Kamer Kilinc

REPERFUSION INJURY AFTER DETORSION OF UNILATERAL TESTICULAR TORSION

SummaryReperfusion injury has been well documented in organs other than testis. An experimental study was conducted to investigate reperfusion injury in testes via the biochemical changes after unilateral testicular torsion and detorsion. As unilateral testicular torsion and varicocele have been shown to affect contralateral testicular blood flow, reperfusion injury was studied in both testes. Given that testicular blood flow does not return after 720° testicular torsion lasting more than 3 h, the present study was conducted after 1 and 2 h of 720° torsion. Adult male albino rats were divided into seven groups each containing ten rats. One group served to determine the basal values of biochemical parameters, two groups were subjected to 1 and 2 h of unilateral testicular torsion respectively, two groups were subjected to detorsion following 1 and 2 h of torison respectively, and two groups underwent sham operations as a control. Levels of lactic acid, hypoxanthine and lipid peroxidation products were determined in testicular tissues. Values of these three parameters obtained from the sham operation control groups did not differ significantly from basal values (P>0.05). All three parameters were increased significantly in both ipsilateral and contralateral testes after unilateral testicular torsion when compared with basal values (P<0.01 and P<0.05, respectively). Detorsion caused significant changes in lipid peroxidation products levels in ipsilateral but not in contralateral testes when compared with values obtained after torsion (P<0.01 and P>0.05, respectively). It is concluded that ipsilateral testicular torsion causes a decrease in perfusion not only in the ipsilateral but also in the contralateral testis. Additionally, detorsion following up to 2 h of 720° torsion causes reperfusion injury in ipsilateral but not in contralateral testis.

The effect of allopurinol pretreatment before detorting testicular torsion.

The resumption of blood flow to organs following ischemia may cause a further increase in tissue damage through an increase in peroxidation of lipids in cell membranes. An experimental study was conducted to investigate the prevention of reperfusion injury after testicular torsion through changes in the lipid peroxide content of the testis. Adult male albino rats were divided into 11 groups, each containing 10 rats. One group served to determine base values of the lipid peroxide content of the testis and kidney; 3 groups were subjected to unilateral testicular torsion lasting 1, 3 and 5 hours; 3 groups were subjected to detorsion following torsion lasting 1, 3 and 5 hours; 3 groups were treated with allopurinol before detorsion following torsion lasting 1, 3 and 5 hours; and 1 group underwent sham operation as a control. Thiobarbituric acid reactive products of lipid peroxidation (TBAR) were assessed in testicular and renal tissues. Testicular torsion caused a significant increase in TBAR in the testis (p < 0.01), but not in the kidneys. Detorsion caused a further significant increase in testicular TBAR (p < 0.01). Pretreatment with allopurinol prevented this further increase (p < 0.01). It is concluded that, biochemically, reperfusion injury occurs in the testis following detorsion after testicular torsion of 720 degrees lasting as long as 5 hours. Pretreatment with allopurinol before detorsion prevents such reperfusion injury.

Ipsilateral and contralateral testicular biochemical acute changes after unilateral testicular torsion and detorsion

OBJECTIVES An experimental study has been conducted to investigate testicular blood flow alterations through acute biochemical changes during unilateral testicular torsion and detorsion. METHODS One hundred twenty male albino rats were divided into 12 groups, each containing 10 rats. One group served to determine basal values of biochemical parameters, 4 groups were subjected to varying periods of unilateral testicular torsion (3, 6, 12, and 24 hours, respectively), 3 groups were subjected to detorsion following varying periods of torsion (6, 12, and 24 hours, respectively), and 4 groups underwent sham operations as controls. Levels of lactic acid, hypoxanthine, and lipid peroxidation products were determined in testicular tissues. RESULTS Values of these 3 parameters obtained from sham operation control groups did not differ significantly from basal values (p > 0.05). All 3 parameters were increased significantly in both ipsilateral torted and contralateral nontorted testes after unilateral testicular torsion when compared with basal values (p < 0.05). Detorsion did not cause significant changes in levels of lipid peroxidation products in both ipsilateral torted and contralateral nontorted testes when compared with values obtained after torsion (p > 0.05). CONCLUSIONS Ipsilateral testicular torsion causes a decrease not only in the ipsilateral torted but also in the contralateral nontorted testicular perfusion. The clues of reperfusion injury do not become evident following detorsion of testicular torsion lasting more than 6 hours.

