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The Role of Hyperbaric Oxygen Therapy (HBOT) in Liver Transplantation

Liver transplantation is a commonly explored treatment option in instances of end-stage liver complications. Some of these include acute liver failure and specific liver disorders. The popular therapeutic modality caters to acute/chronic forms of complications with the objective of improving outcomes after transplantation. One of the most common causes of liver failure after transplantation is liver ischemia/reperfusion injury. Regular blood flow, which is essential after the procedure is interrupted, leads to graft dysfunction and failure. Viral infections occur pretty often after transplantation as well, with the most common being hepatitis B, hepatitis C, or CMV. In other instances, the recipient’s immune system fights the newly replaced organ, leading to tissue damage and, finally, failure. Hyperbaric oxygen therapy (HBOT), a more recent form of treatment, takes care of most of these causes of graft failure and dysfunction. 

Mechanism of Action

Hyperbaric oxygen therapy comes in handy as it protects the liver against organ ischemia/reperfusion (I/R) injury. The latter is the most prevalent form of complication facing liver transplantations. Oxidative stress is handled in the process. HBOT has the effect of curbing hepatocyte apoptosis as it has dominant hepatoprotective effects. The cell membrane and organelles are spared from destruction via lipid peroxidation, protein nitration, and DNA modification. Increased oxygenation also aids in the storage of liver obtained from brain-dead donors. Increased oxygen supply during HBOT also aids in liver tissue regeneration. The latter especially applies if the organ incurs injury during or after the transportation process. The high metabolic demands during regeneration are necessary to restore the hepatic energy demands for mitochondrial oxidative phosphorylation. 

HBO plays a protective role in liver transplantation. Bilirubin levels increase while necrotic foci reduce or are eliminated. Oxygen also prevents liver cirrhosis, treating hepatic artery thrombosis (HAT) and boosting various functions of the liver in the body; its functioning is optimized. The inflammatory response that compromises the liver transplantation process entails the production of inflammatory substances by various cells. The released substances activate leukocytes, platelets, and endothelial cells, which protect the lining of various blood vessels. Hyperbaric oxygen (HBO) reverses the inflammatory response that results in increased adhesion molecules on the surface of endothelial cells. The most prevalent molecules in this scenario are CD11 and CD18; the proteins play a crucial role in leukocyte adhesion. ICAM-1, which expresses itself similarly on endothelial cells, is also reduced. The resultant effect of result white blood cell adhesion to endothelial cells is reduced liver tissue damage. HBOT should be used for perioperative care to improve its efficacy in the host’s body. HBOT helps in improving the quality of life for individuals who have undergone liver transplantation by improving their chances of survival. There are fewer instances of re-transplantation, morbidity, and mortality as a result of various complications after transplantation.

References 

 

Liu, W., Lv, H., Han, C., & Sun, X. (2016). Application of hyperbaric oxygen in liver transplantation. Medical Gas Research, 6(4), 212–219. https://doi.org/10.4103/2045-9912.196903  

Mazariegos, G. V., O’Toole, K., Mieles, L. A., Dvorchik, I., Meza, M. P., Briassoulis, G., Arzate, J., Osorio, G., Fung, J., & Reyes, J. (1999). Hyperbaric oxygen therapy for hepatic artery thrombosis after liver transplantation in children. Liver Transplantation and Surgery, 5(5), 429–436. https://doi.org/10.1002/lt.500050518  

Silveira, M. R., Margarido, M. R., Vanni, J. C., Nejo Junior, R., & Castro-e-Silva, O. de. (2014). Effects of hyperbaric oxygen therapy on the liver after injury caused by the hepatic ischemia-reperfusion process. Acta Cirurgica Brasileira, 29(suppl 1), 29–33. https://doi.org/10.1590/s0102-86502014001300006  

 

 

 

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