Tehran University Medical Journal

Background: The aim of this study was to determine the level of lipid peroxidation and tissue protein after superior mesenteric artery occlusion tissue damage. The effect of melatonin as anti oxidant and free radical scavenger in prevention of tissue damage, were also evaluated.

Methods: Thity six young male Wisatr-Albino rats (weight: 80-120 gr), were divided equally in 6 group with different concentrations of melatonin (10,20,30 mg/kg) treatment. Group 1was control, group 2 the sham that surgical process was applied until superior mesenteric artery dissection and received vehicle solution only in equally volume by intra muscular route. Group 3 was ischemia- reperfusion (I/R), group 4 was I/R plus melatonin 10 mg/kg, group 5 I/R plus melatonin 20 mg/kg and finally group 6 I/R plus melatonin 30 mg/kg. After laparatomy, a microvascular atraumatic clip was placed across the superior mesenteric artery under general anaesthesia and itbremoved after ischemia for 30 minutes. The first dose of melatonin was applied just beforereperfusion, second dose, after reperfusion and third dose on the second day .On third day rats were killed and their bowels were removed. The level of tissue melandialdehyde (MDA) as index of lipid peroxidation and tissue protein was determined.

Results: The level of tissue MDA were significantly lower in group 4, 5, 6 than group 3 (p<0.05). Tissue protein levels were significantly upper in group 4 than group 3. (p<0.001). There was no significant difference tissue protein level in group 5, 6 than group 3(p>0, 05).

Conclusion: These results suggest that melatonin 10 mg/kg has antioxidant effect in prevention of inducing tissue damage during SMA occlusion in rat intestine.

Background: Hypomagnesemia is commonly encountered in patients with a wide variety of diseases including subarachnoid hemorrhage (SAH), cardiovascular emergencies, head trauma, migraine attacks, seizure and preeclampsia. It seems to be associated with a poor clinical outcome. This study considers the prevalence and temporal distribution of hypomagnesemia after aneurysmal SAH and its correlation with the severity of SAH, delayed cerebral ischemia (DCI) as well as the neurological outcome after a period of three months.

Methods: Between 2003 and 2008, 60 patients were admitted to the emergency ward of Imam Khomeini Hospital with acute SAH. Serum magnesium levels were measured during the first 72 hours, days 4-7, and second and third weeks after SAH. The three-month outcome was assessed according to the Glasgow Outcome Scale (GOS). Clinical SAH grading was performed according to the criteria of the World Federation of Neurological Surgeons (WFNS) and the patients were allocated to "Good" (GOS = 4, 5) and "Poor" (GOS= 1-3) outcome groups. The prevalence of hypomagnesemia was assessed in both patient groups. Fisher exact test was used to analyze data.

Results: Hypomagnesemia occurred in 22% of patients during the first 72 hours after SAH. It was associated with more prevalent DCI (p<0.05), whereas low serum magnesium levels during days 4-7 17% of patients) and the second week (22% of patients) after SAH were correlated with poor clinical outcome (p<0.05). No correlation was found between first 72 hour-hypomagnesemia and poor clinical outcome at three months.

Conclusion: Hypomagnesemia occurs after aneurysmal SAH and it may predict the occurrence of DCI, while low serum magnesium levels during days 4-7 and within the second week of event predict poor clinical outcome at three months. Treatment of this electrolyte disturbance may have a favourable effect on the clinical outcome of patients with aneurysmal SAH.

Background: Dimethyl sulfoxide (DMSO) has been used as a solvent for many drugs in ischemic experiments. DMSO has many biological benefits, including antioxidant, anti-inflammatory, platelet aggregation inhibiting and cell membrane stabilizing effects. Moreover, some experimental studies report that DMSO has a neurprotective effect in permanent focal cerebral ischemia. Despite the effect of DMSO on the cortex, striatum injuries and motor neurological dysfunctions in transient focal cerebral ischemia are not completely clear.

