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Capillary growth and Hyperbaric Oxygen

The reason for capillary growth and how it is connected higher levels of oxygen saturation

The new capillary Development does not occur during the oxygen saturations while doing HBOT. IT begins after the HBOT session. The lack of oxygen after return to normal pressure causes angeiogenesis or capillary development.

To explain it better, rats kept at 0.5 ATM which is equal to over 17,000 feet altitude for a few weeks were shown to have a 50% higher capillary count than those at sea level atmospheric pressure. (Ref. 1) As Dr. Philip James explained it, “This enormously increases the surface area for oxygen diffusion. However, below a critical level of oxygenation ATP production fails and eventually no capillary angiogenesis or even metabolism is possible. As oxygen levels fall macrophages, neutrophils and other cells activate a variety of their genes, including the encoding vascular endothelial growth factor. (VEGF)” (Ref. 2) “) Mild hypoxia is often referred to as a ‘stimulus’ to capillary neogenisis. It is difficult to see how the absence of something can be a stimulus! It is more logical to state that adequate oxygen levels inhibit angiogenesis and the reason is obvious. If tissue oxygen levels are adequate then there is no need for additional blood flow and of course oxygen is the primary regulator of flow by controlling vasomotor tone.” (Ref. 3)

This should explain the importance of spending as much time, numerous sessions, in the chamber at higher level of oxygen saturation. When the patient returns to sea level pressure, the oxygen level drops and stimulates angiogenesis or capillary growth. It should be logical then that doing treatments at over 1100 mmHg (hard chamber) would cause more development when returning to sea level 159.6 mmHg than a soft chamber session 207.48 mmHg. When the neurons recognize that the high level of oxygen supply has disappeared then the brain begins to develop more capillaries to compensate for the shortage.

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