Hyperbaric Oxygen Therapy Dampens Inflammatory Cytokine Production and Does Not Worsen the Cardiac Function and Oxidative State of Diabetic Rats

Hyperbaric oxygen therapy (HBOT) is frequently used after soft tissue injuries and in diabetic patients with ulcerated wounds; however, its ability to increase oxidative stress casts doubts. Diabetes (DM) in male Wistar rats (N = 20) weighing 300 g were induced by a single dose of streptozotocin. Ten diabetics (DMHBOT) and 10 controls (CHBOT) underwent a one-hour long hyperbaric oxygen treatment protocol (2.5 bar) 12 times after the 3rd week of diabetes. Ten animals remained untreated. Eight weeks after diabetes induction, we measured the 24-hour blood glucose profile and cardiovascular function (sonocardiography and the relaxation ability of aortae). Malonyl-dialdehyde (MDA) and cytokine levels were measured in blood plasma. Poly(ADP-ribose) polymerase (PARP) activity was estimated in cardiac and aortic tissue. HBOT did not alter most of the cardiovascular parameters. PARylation in cardiac and aortic tissues, plasma MDA levels were elevated in diabetic rats. HBOT prevented the increase of MDA in diabetic animals. In addition, levels of the pro-inflammatory cytokine-induced neutrophil chemoattractant-1 (CINC-1) the levels of anti-inflammatory tissue inhibitor of metalloproteases-1 were not altered in diabetes or in hyperoxia. Our results suggest that HBOT does not increase long-term oxidative stress, and, similar to training, the TBARS products, nitrotyrosine formation and poly(ADP-ribosyl)ation may be eased as a result of hyperoxia