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Hypoxia

Hypoxia

Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...

Acute Respiratory Failure-II

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:

Oxygen Transport in the Blood

Oxygen Transport in the Blood

Hemoglobin (Hb) is a crucial molecule in the human body, consisting of four polypeptide chains, each bound to an iron-containing heme group. This unique structure enables hemoglobin to bind to oxygen, with each molecule capable of combining with four molecules of oxygen, leading to rapid and reversible oxygen loading. When fully loaded with oxygen, it is called oxyhemoglobin, while hemoglobin that has released oxygen is called reduced hemoglobin or deoxyhemoglobin. As hemoglobin binds oxygen,...

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Related Experiment Video

Updated: Aug 13, 2025

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Hyperoxia Induced Hypomyelination.

Weilin Song^1,2, George Hoppe¹, Demiana Hanna¹

¹Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

|January 21, 2023

Summary

This summary is machine-generated.

High oxygen levels can harm preterm infants by causing hypomyelination in the brain

Keywords:

HIF stabilization hyperoxia hypomyelination hypoxia inducible factor myelin basic protein oligodendrocytes periventricular leukomalacia premature birth prolyl hydroxylase

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Last Updated: Aug 13, 2025

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Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents

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Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures

Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures

Published on: November 2, 2015

Area of Science:

Neuroscience
Neonatal Physiology
Developmental Biology

Background:

Periventricular leukomalacia (PVL) is a major cause of neurological disability in preterm infants.
The role of hyperoxia (excessive oxygen) in PVL pathogenesis is not fully understood.

Purpose of the Study:

To investigate if hyperoxia induces hypomyelination in the corpus callosum.
To explore the underlying mechanisms, including vascular changes and oligodendrocyte function.
To assess the role of hypoxia-inducible factor (HIF) in hyperoxia-induced brain injury.

Main Methods:

Mouse pups exposed to hyperoxia (80% oxygen) from postnatal day 4-8.
Analysis of corpus callosum for myelin, oligodendrocytes, apoptosis, fibrosis, and capillary density.
Measurement of hypoxia using Hypoxyprobe and HIF stabilization.
Use of hypoxiamimetics and hepatic HIF-1 knockout models.

Main Results:

Hyperoxia led to hypomyelination, reduced corpus callosal capillaries, decreased oligodendrocytes, and increased apoptosis and fibrosis.
Cerebral hypoxiamimesis mimicked hyperoxia effects, while hepatic hypoxiamimesis promoted myelination.
Hepatic HIF-1 knockout confirmed its role in myelination.

Conclusions:

Hyperoxia can induce corpus callosum hypomyelination in developing brains, potentially via vaso-obliteration and subsequent ischemia.
This suggests a novel oxygen-induced mechanism contributing to PVL in preterm infants.
Targeting hepatic HIF-1 may offer a therapeutic strategy to promote myelination.