Methods: Thirty-six male Sprague-Dawley rats weighing 300-350 g were divided into saline- (control) and DMSO-treated groups. Under chloral hydrate anesthesia (400mg/kg, ip), transient focal cerebral ischemia was induced by 90-min middle cerebral artery occlusion (MCAO) followed by 23-h reperfusion. Rats received saline (n=11) or 2% DMSO intraperitoneally at doses of 0.01 (n=11), 0.1 (n=7) and 0.2 (n=7) ml/kg 30 min prior to induction of ischemia. Twenty-four hours after MCAO, the neurological deficit scores were ascertained. Cortical and striatal infarct volumes determined by triphenyltetra-zolium chloride staining. 

Results: Administration of DMSO at doses of 0.1 and 0.2 ml/kg significantly reduced cortical and striatal infarct volumes (p<0.001), while rats receiving the 0.1 ml/kg dose had infarct volumes similar to those of the control group (p=0.225). Moreover, only 0.2 ml/kg doses of DMSO significantly reduce neurological motor dysfunction (p<0.001).

Conclusions: Findings of this study indicate that DMSO is a potent neuroprotective agent against transient focal cerebral ischemia in rat. Moreover, our data also suggest that DMSO may be a candidate for acute stroke treatment.

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: The effect of ischemia/reperfusion (I/R) injury on kidney has been under investigation for many years. But the changes in liver function and oxidative stress status in renal I/R injury is not well known. Recent studies suggest a crosstalk between liver and kidneys. The aim of the present study was to assess liver changes after induction of various degrees of renal I/R injury.
Methods: This is an experimental study conducted on 20 male rats that were obtained from animal house of Physiology Department. Twenty male rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion periods. Blood samples were drawn post-operatively and plasma creatinine, BUN, ALT and AST were measured. Hepatic glutathione (GSH) and FRAP (ferric reducing antioxidant power) levels and the concentration of IL-10 and tumor necrosis factor (TNF) -alpha were evaluated.
Results: Both 45 and 60 min ischemia followed by 1h reperfusion periods resulted in significant increases in plasma creatinine (11.1±1.7mg/dl and 1.24±0.07mg/dl vs 0.55±0.15mg/dl, p<0.05) and BUN (34±3.85mg/dl and 35.0±2.81mg/dl vs 23.75±1.1mg/dl, p<0.05). These rats showed a significant decrease in liver GSH as well as significant increase in TNF-a & IL-10 concentrations.
Conclusion: Renal ischemia causes changes in liver function and oxidative stress status. A minimum of 45 min ischemia is needed to study the effects of renal injury on liver as a remote affected organ.

Background: Cerebrovascular ischemic accident is the third most common cause of death in community. Management of high-risk patients reduces complications and mortality. Serum lipid profile is one of the most important factors influencing the prognosis.

Methods: In this cross sectional study, 123 (58 female and 65 male) patients with acute ischemic stroke, mean aged 65.1± 11.16 years, were admitted to Sina Hospital between September 2008 and September 2009. The inclusion criteria were age between 40-90 years and ischemic stroke within the anterior or posterior brain blood system. The exclusion criteria were brain tumor or abscess, venous sinus thrombosis, liver disease, renal failure, hypothyroidism or metabolic problems. Serum lipid profile was evaluated during the first 24 hours after stroke and after 12 hours of fasting. Furthermore, the patients' inability was evaluated on the first and fifth day of hospitalization by NIH Stroke Scale (NIHSS).

Results: Patients' total serum cholesterol was 189.93± 51.46 mg/dl and mean total serum triglycerides was 157.72± 72.67 mg/dl. The mean HDL and LDL was 47.70± 14.43 and 105.98± 37 mg/dl, respectively. In the analysis, a significant inverse relationship was found between serum triglyceride levels and fifth day's NIHSS. In addition, age and a history of heart disease had a significant direct relationship with the first day's NIHSS. (p< 0.05)

Conclusion: The study showed a better prognosis in cases with increased plasma triglyceride levels, after cerebral ischemic stroke. Besides, older age and a history of ischemic heart disease were associated with a worse prognosis.

