5 to 25 +/- 4 and to 14 +/- 4 Torr, respectively, without altering arterial blood gases or hemoglobin concentration. Right ventricular systolic pressure increased from 32 +/- 2 to 36 +/- 3 Torr with cyanate erythrocytes and to 44 +/- 5 Torr with Créteil erythrocytes. Cardiac output was unchanged. Control exchange transfusions with normal rat or 2,3-diphosphoglycerate-enriched human erythrocytes had no effect on PvO2 or right ventricular pressure. Alveolar hypoxia plus high O2 affinity blood caused a greater increase in right ventricular systolic pressure than either stimulus alone. We concluded that PvO2 is an important determinant of pulmonary vascular tone in the rat.