Histopathological Damage Scores Research Articles

The Diagnostic Value of Plasma SCUBE1, a Novel Biomarker of Platelet Activation, in Testicular Torsion: A Randomized, Controlled, Experimental Study

To investigate the potential diagnostic value of plasma signal peptide, CUB (complement proteins C1r/C1s, Uegf, Bmp1) domain, epidermal growth factor (EGF)-like 1 (SCUBE1) protein in experimentally induced testicular torsion (TT). In this randomized, controlled, experimental study, 24 mature male Wistar rats were divided into four groups: 2- and 4-hour control (groups I and III, respectively), and 2- and 4-hour torsion (groups II and IV, respectively) groups. Torsion was performed by rotating the left testis 720° clockwise and maintained by fixing the testis. Plasma SCUBE1 levels and histopathological damage scores were compared. There was significantly greater histopathological damage in the 4-hour torsion group compared with the other groups. SCUBE1 levels in this group were also higher than those in the other groups, and the difference was significant. There were significant correlations between histopathological scores and SCUBE1 levels. SCUBE1, a novel marker of platelet activation, is elevated in TT. According to our results, platelet activation may play an important pathological role in tissue injury associated with testicular ischemia. Plasma SCUBE1 measurement may have diagnostic, therapeutic, or prognostic value in TT.

Exposure to a 900 MHz electromagnetic field for 1 hour a day over 30 days does change the histopathology and biochemistry of the rat testis

Purpose: To investigate the effect of exposure to a 900 megahertz (MHz) electromagnetic field (EMF) on the rat testicle.Materials and methods: Twenty-four adult male rats were divided into control, sham and EMF groups. The EMF group rats were exposed to 900 MHz EMF (1 h/30 day), and testicles were extracted at the end of the experiment. Malondialdehyde, superoxide dismutase, catalase and glutathione levels and apoptotic index and histopathological damage scores were compared.Results: Histopathologically, EMF group rats exhibited vacuoles in seminiferous tubules basal membrane and edema in the intertubular space. Seminiferous tubule diameters and germinal epithelium thickness were both smaller, and apoptotic index was higher, in the EMF group than in the other groups. Malondialdehyde, superoxide dismutase, catalase and glutathione values in the EMF group decreased significantly compared to those of the control group.Conclusions: The results show that exposure to 900 MHz EMF causes alterations in adult rat testicular morphology and biochemistry.

The effects of streptozotocin-induced diabetes on ghrelin expression in rat testis: biochemical and immunohistochemical study.

Ghrelin is a hormone which has effects on the secretion of growth hormone, gastrointestinal system, cardiovascular system, cell proliferation and reproductive system. The present study we focused on the relation between ghrelin and GHS-R1a gene expression and the regulation of their expression in the testes of diabetic rats. 40 male Wistar albino rats were divided into four groups: control, and sampled 4, 8 and 12 weeks after induction of diabetes by streptozotocin (STZ) intraperitoneal injection (40 mg/kg). The rats were decapitated under ketamine anesthesia and their testes were removed. Blood was obtained from heart and serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured by ELISA. Tissue ghrelin and GHS-R mRNA levels were determined by qRT-PCR, while ghrelin protein expression was studied by immunohistochemistry. Histopathological damage scores were also assessed. Eight weeks after diabetes induction serum FSH level was increased, whereas LH and testosterone concentrations decreased. The ghrelin and GHS-R1a gene expression and ghrelin immunohistochemistry score first tended to increase after first four weeks of diabetes, and then tended to decrease. Ghrelin-immunopositive cells were detected in Leydig cells in all groups of rats, however, not in the germinal epithelium. Congestion of vessels and hemorrhage, formation of the vacuoles in spermatogonia and spermatocytes, desquamation of spermatids in the lumen and disorganization of seminiferous tubule germinal epithelium were observed in testis of all the diabetic rats. In addition, mean testicular biopsy score and mean seminiferous tubule diameter were getting lower in diabetic animals. Our results suggest that diabetes affects ghrelin expression in rat testis.

Protective effect of β-glucan on acute lung injury induced by lipopolysaccharide in rats.