Background: Numerous studies have shown the protective effects of saffron against oxidative damage in a global model of cerebral ischemia, but its effects on brain edema and oxidative ischemic injury in focal ischemic stroke are not completely understood. Therefore, this study was designed to investigate the effects of saffron on brain edema, infarct volume, antioxidant enzyme activity (glutathione peroxidase and superoxide dismutase) and concentration of malondialdehyde (MDA) in ischemic brain tissue in an experimental model of stroke.

Methods: Focal brain ischemia was established with the temporary occlusion of the middle cerebral artery for one hour in rats. Saffron (100 mg/kg) was given intra-peritoneally at the onset of ischemia. 24 hours later, brain edema and infarct volume were evaluated and glutathione peroxidase and superoxide dismutase activities and MDA concentration were measured in the ischemic brain tissue using a specific kit.

Results: The results showed that saffron reduced infarct volume by 77% (P<0.001) and brain edema by 60% (P<0.001) compared with the control group in 24 hours following ischemia. Moreover, saffron significantly reduced the content of MDA (P<0.001) and increased the activity of superoxide dismutase (P<0.001) and glutathione peroxidase (P<0.001) in the cortex of the ischemic brain tissue.

Conclusion: Saffron has protective effects against oxidative ischemic damage and brain edema in a transient model of focal cerebral ischemia in rats. This protective effect is probably induced by increasing the capacity of antioxidant enzymes and decreasing the production of free radicals.

Background: Creatine kinase is a cardiac biomarker that is used for the assessment of ischemic injuries and myocardial infarction. The present study was designed to evaluate effects of oxytocin administration during ischemia and reperfusion periods on CK-MB levels in the coronary effluent of isolated rat heart and the possible role of oxytocin receptor, nitric oxide (NO), prostacyclin and mitochondrial ATP-dependent potassium channels in this regard.

Methods: Male wistar rats (n=8) were anesthetized with sodium thiopental and their hearts were transferred to a Langendorff perfusion apparatus. All animals were randomly divided into nine groups as follow in the ischemia-reperfusion group, hearts underwent 30 min of regional ischemia followed by 120 min of reperfusion. In oxytocin group, hearts were perfused with oxytocin 5 min after ischemia induction for 25 min. In other groups, 35 min prior to oxytocin perfusion, atosiban (a non-specific oxytocin receptor blocker), L-NAME (an NO synthase inhibitor), indomethacin (a non-specific cyclooxygenase blocker) and 5-HD (a specific mKATP channel blocker) were perfused for 10 min. In all groups, we measured CK-MB levels in the coronary effluent at the end of reperfusion. Moreover, coronary flow (mL/min) was measured at baseline, during ischemia period and 60 and 120 min after reperfusion.

Results: Oxytocin administration significantly reduced CK-MB level in oxytocin group as compared to ischemia-reperfusion group. Administration of atosiban, L-NAME, indomethacin and 5-HD prior to oxytocin perfusion abolished the effects of oxytocin on CK-MB levels.

Conclusion: Administration of oxytocin during ischemia and reperfusion periods deceased CK-MB levels but infusion of atosiban, L-NAME, 5-HD and indomethacin inhibited oxytocin from exerting its effects.

Background: Ischemia/reperfusion induced acute renal failure causes excretory functional disorders of nephrons. Ischemia/reperfusion injury is accompanied by generation of reactive oxygen species that leads to dysfunction, injury, and death of renal cells. Antioxidants of plant origin minimize the harmful effects of reactive oxygen species. The aim of this study was to determine the possible therapeutic potentials of Rosa canina L. in preventing renal functional disturbances during the post-ischemic reperfusion period.

