Nowicki P T, Miller R R, Hansen N B, Hayes J R
Pediatr Res. 1985 Nov;19(11):1197-200. doi: 10.1203/00006450-198511000-00017.
Gastrointestinal (GI) blood flow, O2 transport, and O2 uptake were measured during recovery from severe hypoxemia in newborn piglets. Hypoxemia was induced by lowering the inspired O2 concentration to 0.05 for 15 min. This resulted in an 82% decrease in GI O2 uptake. Recovery measurements were obtained 5 and 65 min after restoration of normoxia. During early recovery (5 min), GI O2 uptake increased above prehypoxemia baseline, presumably to "repay" the O2 deficit incurred during hypoxemia. This was mediated by an increase in the arteriovenous O2 content difference, as GI blood flow did not increase above prehypoxemia baseline. During late recovery (65 min), GI blood flow, O2 delivery, and arteriovenous O2 content difference decreased below prehypoxemia baseline. This resulted in a 52% decrease in GI O2 uptake below prehypoxemia baseline. Therefore, early recovery was characterized by an appropriate increase in GI O2 uptake; however, late recovery was characterized by a significant reduction in GI O2 transport and uptake. Circulatory homeostasis was not reestablished during the late recovery period.
在新生仔猪从严重低氧血症恢复过程中，测量了胃肠道（GI）血流、氧气运输和氧气摄取情况。通过将吸入氧气浓度降至0.05并持续15分钟来诱导低氧血症。这导致胃肠道氧气摄取减少了82%。在恢复正常氧合5分钟和65分钟后进行恢复测量。在早期恢复阶段（5分钟），胃肠道氧气摄取增加至低氧血症前基线以上，推测是为了“偿还”低氧血症期间产生的氧气亏空。这是由动静脉氧含量差增加介导的，因为胃肠道血流并未增加至低氧血症前基线以上。在晚期恢复阶段（65分钟），胃肠道血流、氧气输送和动静脉氧含量差降至低氧血症前基线以下。这导致胃肠道氧气摄取比低氧血症前基线减少了52%。因此，早期恢复的特征是胃肠道氧气摄取适当增加；然而，晚期恢复的特征是胃肠道氧气运输和摄取显著减少。在晚期恢复阶段，循环稳态并未重建。
