From
StayCurrentMD
CDH Live Webinar Series Part 1: Research: Lung Compression in CDH Generates Cellular Chronic Hypoxia and Energy Failure
With CCHMC Pediatric Surgery · hosted by Dr. M Thambash
Educational content from recorded physician discussions — not medical advice. Talk to your (or your child's) care team about your situation.
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What the experts said
According to the US Centers for Disease Control and Prevention, the incidence of CDH is 2.6 per 10,000 births.
The pathophysiology of CDH is not well understood, and we don't know why these babies have lung hypoplasia and severe pulmonary hypertension.
The diaphragmatic defect causes abdominal viscera to herniate to the chest, creating lung compression and lung hypoperfusion.
In the nitrofen model, rats were given intragastrically 100 milligrams of nitrofen dissolved in 1 milliliter of olive oil at 9.5 days, with euthanization on day 21.5 before pups were born.
All pups' lungs were harvested in less than 50 minutes to minimize hypoxia.
HIF mRNA and protein levels are elevated in the fetal lung with the entire HIF system activated at eight weeks of gestation in the human.
When HIF-1 Alpha is exposed to oxygen in normoxia, it has a short half-life which is less than five minutes.
HIF-1 Alpha gene expression analyzed by qPCR is significantly different between the nitrofen CDH and vehicle control.
Under decreased concentrations of oxygen, the degradation of HIF alpha is retarded, which can explain why protein expression of HIF is increased in the periphery of CDH lungs.
Glucose is the primary energy source of the lungs and is essential for energy production and surfactant synthesis.
Glucose Transporter One (GLUT1) increases in lung tissue under hypoxia.
In fetal rats, GLUT1 mRNA expression increases to maximum levels at gestation day 20 and falls to very low levels by postnatal day 8.
GLUT1 gene expression evaluated by qPCR is upregulated in CDH.
Glucose is not decreased in the lungs with CDH when evaluated by NMR spectroscopy.
Both HIF-1α and GLUT1 manifest in the airways.
Metabolomic investigation of complete fetal lungs published last year indicates the presence of a unique metabolic profile in the nitrofen-induced CDH fetal lungs.
CDH lungs show evident changes in energy production, redox control state, and cell proliferation, associated with lung hypoplasia caused by nitrofen and aggravated by lung compression.
Healthy cells must maintain a high ratio of ATP to ADP in the order of 10 ATPs for each ADP, and ADP to AMP in the order of 100 ADPs for each AMP.
In CDH lungs, ADP is decreased and AMP is increased.
Normal energy charge varies between 0.7 and 0.95, and oxidations in this range are very frequent and normal.
CDH lungs are in energetic failure with an energy charge level of 0.15.
Fetal CDH lungs are compressed and probably with chronic hypoxia, have a different metabolism with significant alteration in glycolytic energy, antioxidant, and nucleotide metabolites.
The metabolic changes found in fetal CDH are compatible with growth arrest and tissue remodeling.