Mitigation of indomethacin-induced gastric mucosal lesions by a potent specific type V phosphodiesterase inhibitor.

AIM: To investigate the gastroprotective effect of vardenafil against indomethacin-induced gastric damage. METHODS: Forty-eight female Wistar albino rats were randomly divided into 6 groups. Group 1 received saline only. Group 2 (indomethacin) received indomethacin. Rats in group 3 and 4 were pretreated with different doses of famotidine. Group 5 and 6 were pretreated with different doses of vardenafil. Rats in groups 3 to 6 received 25 mg/kg indomethacin 30 min after pretreatment. The animals were sacrificed 6 h later and their stomachs were opened. Gastric lesions were counted and measured. The stomach of each animal was divided in two parts for histopathological examinations and nitric oxide (NO) and malondialdehyde (MDA) assays, respectively. RESULTS: There were no gastric mucosal lesion in the saline group but all rats in the indomethacin group had gastric mucosal ulcerations (ulcer count; 6.25 +/- 3.49, and mean ulcer area; 21.00 +/- 12.35). Ulcer counts were diminished with famotidine 5 mg/kg (4.12 +/- 2.47, P > 0.05), 20 mg/kg (2.37 +/- 4.43, P < 0.05), vardenafil 2 mg/kg (4.37 +/- 3.06), and vardenafil 10 mg/kg (1.25 +/- 1.38, P < 0.05) compared to the indomethacin group. Gastric mucosal lesion areas were diminished with famotidine 5 mg/kg (8.62 +/- 2.97, P < 0.001) , famotidine 20 mg/kg (0.94 +/- 2.06, P < 0.001), vardenafil 2 mg/kg (6.62 +/- 5.87, P < 0.001), and vardenafil 10 mg/kg (0.75 +/- 0.88, P < 0.001) compared to the indomethacin group. MDA levels were significantly higher in indomethacin group (28.48 +/- 14.51), compared to the famotidine 5 mg/kg (6,21 +/- 1.88, P < 0.05), famotidine 20 mg/kg (5.88 +/- 1.60. P < 0.05), vardenafil 2 mg/kg (15.87 +/- 3.93, P < 0.05), and vardenafil 10 mg/kg (10.97 +/- 4.50, P < 0.05). NO concentration in gastric tissues of the famotidine groups were significantly increased (P < 0.05), but the NO increases in the vardenafil groups were not statistically significant. Histopathology revealed diminished gastric damage for pretreatment groups compared to the indomethacin group (P < 0.05). CONCLUSION: Vardenafil affords a significant dose-dependent protection against indomethacin induced gastric mucosal lesions in rats.

Evaluation of a new hemostatic agent Ankaferd Blood Stopper in experimental liver laceration.

INTRODUCTION: Hemorrhage is a leading cause of death after trauma. It is also the major cause of operating room deaths among patients who undergo liver surgery. Various techniques and materials have been attempted to manage bleeding, but a standard method has not been defined yet. We studied the hemostatic effects of Ankaferd Blood Stopper on liver injury in comparison with regenerated oxidized cellulose. MATERIALS AND METHODS: Thirty Wistar albino rats underwent partial hepatic laceration by scissors. The animals were randomized to the treatment of resected surface with either Ankaferd Blood Stopper (ABS, n = 11) or regenerated oxidized cellulose (Surgicel, n = 9), or were left untreated (controls, n = 10). All the animals were resuscitated with lactated Ringer's solution at 3.3 ml/min/kg to a mean arterial pressure (MAP) of 100 mmHg. Survival time, total blood loss, resuscitation volume, and MAP were recorded for 30 min or until death. The rats that were alive at the end of 30 min were sacrificed with blood withdrawal from catheters. RESULTS: Rats in the ABS and Surgicel groups survived significantly longer than rats in the control group (p =.0001). There were no significant differences between the ABS and the Surgicel groups in survival (p =.91). Application of ABS and Surgicel was associated with a significant reduction in blood loss compared to controls (p =.008), with no significant differences between active treatment groups (p =.74). The resuscitation volume was not different. CONCLUSIONS: ABS is as effective as Surgicel in achieving hemostasis following partial liver excision in an experimental rat model.