ABSTRACT
The objective of this study was to examine whether a decrease in neutrophil-mediated tissue injury using Fucoidin, a nontoxic neutrophil rolling inhibitor, would improve flap survival in an island flap model after ischemia-reperfusion. Myeloperoxidase activity (an indirect index of tissue neutrophil count) and malondialdehyde (an indicator of lipid peroxidation), the degree of neutrophil infiltration by direct counting, and macroscopic flap survival were assessed in the flap after arterial ischemia-reperfusion. Epigastric island skin flaps were elevated in 56 rats. The first group of 21 rats was subjected to 6 hours of arterial ischemia. The second group of 21 rats was subjected to 10 hours of arterial ischemia, and the rest of the rats were used as nonischemic controls (sham flaps). For inhibiting neutrophil rolling, a nontoxic polysaccharide agent-Fucoidin-was used. Each ischemic group was divided further into three subgroups: Subgroup I (control rats) received saline, subgroup II received 10 mg per kilogram Fucoidin, and subgroup III received 25 mg per kilogram Fucoidin before reperfusion. The results were evaluated as tissue neutrophil counts, tissue malondialdehyde content, tissue myeloperoxidase activity, and flap survival. Neutrophil counts and tissue myeloperoxidase activity were decreased significantly (p <0.001) in subgroup III, but lipid peroxidation by means of tissue malondialdehyde content was not affected by Fucoidin administration. The authors conclude that administration of Fucoidin before reperfusion can limit tissue injury apparently by inhibiting neutrophil rolling in a dose-dependent manner.
Subject(s)
Fucose/therapeutic use , Neutrophil Infiltration/drug effects , Polysaccharides/therapeutic use , Reperfusion Injury/prevention & control , Surgical Flaps/blood supply , Animals , Graft Survival , Malondialdehyde/metabolism , Neutrophils/pathology , Peroxidase/metabolism , Rats , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Reperfusion Injury/pathology , Surgical Flaps/pathologyABSTRACT
The viability of human split thickness skin grafts stored in plasma and saline at +4 degrees C had been evaluated by means of viable keratinocytes by trypan blue method. Skin grafts which were stored in plasma showed better percentage of viable keratinocytes at the end of 30 days than saline. It is concluded that plasma is a better storage medium than saline for preservation of skin grafts.
Subject(s)
Keratinocytes/physiology , Surgical Flaps , Tissue Preservation/methods , Cell Survival/drug effects , Humans , Keratinocytes/drug effects , Plasma , Sodium Chloride/pharmacologyABSTRACT
BACKGROUND/AIM: In the present study our purpose was to investigate the effect of pentoxyfilline, that plays a role in microcirculation and tissue oxygenation, alone and in combination with an antioxidant vitamin E on tissue damage in the rat liver induced by ischemia-reperfusion. METHODOLOGY: Thirty-one albino rats were divided into four groups. Rats in group I (n= 7), group II (n= 8) and group III (n= 8) were given, respectively, pentoxyfilline (25 mg/kg), pentoxyfilline and vitamin E in combination (25 mg/kg and 50 mg/kg, respectively) and equal volume of saline solution intraperitoneally for 7 days. Rats in group IV (n= 8) served as controls and received no treatment. On day 7 ischemia was induced by cross-clamping the hepatic artery, portal vein and left branch of the biliary duct for 30 minutes. Malondialdehyde (MDA) and catalase activity were assessed in tissue sample, and the level of ALT was measured in serum obtained after reperfusion for 30 minutes. Histological examination of tissue sample was also carried out. RESULTS: There was no significant difference in ALT level between three study groups. Group I and group II had significant lower MDA and catalase levels than those of group III. The results of histopathologic examination in group I and group II were better than that of group III. CONCLUSION: Our findings suggested that the treatment of pentoxyfilline alone and in combination with vitamin E decreased liver damage induced by ischemia-reperfusion and that the effect of latter was more effective but the difference between the two treatment patterns was not statistically significant.
Subject(s)
Antioxidants/pharmacology , Liver/blood supply , Pentoxifylline/pharmacology , Reperfusion Injury/pathology , Vasodilator Agents/pharmacology , Vitamin E/pharmacology , Alanine Transaminase/metabolism , Animals , Catalase/metabolism , Liver/metabolism , Liver/pathology , Malondialdehyde/metabolism , Rats , Reperfusion Injury/metabolismABSTRACT
The effect of VIP on mast cell invasion/degranulation in testicular interstitium of stressed (immobilization and cold) and beta-endorphin-treated rats were investigated. Fifty-three Wistar male rats were used in four series of experiments. Initially, the effect of immobilization and cold stress on mast cell invasion and degranulation in testicular interstitium was examined in three age group of rats: 15 (n = 6), 30 (n = 6), and 45 (n = 7) days of age. Five animals per age group were used as controls. Because the most obvious effect of the stress on mast cell invasion/degranulation in testicular interstitium was observed in 45-day-old rats, the action of VIP in stressed and beta-endorphin-treated rats was only investigated at this age group. Mast cells and Leydig cells were evaluated by using histochemical and light microscopic protocols. Stress caused mast cell accumulation and degranulation in the testicular interstitium. Stress decreased heparin synthesis and possibly increased histamine content of mast cells. The effect of beta-endorphin was not as high as seen with stress. In some areas of testicular interstitium of stressed rats, there were aplasic and/or inactive Leydig cells. VIP inhibited proliferation and degranulation of mast cells, increased heparin content of the cells, and protected Leydig cells. By way of mast cell accumulation and degranulation in the testicular interstitium, exposure to stress may lead to Leydig cell damage and infertility. VIP may be involved in the protection of normal testicular function under stress conditions.