This study validates a new animal model to study the effects of acute systemic hypoxia on colonic anastomotic healing. In this model, systemic hypoxia directly translated into local tissue hypoxia, and anastomotic healing was impaired. Contrary to our original hypothesis, hypoxia led to a significant increase in vascular endothelial growth factor and inducible nitric oxide synthase protein expression at the colonic anastomotic site. Impairment in anastomotic integrity despite upregulation of these angiogenic factors could be a result of the inability of wounded tissue to respond to vascular endothelial growth factor and inducible nitric oxide synthase or alternatively, hypoxia may adversely affect collagen synthesis and deposition directly.
The effects of discontinuous hypoxia on cerebrovascular regulation in humans are unknown. We hypothesized that five nocturnal hypoxic exposures (8 h/day) at a simulated altitude of 4,300 m (inspired O2 fraction = approximately 13.8%) would elicit cerebrovascular responses that are similar to those that have been reported during chronic altitude exposures. Twelve male subjects (26.6 +/- 4.1 yr, mean +/- SD) volunteered for this study. The technique of end-tidal forcing was used to examine cerebral blood flow (CBF) and regional cerebral O2 saturation (Sr(O2)) responses to acute variations in O2 and CO2 twice before, immediately after, and 5 days after the overnight hypoxic exposures. Transcranial Doppler ultrasound was used to assess CBF, and near-infrared spectroscopy was used to assess Sr(O2). Throughout the nocturnal hypoxic exposures, end-tidal Pco2 decreased (P < 0.001) whereas arterial O2 saturation increased (P < 0.001) compared with overnight normoxic control measurements. Symptoms associated with altitude illness were significantly greater than control values on the first night (P < 0.001) and second night (P < 0.01) of nocturnal hypoxia. Immediately after the nocturnal hypoxic intervention, the sensitivity of CBF to acute variations in O2 and CO2 increased 116% (P < 0.01) and 33% (P < 0.05), respectively, compared with control values. Sr(O2) was highly correlated with arterial O2 saturation (R2 = 0.94 +/- 0.04). These results show that discontinuous hypoxia elicits increases in the sensitivity of CBF to acute variations in O2 and CO2, which are similar to those observed during chronic hypoxia.
Validation of pulse oximetry in commercially available normobaric hypoxic chambers (NHC) has not been previously reported. The present study examined the validity of pulse oximetry (SpO2) against direct measurements of arterial oxygen saturation (SaO2) via co-oximetry (AVOXimeter 4000) in 13 young adults age 21.3 +/- 0.6 years. Over a period of 2.5 hrs, the inspired fraction of oxygen inside a NHC (Hypoxico, Inc.) was progressively reduced from 20.9% to 11.5%. Measurements of SaO2 at baseline and at 15, 30, 60, 90, 120, and 150 min during the hypoxic exposures were compared with SpO2 estimates of oxygen saturation (Nellcor 295) using reflectance (RS-10, temporal) and transmission (D-25, finger) sensors. Regression analysis and methods for assessing agreement (bias, b; precision, p) of SaO2 with SpO2 were similar (R2 = 0.92, 0.89; b = 0.016, -0.47; p = 2.47, 3.03; RS-10 and D-25, respectively). When SaO2 < 85%, RS-10 had greater validity than D-25 (R2 = 0.73, 0.56; b = 1.38, 1.13; p = 2.72, 4.34; RS-10 and D-25, respectively). In light of these findings, caution should be exercised when monitoring individuals with pulse oximetry during desaturation episodes below 85%. When employing frequent NHC exposures, a priori validation of SpO2 utilized to assess blood oxygen status appears warranted.
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