Chapler C K, Cain S M, Stainsby W N
Can J Physiol Pharmacol. 1984 Jul;62(7):809-14. doi: 10.1139/y84-133.
The effects of normobaric hyperoxia on the oxygen uptake (VO2) and cardiovascular responses of the whole body and hindlimb during anemia were investigated. Anesthetized, paralyzed dogs were ventilated for 20-min periods with room air (normoxia), 100% O2 (hyperoxia), and returned to room air. Anemia (hematocrit = 15%) was then induced by isovolemic dextran-for-blood exchange and the normoxia, hyperoxia, normoxia sequence was repeated. Whole body VO2 and cardiac output rose following anemia, and then fell (p less than 0.05) with hyperoxia during anemia. These responses were not abolished by beta-blockade with propranolol (1 mg/kg, iv) or bilateral vagotomy. The hindlimb data for blood flow and VO2 were similar in direction to those of the whole body but were more variable. Section of the sciatic and femoral nerves did not appear to have significant effect on the limb responses to hyperoxia. The decrease in whole body and hindlimb VO2 with hyperoxia during anemia may have resulted from a redistribution of capillary blood flow away from exchange vessels in response to the elevated PO2.
研究了常压高氧对贫血期间全身及后肢摄氧量(VO2)和心血管反应的影响。对麻醉、麻痹的犬只分别进行20分钟的室内空气(常氧)、100%氧气(高氧)通气,然后恢复至室内空气通气。通过等容右旋糖酐-血液交换诱导贫血(血细胞比容 = 15%),并重复常氧、高氧、常氧序列。贫血后全身VO2和心输出量升高,然后在贫血期间高氧时下降(p < 0.05)。这些反应未被普萘洛尔(1 mg/kg,静脉注射)β受体阻滞或双侧迷走神经切断术消除。后肢血流和VO2数据在方向上与全身相似,但变异性更大。坐骨神经和股神经切断似乎对肢体对高氧的反应没有显著影响。贫血期间高氧导致全身和后肢VO2下降可能是由于毛细血管血流重新分布,远离交换血管以应对升高的PO2。