Lipopolysaccharide (LPS)-induced endotoxemia can cause serious organ damage such as acute lung injury and death by triggering the secretion of proinflammatory cytokines and acute-phase reactants. The goal of this study was to evaluate the effects of β-glucan on inflammatory mediator levels and histopathological changes in LPS-induced endotoxemia. Forty-seven male Wistar albino rats were randomly allocated into four groups as follows: control group, LPS group (10 mg/kg LPS), LPS + β-glucan group (100 mg/kg β-glucan before LPS administration), and β-glucan group. Twelve hours after LPS administration, lung and serum samples were collected. Concentrations of IL-6, IL-8, C-reactive protein (CRP), and procalcitonin were measured in the serum at hours 0 (basal) and 12. The severity of lung damage was assessed by an appropriate histopathological scoring system. Serum levels of CRP in the LPS group at 12 h were significantly higher than in the other groups, whereas serum IL-6 levels in the LPS and LPS + β-glucan groups at 12 h were significantly decreased. The mean histopathological damage score of the LPS group was slightly higher than that of the LPS + β-glucan group. Moreover, mortality rate was significantly decreased in the LPS + β-glucan group versus the LPS group. β-glucan reduces endotoxemia-induced mortality and might be protective against endotoxemia-induced lung damage.

Protective effect of early placement of nasogastric tube with solid dilator on tissue damage and stricture formation after caustic esophageal burns in rabbits

BackgroundThe ingestion of caustic substances remains an important public health issue worldwide. Children represent 80% of the ingestion injury population globally. Accidental alkaline material accounts for most caustic ingestions. There is no conclusive evidence of tissue damage and stricture protection of a nasogastric-tube with a solid dilator in the literature, therefore it was hypothesized that early intraesophageal tube placement does not cause additional histopathologic damage and prevents strictures. MethodsAn exploratory study on experimental caustic esophageal burns in a rabbit model was designed. In the treated group a silicone tube was placed immediately after causing the burns, while the untreated group followed the natural course of the burn. On the twenty-secondday, an esophagectomy was performed on all animals for microscopic (Histopathologic Damage Score and Stenosis Index) and macroscopic analysis. ResultsForty animals were randomly divided into two groups. The Histopathologic Damage Score was 3.7±1.1 in the treated group versus 3.9±1.2 in the untreated group (p=.9690). The Stenosis Index was 0.6±0.1 in treated rabbits versus 2.3±0.2 in untreated (p<.0001). ConclusionThe early placement of an intraesophageal tube with solid dilator prevents stenosis formation and does not produce greater tissue damage.

The effect of exogenous oxytocin on streptozotocin (STZ)-induced diabetic adult rat testes

Oxytocin (OXY) plays a crucial role in reproduction. The aim of this study is to investigate the therapeutic and protective effects of oxytocin treatment on streptozotocin (STZ) induced diabetes in testicular tissue. The rats were randomly divided into four experimental groups: (I) Control Group, (II) STZ induced Diabetic Group (STZ Group), (III) STZ induced Diabetic Group with Pre-Oxytocin treatment (Pre-OXY Group) and (IV) STZ induced Diabetic Group with Post-Oxytocin treatment (Post-OXY Group); each group contains six animals. The rats whose blood glucose levels were more than 200mg/dl were included to the experiment. At the end of the 4th week, testes tissue samples were taken to be processed for light microscopy and transmission electron microscopy. Malondialdehyde (MDA), Glutathione (GSH) and Advanced Oxidation Protein Products (AOPP) levels were determined biochemically in blood samples. Testicular tissue samples stained with Hematoxylin and Eosin (H&E) and Periodic acid-Schiff (PAS) reaction were evaluated under light microscope. The histopathological damage score of testicular tissue, which was significantly increased in STZ group, was decreased by oxytocin treatment. According to biochemical data, MDA and AOPP levels have been increased in the blood of STZ Group compared to the Control Group whereas they decreased significantly in Oxytocin-treated Groups compared to STZ Group. GSH levels were significantly decreased in the blood of STZ Group and increased in the blood of Oxytocin-treated Groups compared to STZ Group. In conclusion, oxytocin has a potential protective effect on the testes tissue of STZ-induced diabetic rats.

Methylene blue attenuates renal ischemia–reperfusion injury in rats

Background and purposeIn our study, we investigated the effects of methylene blue (MB) on histopathological changes in renal ischemia/reperfusion (I/R) injury rat model. Material and methodsTwenty-one Sprague–Dawley male rats were divided equally into three groups. Group 1 (control) was administered intraperitoneal saline solution. In Groups 2 (untreated group) and 3 (MB treatment), the renal arteries were clamped, and ischemia (for 1hour) and then reperfusion (for 4hours) were applied. Thirty minutes before ischemia, the untreated group received physiological saline, whereas the treatment group was administered 30mg/kg MB through an intraperitoneal route. Blood samples were drawn, and renal specimens were harvested 5.5hours after physiologic saline injection in the control and immediately after the reperfusion period in the other groups. The levels of tissue superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total oxidant status (TOS), total antioxidant status (TAS), plasma urea, creatinine and ischemia modified albumin (IMA) were measured. Moreover, the histopathological damage score of the renal tissue was determined. ResultsMB significantly alleviated the severity of histopathological damage by increasing the levels of tissue SOD and TAS and decreasing TOS concentrations in the renal I/R model (p<0.05). ConclusionAdministration of MB in renal I/R damage may play a protective role.

