Hyperbaric Oxygen Exposure Attenuates Circulating Stress Biomarkers: A Pilot Interventional Study

Hyperbaric oxygen therapy (HBOT) has been used to provide oxygen to underperfused organs following ischemia or carbon monoxide intoxication. Various beneficial consequences of HBOT have been reported, including wound healing, anti-inflammatory action, and cell survival; however, the molecular mechanisms underlying these effects have not been elucidated yet. We applied a single HBOT program consisting of administration of 2.8 atmospheres absolute (ATA) for 45 min, followed by 2.0 ATA for 55 min, to 10 male volunteers without any metabolic disease. Within 1 week of HBOT, there was no alteration in serum biochemical variables, except for an increase in triglyceride content. As a mitochondrial stress indicator, the serum concentration of growth differentiation factor 15 was reduced by HBOT. The circulating level of γ–glutamyltransferase was also decreased by HBOT, suggesting an attenuation of oxidative stress. HBOT increased adiponectin and reduced leptin levels in the serum, leading to an elevated adiponectin/leptin ratio. This is the first study to investigate the effect of HBOT on serum levels of metabolic stress-related biomarkers. We suggest that HBOT attenuates mitochondrial and oxidative stresses, and relieves metabolic burdens, indicating its potential for use in therapeutic applications to metabolic diseases.

Expression of Aquaporin-1 and Aquaporin-5 in a Rat Model of High-Altitude Pulmonary Edema and the Effect of Hyperbaric Oxygen Exposure

Objective: To investigate the therapeutic roles of hyperbaric oxygen exposure on high-altitude pulmonary edema and to determine whether aquaporin-1 and aquaporin-5 were involved in the pathogenesis of HAPE in rats. Methods: Rats were divided into 5 groups: The control group, the HAPE group (HAPE model), the HBO group (hyperbaric oxygen exposure), the NBO group (normobaric oxygen exposure), and the NA group (normal air exposure). Western blot and real-time PCR were used to analyze the pulmonary expressions of AQP1 and AQP5. The wet-to-dry (W/D) weight ratio and the morphology of the lung were also examined. Results: The lung W/D weight ratio in the HAPE group was increased compared with the control group. The injury score in the HBO group was noticeably lower than that in the control group. The mRNA and proteins expressions of AQP1 and AQP5 were significantly downregulated in the HAPE group. Conclusions: Oxygen exposure alleviated high-altitude hypobaric hypoxia-induced lung injury in rats. Additionally, HBO therapy had significant advantage on interstitial HAPE.

Decreased Blood Glucose and Histopathology Improvement in Hyperbaric Hyperoxic Conditions Alloxan-induced rats(Laboratory Experimental Study)

Background: Diabetes mellitus is still a problem in Indonesia, related to the number of organs involved. This disease has relatively high morbidity and mortality rates. Adjuvant therapy is needed considering the long-term therapy that must be consumed by patients. Objective: To explain the effect of hyperbaric oxygen in reducing blood glucose levels, and repairing histopathological damage to the pancreas and liver. Method : this study was an experimental laboratory study using whistar strain rats (Rattus Norvegicus) which were given a normal diet then induced alloxan to create a hyperglycemia condition. After that, 12 rats from the treatment group were given 3 x 30’ hyperbaric oxygen exposure for 6 days. Blood glucose levels, histopathological changes in the pancreas and liver was measured between the treatment group and the control group were not given hyperbaric oxygen exposure. Results: There was a significant difference (α< 0,05) in decreasing blood glucose and repairing histopathological damage in pancreatic and liver tissue between treated group and control group. Conclusion: hyperbaric oxygen treatment as much as 3 x 30'for days at 2.4 ATA O2 100% reduce blood glucose levels and repair histopathological damage to pancreatic tissue and liver of alloxan- induced white rats.