Methods: In this experimental study undertaken for evaluating renal excretory function in 30 male Wistar rats, renal ischemia was induced by occluding both renal arteries for 45 min, followed by 24 h of reperfusion. The rats received 2 ml of tap water or a hydroalcoholic extract of Rosa canina (500 mg/kg) orally for 7 days before induction of ischemia. In plasma samples, creatinine and urea nitrogen levels were measured, and in renal tissue samples, red blood cells were counted. The data were analyzed using ANOVA and Duncan tests.

Results: Renal ischemia for 45 minutes increased plasma levels of creatinine (P<0.001) and nitrogen urea (P<0.01) while reducing red blood cell counts in renal glomeruli (P<0.001). Rosa canina administration diminished the increase in creatinine (P<0.001) and nitrogen urea concentrations (P<0.01), and prevented reductions in red blood cell counts in renal glomeruli (P<0.001).

Conclusion: Rosa canina seems to be useful as a preventive agent against renal damages induced by ischemia/reperfusion injuries in rats.

Background: In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR (60 min of bilateral renal artery occlusion and 3 hrs reperfusion) injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors.

Methods: Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group (Sham recipient) and the intact recipient mice that received leukocytes from IR donor group (IR recipient). After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected.

Results: Renal malondialdehyde (MDA) increased and glutathione and superoxide dismutase (SOD) decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group.

Conclusion: These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury.

Background: Random pattern flap is a common reconstructive surgery procedure but its necrosis is a challenging problem. A lot of pharmacological agents and surgical procedures have been examined for the prevention of this complication to maximize the length to width ratio of these surgical flaps. Therefore, we designed an experimental study to evaluate the effects of aspirin, clopidogrel bisulfate (Plavix) and their combination on random skin flap survival in rats.
Methods: Forty male rats were randomly assigned to four equal groups. Surgery was done under general anesthesia. A random, rectangular 3×11 cm dorsal skin flap was designed, elevated and sutured back into its primary site. In group one, 100 mg/kg Aspirin and in group two, 25 mg/kg Plavix were administered orally for 7 days postoperatively. Aspirin and Plavix were co-administered in the third group for the same period of time while the control group received no medication. After 7 days, the total surface of flaps, the viable and also the necrotic parts were measured by Image J software. Mean standard deviation and analysis of variance were calculated to compare the results.
Results: The mean area of flap survival was 62.49% in the control, 64.04% in Aspirin, 65.09% in Plavix and 64.06% in combination groups. No statistically significant differences were found between treatment groups and control rats.
Conclusion: In this study, we found no significant differences between Aspirin, Plavix or their combination on the survival of random skin flaps.

Background: The use of random flaps is one of the most common methods of reconstructive surgery because they are easy to use and quick to do. However, the absence of axial vessels especially in the distal areas can cause ischemia and loss of total or part of the flap. Different methods and systemic and topical medications have been recommended to prevent ischemia in random flaps. The aim of this study was to evaluate the effect of stem cells derived from umbilical cord blood in random flap survival in rats.

Methods: This experimental study was conducted in Animal Laboratory of Hazrat Fatemeh Hospital in 2012. In this study twenty Sprague-Dawley male rats weighing approximately 300 to 350 g were selected and divided randomly into two groups. In both groups after anesthesia, a flap was created in the posterior part of each rat with a size of 2 x 6 cm. In the intervention group we injected stem cells derived from umbilical cord blood into the flap, and after eight days the effects on the survival of flaps were examined by digital photography and then pathological examination was performed.

Results: The mean of viable flap in the stem cell group was 6.57 cm² and in control group 4.71 cm². The minimum and maximum flap survival in the intervention group were 4.71 and 8.75, and the minimum and maximum flap survived in control group were 1.86 and 7.77. This difference was significant and showed that the viable parts of flap were more in the intervention group (P=0.49). In pathologic examinations epidermal and muscle necrosis of the skin were reported in 3 cases in the intervention group and 5 cases in control group.

Conclusion: It was observed that in the case of ischemia, the temperature drop was higher than normal. So, during brain injuries to prevent serious damage, the brain metabolism can be reduced by cooling the spinal fluid.