scholarly journals Mannitol in reperfusion skin island flaps injury

1999 ◽  
Vol 14 (3) ◽  
Author(s):  
Alberto Schanaider ◽  
Antônio Ambrósio de Oliveira Neto ◽  
Ilson Rosique da Costa ◽  
Gustavo Luiz Simões Leite ◽  
Daniela Peixoto Considera ◽  
...  

In the skin, the concept of reperfusion injury is well established. The application of this knowledge to deal with skin flap surgery problems, has a great prophylactic potential. This experimental study was performed to evaluate the action of mannitol as a scavenger of oxygen-free radicals, after an ischemia-reperfusion injury on skin island flaps. Thirty six male Wistar rats were divided into three test groups (n = 12): a non-ischemic group (group I), and two others (groups II and III) which were subjected to nine hours of ischemia following by 30 minutes of reperfusion. After seven days, all animals of group II, treated with saline, showed full skin flap necrosis. The assessment of group III, that received a 20% solution of mannitol prior to the onset of reperfusion, revealed 75% (9/12) of flap viability. These results suggest that pre-treatment with mannitol is able to enhance flaps survival with significantly less tissue necrosis (p <0.02).

2017 ◽  
Vol 10 (16) ◽  
pp. 106
Author(s):  
Rajan Kumar ◽  
Navneet Khurana ◽  
Barinderjit Kaur

Objective: Cardioprotective effect of INM-176 in ischemia reperfusion (I/R) injury in rat heart was evaluated by measuring the extent of release of the enzyme lactate dehydrogenase (LDH) and creatine phosphokinase (CK) and by measuring the myocardial infarction (MI) size.Methods: Five groups of animals were employed. Animals were sacrificed, and heart was mounted over the Langendorff’s apparatus. Group I was employed as control group, Group II was the myocardial ischemic (MI) group, and Group III, IV, and V were pre-treated with different doses of INM- 176 (150, 300, and 600 mg/kg). After this, global ischemia accompanied by reperfusion for 30 and 120 minutes was given, respectively. The effluent was collected from coronary vessel before the initiation of ischemia, immediately, after 5 and 30 minutes of reperfusion. The magnitude of myocardial injury was measured by LDH and CK release in coronary effluent. MI size was also evaluated macroscopically using triphenyl tetrazolium chloride staining.Results: In the present study, INM-176 was found to produce a dose-dependent cardioprotective effect against I/R injury, as observed by a decrease in the level of LDH, CK, and infarct size. Pre-treatment with a dose of 600 mg/kg was found to be more effective as compared to 150 and 300 mg/kg dose of INM-176.Conclusion: INM-176 pre-treatment at a dose of 600 mg/kg provides cardioprotection against I/R-induced myocardial injury.


2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Fadhil G. Al-Amran ◽  
Najah R. Hadi ◽  
Haider S. H. Al-Qassam

Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, and ICAM-1 and plasma level of cTnI (). Morphologic analysis showed that both MK-886 and DITPA markedly improved () the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.


2014 ◽  
Vol 9 (6) ◽  
pp. 2124-2130 ◽  
Author(s):  
NAN KANG ◽  
YONG HAI ◽  
FANG LIANG ◽  
CHUN-JIN GAO ◽  
XUE-HUA LIU

2017 ◽  
Vol 95 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Neslihan Pınar ◽  
Oya Soylu Karapınar ◽  
Oğuzhan Özcan ◽  
Esin Atik Doğan ◽  
Suphi Bayraktar

The aim of this study was to investigate the antioxidant effects of tempol on ovarian ischemia–reperfusion (I/R) injury in rats. Forty female Wistar albino rats were randomly divided into 5 groups: Group I, sham; Group II, ischemia (I); Group III, I/R; Group IV, I/R + tempol 30 mg/kg i.p; Group V, I/R + tempol 50 mg/kg i.p. Oxidative stress index (OSI) was significantly higher in the ischemia group and the I/R group than in the sham group. Catalase levels were significantly lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. Glutathione peroxidase levels were lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. MDA levels were significantly lower in the I/R + tempol 30 mg/kg i.p. group and the I/R + tempol 50 mg/kg i.p. group than in the I/R group. The levels of the histopathological parameters were significantly decreased in the I/R + tempol 50 mg/kg i.p. group compared with the I/R group. Tempol can be used for reducing ovarian I/R injury.


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