Numerous experimental studies demonstrate the anti-inflammatory effect of HBOT. This effect has been demonstrated for classic clinical situations:
In a chronic wound model in rats, HBOT has been shown to decrease cell death and inflammation by preventing white blood cells from migrating from the blood to the wound .
Vascular wall cells in a chronic wound situation show fewer harmful inflammatory signs thanks to HBOT. This effect is genetically controlled and lasts 22 hours, which justifies the daily application of HBOT in chronic wound situations .
White blood cells trigger an inflammatory reaction when in a chronic wound they stick to the walls of the vessels. OHB stops this inflammatory reaction by preventing white blood cells from sticking to the vascular walls . HBOT causes immediate increase in a crucial defense protein contained in white blood cells.
HBOT decreases the size of myocardial infarction by preventing lipid perxidation, production of nitric oxide synthetase as well as the aggregation of white blood cells to the vascular wall which causes a slowdown in local circulation.
HBOT improves the formation of new blood vessels in the experimental infarction in rats .
HBOT also decreases the volume of myocardial infarction caused in rabbits when it is used in conjunction with dilation blocked coronary vessels.
HBOT increases the migration and nesting in the brain of stem cells in rats which have been interrupted of the cerebral circulation . Brain function was improved. The number of migration increases with the number of HBOT sessions.
HBOT was able to decrease the volume of brain damage in rats that have suffered brain trauma. This protective effect is related to the production of nitric oxide synthetase.