No abstract

No abstract

Purpose: Diabetic patients receive hyperbaric oxygen therapy for non-healing lower extremity ulcers. Exposure to hyperbaric hyperoxia during hyperbaric oxygen therapy may affect cardiovascular functions by different mechanisms. Patients may experience serious problems such as pulmonary edema and death during hyperbaric oxygen therapy. The effect of hyperbaric oxygen therapy on cardiovascular functions in diabetic patients is not well documented. N-terminal pro-B-type natriuretic peptide (NT-proBNP) has been suggested as powerful biochemical marker of cardiac function. The aim of this study was to investigate the effect of hyperbaric oxygen therapy on NT-proBNP levels in diabetic patients. Methods: Twenty-five diabetic patients (19 male and 6 female, 64.7 ± 10.2 yr), who were planning to undergo hyperbaric oxygen therapy for non-healing lower extremity ulcers, were prospectively enrolled into the study. All patients were evaluated with echocardiography before the study. Heart rate and arterial blood pressure of patients were measured, and venous blood samples were drawn from each patient for NT-proBNP analysis before and immediately after the hyperbaric oxygen therapy. Results: NT-proBNP levels increased from 815 ± 1096 pg/ml to 915 ± 1191 pg/ml after HBO2 therapy (P < 0.05). Heart rate and arterial blood pressure did not change with HBO2 therapy (P > 0.05). Conclusion: Hyperbaric oxygen therapy induces considerable ventricular wall stress in diabetic patients. Care should be taken when a diabetic patient with cardiovascular disease is treated with hyperbaric oxygen therapy.

Myoglobinuric acute renal failure (MARF) may develop after severe muscle injury. Heme oxygenase-1 (HO-1), a stress-response protein, has been implicated as a protective agent against MARF. We hypothesized that hyperbaric oxygen therapy (HBOT) may alleviate MARF by inducing renal HO-1 expression. Wistar-Albino rats were randomly assigned into three groups: Control (n = 4), MARF (n = 8), MARF + HBO (n = 8). MARF was induced by intramuscular glycerol (50%, 8 mL/kg) injection. Saline (8 mL/kg) was injected into the hind limb of the animals in the control group. Animals in the MARF + HBO group received two sessions of HBO therapy (90 min at 2.5 atm) 2 and 18 h after glycerol injection. Serum and tissue samples were taken at 24 h. Serum urea and creatinine levels increased in the MARF and MARF + HBO groups confirming the development of MARF. But, serum urea and creatinine levels were similar in MARF and MARF + HBO groups. Oxidative stress parameters were similar among all groups. Histological renal injury score was similar in MARF and MARF + HBO groups. HO-1 level, determined by immunohistochemistry, was significantly higher in MARF and MARF + HBO groups, compared to the control group. Although HO-1 level in MARF + HBO group was higher than MARF group, it was not statistically significant. We found that HBOT did not reduce renal injury in experimental MARF model. HBOT is used to reduce the muscle damage after crush injury, which may be accompanied by MARF. Therefore, more studies are needed to understand the effects of HBO treatment on renal functions after MARF.

Letters to the Editor should be submitted online to www.editorialmanager.com/ amsurg. (See details online under ''Instructions for Authors''.) They should be no more than 3 double-spaced pages excluding an Abstract and sub-headings with a maximum of four (4) references. If figures are included, they should be limited to two (2). The cost of printing color figures is the responsibility of the author.