Investigation of the effect of hyperbaric oxygen on experimental cyclosporine nephrotoxicity.

Hyperbaric oxygen interacts with drugs which patients use concurrently with hyperbaric oxygen treatment, which may cause in potentiation or inhibition of both therapeutic and toxic effects. We examined the effect of hyperbaric oxygen therapy on experimental cyclosporine A nephrotoxicity. The study comprised four groups of rats: a control group, a cyclosporine A group (25 mg/kg/day intraperitoneally for four days), a hyperbaric oxygen group (60 min. every day for four days at 2.5 atmospheric pressure), and a cyclosporine A+hyperbaric oxygen group (CsA 25 mg/kg/day intraperitoneally for four days+hyperbaric oxygen for 60 min. every day for four days at 2.5 atmospheric pressure). Hyperbaric oxygen did not alter biochemical parameters. Cyclosporine A increased serum urea and serum creatinine levels and decreased creatinine clearance. In the cyclosporine A+hyperbaric oxygen group serum urea level increased more than in the cyclosporine A group. Cyclosporine A increased tubular epithelial cell apoptosis and necrosis score values. The numbers of apoptotic cells in proximal tubule epithelial cells in the cyclosporine A+hyperbaric oxygen group were significantly higher than those of the cyclosporine A group. We recommend that renal functions of the patients receiving cyclosporine A should be monitored during hyperbaric oxygen therapy.

Visual loss as a late complication of carbon monoxide poisoning and its successful treatment with hyperbaric oxygen therapy.

PURPOSE: To present recovery from vision loss due to CO poisoning with Hyperbaric Oxygen (HBO) therapy in two patients. METHODS: Two female patients developed visual deterioration after carbon monoxide (CO) poisoning and were treated with hyperbaric oxygen therapy (HBO). Clinical examination, including visual acuity assessment, visual field examination and visual evoked potentials (VEPs) before and after the HBO therapy were performed. RESULTS: In Case 1 the visual loss started on the third day with visual acuity at the level of perception of hand movements at 10 cm in the right eye and finger count at 10 cm in the left eye. The visual evoked potentials (VEPs) had low amplitudes and prolonged (128 msec bilaterally) latencies (implicit times). After 48 sessions and 52 days of HBO therapy, the visual acuity became 0.2 in the right eye and 0.15 in the left eye. Visual field examination revealed homonymous right lower quadrant anopsia. The VEPs also improved. In Case 2 the visual acuity was 0.2 in the right eye and 0.1 in the left eye on the 6th day following the accident when the patient was admitted for treatment. The VEP latencies were within normal limits. After 36 days and 35 sessions of HBO therapy, the visual acuity became 0.7 on both eyes. The visual fields completely normalised. The VEP latencies in this case also became shorter. CONCLUSION: It appears that the adverse effects of CO poisoning continue to progress during the late period and we believe that HBO treatment in this period may still be effective and will prevent some of the neurological sequelae such as visual loss from becoming permanent. Clinical, neurological, neuropsychological, visual outcome seems to be favourable even if HBO treatment started as late as 6 or 8 days after the exposure to CO.