Hyperbaric oxygen therapy prevents subarachnoid hemorrhage-induced apoptosis and impaired contractility of the rabbit bladder.

AIM: To explore the effects of experimental subarachnoid hemorrhage (SAH) on rabbit urinary bladder and to assess the potential protective effects of hyperbaric oxygen therapy (HBOT). METHODS: A total of 15 male New Zealand white rabbits were divided randomly to one of three groups: group I was spared as the control group (n = 5), group II was exposed to SAH, received no treatment, and acted as the SAH group (n = 5) and group III was exposed to SAH and received five sessions of HBOT (started 12 hours after SAH induction and was given twice daily for the first 2 days and once on the third day) and acted as the treatment group (n = 5). At 72 hours after the SAH induction, bladders from all animals were removed for in vitro organ bath experiments and biochemical analyses. RESULTS: Isometric tension studies revealed that compared to group I, the contractile responses of the strips to carbachol in group II were significantly decreased whereas HBOT restored the contractile responses (P < .05). Caspase-3 and nitric oxide synthase (NOS) activities of bladder tissues were significantly increased in group II when compared with group I, whereas caspase-3 and NOS activities were significantly decreased in the tissues of group III (P < .01). CONCLUSIONS: Subarachnoid hemorrhage stimulates apoptosis of the rabbit bladder and impairs the contractile response of the rabbit bladder to carbachol. HBOT creates a protective effect in rabbit bladder tissues and restores SAH-induced changes.

Cervical Necrotizing Fasciitis of Odontogenic Origin and Hyperbaric Oxygen Therapy.

Necrotizing fasciitis (NF) is an infection of the soft tissues pathology with high mortality that spreads through the fascial planes and rarely seen in head and neck region. The cause of infection is often odontogenic problems. Broad-spectrum antibiotics, surgical debridement, and hyperbaric oxygen therapy (HBO) are important for the treatment of disease. We report a case of cervical NF in a 33-year-old woman who was treated with rapid surgical debridement and simultaneous HBO.

Effect of hyperbaric oxygen therapy on cerebral vasospasm: a vascular morphometric study in an experimental subarachnoid hemorrhage model.

This study was undertaken to investigate the preventive or therapeutic effect of hyperbaric oxygen therapy (HBOT) on cerebral vasospasm following experimental subarachnoid hemorrhage (SAH). Twenty rabbits were assigned randomly to one of four groups. Animals in Group I were not subjected to SAH or sham operation (control group, n = 5). Animals in Group II were subjected to sham operation and received no treatment after the procedure (sham group, n = 5). Animals in Group III were subjected to SAH and received no treatment after SAH induction (SAH group, n = 5). Animals in Group IV were subjected to SAH and received five sessions of HBOT at 2.4 atmospheres absolute (ATA) for 2 h (treatment group, n = 5). Animals were euthanized by perfusion and fixation 72 h after procedures. Basilar artery vasospasm indices, arterial wall thicknesses, and cross-sectional luminal areas were evaluated. Statistical comparisons were performed using Kruskal-Wallis and Mann-Whitney U tests. Mean basilar artery vasospasm index in the treatment group was significantly smaller than in the SAH group. Mean basilar artery wall thickness in the treatment group was significantly smaller than in the SAH group. Mean basilar artery cross-sectional luminal area in the treatment group showed an increase relative to the SAH group, but this difference remained statistically insignificant. Our results demonstrated that repeated application of HBOT at 2.4 ATA for 2 h attenuated vasospastic changes such as increased vasospasm index and arterial wall thickness. HBOT is thus a promising candidate for SAH-induced vasospasm. Further studies are needed to evaluate maximal effect and optimal application regimen.

Effect of hyperbaric oxygen therapy on tense repair of the peripheral nerves.

BACKGROUND: After a peripheral nerve cut, tense repair of a nerve compromises circulation of the nerve at the injury site, making the site hypoxic. Hyperbaric oxygen might increase tissue oxygenation and therefore diminish the effects of injury. We investigated whether hyperbaric oxygen treatment affects peripheral nerve healing when repaired nerves are under tension. METHODS: Sixteen young female albino Wistar rats were used. Sciatic nerves of the animals were cut and a 3mm part of each nerve was excised. The animals were distributed into two groups: 1) The HBO2 group (n = 8), which received surgical repair and HBO2 therapy; and 2) The Control group (n = 8), which received only surgical repair. Walking track analysis was performed five times, on Days 12, 15, 18, 20 and 22 after surgery. The healing of sciatic nerves was evaluated by histopathological study and electrophysiological study. Pillai's Trace test and Mann-Whitney U-test were used for statistical analysis. RESULTS: Walking track analysis: Sciatic function index (SFI) scores of HBO2 group were significantly higher than SFI scores of Control group (p:0.026). Electrophysiological study: A statistical difference was not found between groups. Histopathological study: Counts of HBO2 group axons were significantly greater than in the control group (p: 0.008). CONCLUSIONS: In clinical practice, tension after nerve repair frequently occurs. However, neither grafting nor other current surgical methods are functionally perfect. Since primary end-to-end repair is known to be the best repair when possible, we think HBO2 allows for the use of primary repair even when nerve tension is foreseen.