Cellular hypoxia, caused by a lack of oxygen, leads to cell death and can be caused by injury or disease. It triggers a complex breakdown of cells, impairs cellular function, and can cause tissue damage. Treatment involves supplemental oxygen, fluids, nutrition, and medication to inhibit inflammation.
Cellular oxygen deprivation is called cellular hypoxia. Unless corrected or reversed, intracellular function ceases, eventually leading to cell death. Depending on the extent of depletion, cells can chemically signal systemic mechanisms that attempt to compensate for the lack of energy and oxygen. Injury and disease can initiate cellular hypoxia. Treatment of cellular hypoxia involves replacement of oxygen, fluids, and nutrition.
Without an adequate supply of oxygen, the transport of electrons within the cell does not work properly. The electrons accumulate, causing a complex progression of cellular breakdowns. Mitochondria, the energy-producing organelles within cells, lose their membrane potential and stop producing adenosine triphosphate (ATP). Without a constant supply of nutrition, cells deplete their ATP stores. This action could also trigger an inflammatory process, creating tissue damage.
Cells send out chemical signals that encourage blood flow in an effort to get more oxygen. Lactic acid and nitric oxide are formed, resulting in an acidic environment. Ineffective electrical impulses affect the lysosomes which cease to metabolize cellular waste products. The accumulation of electrons also interferes with the activity of the sodium-potassium pump, allowing potassium to flood the extracellular spaces and sodium and water to enter the cell, in turn causing cell edema and possible rupture. Cellular hypoxia also impairs cellular calcium stores necessary for proper membrane function and the release of neurotransmitters into the cell.
Membrane damage triggers the release of enzymes that begin digesting the cell. Lacking a protective membrane, the cell dies, causing cellular waste, enzymes, and other chemicals to enter the bloodstream. Lactic acid and nitric oxide in sufficient quantities initiate systemic responses. Lactic acid reduces the heart’s ability to contract. Acid signals also desensitize arterioles, decreasing the vascular response to central nervous system hormones. Nitric oxide causes vasodilation, increases capillary permeability and initiates clotting mechanisms to inhibit blood loss. The outward signs of hypoxia can include an increased rate of breathing as the body struggles to replace oxygen.
Hypoxia is caused by any circumstance that interferes with access to oxygen, including blunt force trauma, fluid loss, and tissue damage caused by prolonged applied pressure. Diseases that impede normal blood flow or that reduce oxygen intake also contribute to cellular hypoxia. Some researchers believe that maintaining a diet high in polyunsaturated fat reduces membrane permeability and the cell’s ability to absorb oxygen. Scientists speculate that oxygen-starved cells and their ensuing processes may create environments that encourage the growth of cancerous tumours.
Treatment and management of hypoxia involves measures of general care. Supplemental oxygen and intravenous fluids prevent further cellular damage and encourage cell replication by ensuring adequate blood flow and oxygen supplies. Providing oral or intravenous nutrition helps cells acquire the nutrients needed for cellular function. Healthcare professionals might also prescribe medications that inhibit the inflammatory process.
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