Time-Level Relationship for Lipid Peroxidation and the Protective Effect of α-Tocopherol in Experimental Mild and Severe Brain Injury

OBJECTIVE Oxygen free radical-mediated lipid peroxidation has been proposed to be one of the major mechanisms of secondary damage in traumatic brain injury. The first purpose of this study was to establish the time-level relationship for lipid peroxidation in injured brain tissue. The second purpose was to examine the protective effect of alpha-tocopherol against lipid peroxidation. METHODS For this study, 65 guinea pigs in five groups were studied. Five of the animals were identified as a control group, and the remaining 60 animals were divided equally into four groups (Groups A, B, C, and D). Mild injury (200 g x cm) (Groups A and C) and severe injury (1000 g x cm) (Groups B and D) were produced by the method of Feeney et al. Alpha-tocopherol (100 mg/kg) was administered intraperitoneally before brain injury in Groups C and D. Five animals from each group were killed immediately after trauma, five after 1 hour, and the remaining five animals after 36 hours. Lipid peroxidation in traumatized brain tissues was assessed using the thiobarbituric acid method. RESULTS In all groups with traumatic brain injuries, levels of malondialdehyde, a lipid peroxidation product, were higher than in the control group. The amount of lipid peroxidation was increased by the severity of the trauma. Alpha-tocopherol significantly suppressed the rise in lipid peroxide levels in traumatized brain tissues. CONCLUSION This study demonstrates that lipid peroxidation is increased by the severity of trauma and that alpha-tocopherol has a protective effect against oxygen free radical-mediated lipid peroxidation in mild and severe brain injury.

Sildenafil attenuates renal ischemia reperfusion injury by decreasing leukocyte infiltration

The aim of the study was to investigate the effects of sildenafil citrate (SC) on renal ischemia reperfusion (I/R) injury in a rat model. Forty eight male Wistar albino rats were randomly assigned into six groups: sham, ischemia, I/R, SC+sham, SC+ischemia and SC+I/R. In the I/R groups, the right kidney was removed and the artery and vein of the left kidney were clamped for 45 min followed by reperfusion for 1 h. In the SC-treated groups, SC dissolved in saline solution was given as a single dose (1 mg/kg) 60 min before the operation. Renal histology was analyzed by scoring the tubular damage and neutrophil infiltration. Tissue myeloperoxidase activity and lipid peroxidation were analyzed. The histological damage and the neutrophil infiltration induced by I/R were significantly less in the SC+I/R group (p = 0.004 and p = 0.003, respectively). Pretreatment with SC significantly diminished the tissue myeloperoxidase activity, indicating the prevention of the neutrophil sequestration into the kidney in the SC+I/R group (p = 0.004); however, it did not result in any changes in lipid peroxidation. Our results in a rat model of ischemia-reperfusion indicate that pre-ischemic treatment with sildenafil citrate can significantly attenuate ischemia/reperfusion-induced renal injury by decreasing leukocyte infiltration.

Antioxidant actions and early ultrastructural findings of thiopental and propofol in experimental spinal cord injury.

Thiopental and propofol are effective antioxidant agents. The current study was undertaken to examine the neuroprotective effects of a single intraperitoneal dose of thiopental and propofol. Effects of the drugs were evaluated by lipid peroxidation and ultrastructural findings. Fifty male Wistar rats were divided into five groups. Group 1 was the control group. Rats underwent laminectomy only, and nontraumatized spinal cord samples were obtained 1 hour after surgical intervention. All other rats sustained a 50-g/cm contusion injury by the weight drop technique. Group 2 rats underwent spinal cord injury alone, group 3 rats received 1 mL intralipid solution intraperitoneally immediately after trauma as the vehicle group, group 4 rats received a 15-mg/kg single dose of thiopental, and group 5 rats received a 40-mg/kg single dose of propofol intraperitoneally following the trauma. Samples from groups 2, 3, 4, and 5 were obtained 1 hour after injury. Lipid peroxidation was determined by measuring the concentration of malondialdehyde in the spinal cord tissue. The ultrastructure of the spinal cord was determined by electron microscopy. The contusion injury was associated with a rise in lipid peroxidation. Compared with the trauma group there was significant attenuation in lipid peroxidation of groups 4 and 5. Ultrastructural findings showed that the rats of group 4 sustained minor damage after spinal cord injury, but there was more evident damage in group 5 rats. These results indicate that thiopental decreases lipid peroxidation and improves ultrastructure, whereas propofol decreases lipid peroxidation without improving ultrastructure 1 hour after spinal cord injury in rats.

Increased xanthine oxidase activity after traumatic brain injury in rats.

