Hyperoxia inhibits several critical aspects of vascular development

Abstract

Normal human retinal vascular development uses angiogenesis and vasculogenesis, both of which are interrupted in the vaso-obliteration phase of retinopathy of prematurity (ROP). Canine oxygen-induced retinopathy (OIR) closely resembles human ROP. Canine retinal endothelial cells (ECs) and angioblasts were used to model OIR and characterize the effects of hyperoxia on angiogenesis and vasculogenesis. Cell cycle analysis showed that hyperoxia reduced the number of G1 phase cells and showed increased arrest in S phase for both cell types. Migration of ECs was significantly inhibited in hyperoxia (P < 0.01). Hyperoxia disrupted the cytoskeleton of angioblasts but not ECs after 2 days. Differentiation of angioblasts into ECs (determined by acetylated low-density lipoprotein uptake) was evaluated after basic fibroblast growth factor treatment. Differentiation of angioblasts into pericytes was determined by smooth muscle actin expression after treatment with platelet-derived growth factor. Differentiation into ECs was significantly inhibited by hyperoxia (P < 0.0001). The percentage of CXCR4 ؉ cells (a marker for retinal vascular precursors) increased in both treatment groups after hyperoxia. These data show novel mechanisms of hyperoxia-induced disruption of vascular development. Developmental Dynamics 236:981-990, 2007.

Wound angiogenesis as a function of tissue oxygen tension: A mathematical model

“…3) in the case when the base level represented the hyperoxic concentration of 2 showed no improvement in endothelial cell density when the oxygen level is increased to 3 or 4 for 90 min per day. This agrees with the result that high levels of oxygen are known to cause growth arrest and senescence of cells (19,65). Fig.…”

“…Oxygen therapy is commonly used in the wound clinics to treat wound hypoxia (20)(21)(22)(23)(24). Extreme hyperoxia, on the other hand, can cause oxygen toxicity and derail tissue repair (16,17,19).…”

Cerebral Oxygenation and Oxygen Extraction in the Preterm Infant during Desaturation: Effects of Increasing FiO₂ to Assist Recovery

“…One has to consider that the accepted arterial pO 2 values in the newborn preterm baby are substantially higher than the physiologic (in utero) norm for the same post-conceptional age and that there are poor enzymatic and cellular anti-oxidant defenses [38][39][40][41] . In the immature baby, hyperoxia interferes with vascular development of the lungs and the eyes and is capable of causing cell death in these organs [10,[40][41][42][43][44][45] . There is an growing body of evidence that exposure to an excess of oxygen may be equally damaging to the developing brain [12][13][14][15] .…”

Brain Natriuretic Peptide: A Predictor for Severity Respiratory Distress Syndrome in Newborns

“…RDS is a hyaline membrane disease in which due to preterm delivery of the infants -age of birth less than 37 weeks, production of surfactants decreases and consequently, acidosis, hypoxia, ischemia, infection and pulmonary disease mainly occur (5) then as a result, low alveolar radius, weak chest wall and decrease of the lung compliance cause pulmonary atelectasis (6). In the end, V/Q miss match, hypoventilation, hypoxia, pulmonary vasoconstriction increase and vascular damage occur which result in RDS (7)(8)(9)(10)(11)(12).…”