Efficiency of Ozone Therapy in a Rat Model of Experimental Uveitis.

PURPOSE: To investigate efficiency of ozone therapy in uveitis. METHODS: A total of 24 albino Wistar rats were randomly assigned to four groups (n = 6); (a) control group; (b) sham group; (c) infliximab treatment group; (d) ozone therapy group. Vitreous haze scores of all groups were evaluated. Vitreous cytokine levels (TNF-α, IL-1, IL-6) measured by ELISA and eyes were enucleated for histopathologic examination. RESULTS: According to vitreous haze scores, there was statistically significant inflammation in Group (b) compared with Group (a), and there was less inflammation in infliximab and ozone groups compared with Group (b) (p < 0.05). Cytokine levels in infliximab and ozone groups were lower but not statistically significant when compared with Group (b) (p > 0.05). There was significantly less inflammation in histopathologic examination in treatment groups when compared with the sham group (p < 0.05). CONCLUSIONS: Clinical and histopathologic examination results indicate that systemic application of ozone may be efficient in the treatment of uveitis.

Is Tracheal Transplantation Possible With Cryopreserved Tracheal Allograft and Hyperbaric Oxygen Therapy? An Experimental Study.

BACKGROUND: Allografts have achieved prominence for tracheal reconstruction because of their natural physiologic and anatomic structure, which preserves respiratory tract flexibility and lumen patency. The immunomodulatory effects of cryopreservation prevent tracheal allograft rejection. In addition, hyperbaric oxygen therapy (HBOT) accelerates wound healing by promoting epithelization and neovascularization. This experimental study investigated the early and late effects of HBOT on cryopreserved tracheal allografts (CTAs). METHODS: The study used 33 outbred Wistar rats weighing 300 to 350 g as allograft transplantation donors and recipients. Among these, 22 recipient rats were randomly assigned to the HBOT (n = 11) and control (n = 11) groups. Rats in the HBOT group were treated with 100% oxygen for 60 minutes at 2.5 atmospheres of absolute pressure for 7 days. Recipient rats in both groups were euthanized at 1 week (n = 5) and 4 weeks (n = 6) after transplantation, defined as the early and late periods, respectively. RESULTS: In the early period, no significant histopathologic differences were observed between groups (p > 0.05). However, microscopic evaluation of the control group during the late period showed low epithelization of the CTA. In contrast, microscopic evaluation of the HBOT group during this same period revealed epithelium covering the transplanted CTA lumen. Significant epithelization and vascularization and significantly reduced inflammation and fibrosis were found in the HBOT group compared with the control group (p < 0.05). CONCLUSIONS: HBOT may be effective in tracheal reconstruction by increasing epithelization and neovascularization after extended tracheal resection. HBOT, therefore, should be considered in CTA transplantation.

Effects of dexpanthenol and N-acetylcysteine pretreatment in rats before renal ischemia/reperfusion injury.

BACKGROUND: We investigated the anti-inflammatory and protective effects of concomitant use of dexpanthenol (DXP) and N-acetylcysteine (NAC) induced ischemia/reperfusion (I/R) injury of kidney. METHODS: Forty rats were randomly divided into 5 groups. In all groups except for Group 1(Sham), renal arteries bilaterally occluded with vascular clamp for IR injury. Group 1(Sham), received a single dose of 10 mL/kg isotonic saline daily by intraperitoneal (IP) injection for three days. Group 2(IR), received a single dose of 10 mL/kg isotonic saline daily by IP injection for three days. Group 3(IR + NAC), received 300 mg/kg NAC daily by IP injection for three days. Group 4(IR + DXP), received 500 mg/kg DXP daily by IP injection for three days. Group 5(IR + NAC + DXP), received 500 mg/kg DXP and 300 mg/kg NAC daily by IP injection for three days. Serum urea (BUN), creatinine (Cr) and neutrophil gelatinase-associated lipocalin (NGAL, lipocalin 2, siderocalin) levels were measured as kidney function tests. TNF-α levels were measured as inflammatory marker. Tissue sections were evaluated histopathologically under light microscopy. RESULTS: IR + NAC + DXP group received both NAC and DXP before induction of renal I/R and as the biochemical and histopathological data revealed the results of the IR + NAC + DXP group and sham group were similar. Biochemically and histopathologically, combined use of NAC and DXP has better results when each of them used alone. CONCLUSION: We concluded that concomitant use of DXP and NAC plays a major role against I/R injury and may be useful in acute treatment of I/R induced renal failure.

Hyperbaric oxygen therapy does not potentiate doxorubicin-induced cardiotoxicity in rats.

The current use of doxorubicin is regarded as an absolute contraindication for hyperbaric oxygen (HBO2) therapy because of the increased risk of cardiotoxicity. The aim of this study was to investigate whether additional exposure to HBO2 during the course of doxorubicin treatment would further increase the cardiotoxicity of doxorubicin in rats. Female Wistar rats were treated with either HBO2 (n = 10) or doxorubicin (n = 8) or a combination of both treatments (n = 10) for 4 consecutive weeks and followed up for an additional 4 weeks. Cardiomyopathy was evaluated using two-dimensional and M-mode echocardiography at baseline, at the fourth, sixth and eighth weeks, and by histopathological investigation of the rat hearts at the eighth week. Doxorubicin treatment significantly reduced ejection fraction and fractional shortening (P < 0.001) and caused severe histopathological injury (P < 0.05) indicating development of cardiotoxicity. Although the combination of doxorubicin and HBO(2) also markedly reduced ejection fraction and fractional shortening (P < 0.001), this reduction was significantly less than that of doxorubicin treatment (P < 0.05). HBO2 therapy also attenuated doxorubicin-induced histopathological changes in rat hearts (P < 0.05). HBO2 alone did not alter echocardiographic parameters or histopathological findings (P > 0.05). In conclusion, HBO2 therapy does not potentiate doxorubicin-induced cardiotoxicity in rats. Cardioprotection conferred by HBO2 against doxorubicin warrants further investigation.