Oxidative stress may contribute to many of the pathophysiologic changes that occur after traumatic brain injury (TBI). There are a number of potential sources and mechanisms for oxygen free radical (OFR) production and lipid peroxidation after TBI. In this study, we investigate the time-dependent changes in xanthine oxidase (XO) activity and lipid peroxidation using a focal TBI animal model. We demonstrate that there is an immediate increase in lipid peroxidation by-products and in XO enzyme activity after TBI.

A New Model for Tethered Cord Syndrome: A Biochemical, Electrophysiological, and Electron Microscopic Study

In order to investigate the pathophysiology of the tethered cord syndrome, a few experimental models have been developed and used previously. In this study, the authors present a new experimental model to investigate the biochemical, electrophysiological, and histopathological changes in the tethered spinal cord syndrome. A model was produced in guinea pigs using an application of cyanoacrylate to fixate the filum terminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were performed on 40 animals divided into two groups. The responses to tethering were evaluated with hypoxanthine and lipid peroxidation, somatosensory and motor evoked potentials, and transmission electron microscope examination. The hypoxanthine and lipid peroxidation levels significantly increased, indicating an ischemic injury (p < 0.01). The average hypoxanthine level in the control group was 478.8 +/- 68.8 nmol/g wet tissue, while it was 651.2 +/- 71.5 nmol/g in the tethered cord group. The lipid peroxidation level in group I was 64.0 +/- 5.7 nmol/g wet tissue, whereas it was 84.0 +/- 4.7 nmol/g in group II. In the tethered cord group, the latencies of the somatosensory and motor evoked potentials significantly increased, and the amplitudes decreased. These changes indicated a defective conduction in the motor and sensorial nerve fibers. In the transmission electron microscopic examinations, besides the reversible changes like edema and destruction in the gray-white matter junction, irreversible changes like scarcity of neurofilaments and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for tethered cord syndrome.

Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats

Abstract Oxygen free radical-mediated lipid peroxidation is one of the major mechanisms of secondary damage in traumatic brain injury. We assessed the effects of nimodipine on lipid peroxidation 1 h after head trauma in rats. Nimodipine (1.5 µg/kg IV bolus injection) was given immediately after head trauma by either the carotid artery or the jugular vein. Placebo treated rats received saline by the same routes. Control rats received head trauma only. Sham-operated rats were the group without head trauma. Malondialdehyde (MDA), which is the end product of lipid peroxidation, was measured as an indicator of oxygen free radical formation in the brain tissue. The mean values for MDA in sham operated rats were 92.4±4.9 nanomoles/gram wet weight (nmol/gww) of brain tissue. In the control group, MDA content of the brain tissue was 120.8±9.4 nmol/gww. In placebo treated rats, the results were similar. In the groups receiving nimodipine via carotid artery or jugular vein, the mean values were 101.1±6.9 and 106.5±6.0 nmol/gww, respectively. These results indicate that nimodipine caused a significant decrease in lipid peroxidation when given in the acute phase of head trauma in rats. This occurred regardless of the route of injection.

Effect of Melatonin on Cerebral Edema in Rats

OBJECTIVE Melatonin (5-methoxy-N-acetyltrypamine), a chemical naturally produced in the pineal gland, has been suggested to be a free radical scavenger and an antioxidant. In the present study, the effect of melatonin on cold-induced brain edema was evaluated by determination of cerebral water content, blood-brain barrier permeability, and areas of infarct; the effects were also studied histopathologically. METHODS Brain edema was produced in rats by creating a lesion via cortical freezing. Animals were separated into four groups: sham-operated (craniectomy only); control (cold injury); sham-vehicle (cold injury plus saline); and melatonin treatment (cold injury plus melatonin). Melatonin was administered (50 mg/kg intraperitoneally) 15 minutes after the cold injury was induced. Twenty-four hours later, tissue samples from the core, from the periphery of the cold-injured hemisphere, and from the contralateral hemisphere symmetrical to the cold injury were obtained. RESULTS Melatonin treatment reduced edema (mean +/- standard deviation; 86.22 +/- 1.54% in the control group versus 80.78 +/- 2.76% in the melatonin treatment group, P < 0.001) and blood-brain barrier permeability (45.34 +/- 2.75% in the control group versus 38.26 +/- 3.40% in the melatonin treatment group, P < 0.001) at the periphery of cold injury. Area of infarct reduced from 5.84 +/- 0.58% in the control group to 3.30 +/- 0.89% in the melatonin treatment group (P < 0.001). The effect of melatonin was also confirmed histopathologically. CONCLUSION Melatonin was found to be neuroprotective in instances of cold-induced brain edema. Thus, melatonin may be a valuable therapeutic agent in the treatment of cerebral edema.