Effect of detorsion alone and in combination with enoxaparin therapy on ovarian reserve and serum antimüllerian hormone levels in a rat ovarian torsion model

To investigate the effect of enoxaparin on ovarian reserve and serum antimüllerian hormone (AMH) levels in a rat ovarian torsion model. Experimental study. Experimental surgery laboratory in a training and research hospital. Fourteen female Wistar Hannover rats. 1) Control group received no special treatment other than abdominal exposure; 2) detorsion-only group received bilateral adnexal torsion (3-hour ischemia), and then after 3-hour torsion period, detorsion (reperfusion) was performed; and 3) detorsion-enoxaparin group received 0.5mg/kg enoxaparin subcutaneously 2hours before the same surgery as the detorsion-only group and a second 0.5mg/kg dose of enoxaparin 24hours after the first surgeries. Apart from the surgeries, preoperative and postoperative 1-mL blood samples were drawn from the right jugular vein of each rat. Preoperative and postoperative serum AMH levels, histopathologic damage scores, and follicle counts in the ovarian tissue of the rats. Vascular congestion and hemorrhage scores were higher in the detorsion-enoxaparin group than in the detorsion-only and control groups. The number of small antral follicles was smaller in the detorsion-only group than in the control group. The difference in the pre- and postoperative AMH levels was higher in the detorsion-only group than in the control and detorsion-enoxaparin groups. The combination of enoxaparin therapy with conventional ovarian detorsion is more effective in protecting the ovarian reserve than detorsion alone.

Effects of tenoxicam in experimental corrosive esophagitis model

Esophageal stricture, one of the important complications of corrosive esophagus, develops following edema and granulation tissue that forms during and after the inflammatory reactions. Tenoxicam, a non-steroid anti-inflammatory drug with a long half-life, prevents various leukocyte functions including phagocyte and histamine secretion by inhibiting prostaglandin synthesis and removes various oxygen radicals in the region of inflammation. We designed this as a histopathological study using tenoxicam in rats for which we created a corrosive esophagus model. After necessary authorizations were obtained, the study was performed in Çanakkale 18 Mart University experimental animal laboratory. Twenty-four Wistar albino rats, weighing 220-240 g, were used for the experiment. Experimental animals were randomized into three groups: tenoxicam group (group T, n:8), control group (group C, n:8), and sham group (group S, n:8). Tenoxicam 0.5 mg/kg/day was administered to animals in group T, where esophageal burn was developed experimentally, 5 mg/kg 0.9% NaCL was administered i.p. to rats in group C for 15 days, once in 24 hours. No procedure was applied to rats in group S. After 15 days, all animals were sacrificed under general anesthesia and their esophagi were extracted. As a result of histopathological evaluation, inflammation and fibroblast proliferation was not observed in rats in the sham group (group S). Intense inflammation was observed in six rats (6+/2-) in the control group, and fibroblast proliferation was observed as 5+/3-. And in treatment groups, inflammation was evaluated as 3+/5-, and fibroblast proliferation as 3+/5-. In our study, histopathologic damage score was higher in the control group (P < 0.005). We deduce that tenoxicam can be useful in the treatment of caustic esophageal injuries in the acute phase, but think that these drugs require further researches and clinical studies before routine clinical use.

The short term effects of resveratrol on ischemia–reperfusion injury in rat testis

PurposeThe purpose of this study was to identify changes taking place in the rat testis at the 24th hour of reperfusion following testicular torsion and to evaluate the effects of resveratrol (RSV), a powerful antioxidant, in preventing these changes using novel biochemical parameters and histopathology. MethodsEighteen adult male rats were divided into three groups: Sham-operated (S), torsion/detorsion (T/D), and T/D+RSV groups. In the T/D group, testicular ischemia was achieved by rotating the left testis 720° clockwise for 4h. In the T/D+RSV group, 20mg/kg RSV was administered intraperitoneally 30min before detorsion. All rats were sacrificed 24h after detorsion. Serum and tissue malondialdehyde (MDA) concentrations, ischemia modified albumin (IMA), total oxidative status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and histopathological damage score were analyzed. ResultsSerum MDA, IMA, TOS, and OSI levels rose significantly in the T/D group. Serum MDA and IMA values were lower in the T/D+RES groups, but not significantly. OSI and TOS values were lower in the T/D+RES group, and the difference was significant. TAS values decreased significantly in the T/D group and rose in the T/D+RSV group, but not significantly. Ipsilateral tissue MDA values were significantly elevated in the T/D group and decreased in the T/D+RSV group, but not significantly. Apoptosis and histopathological damage increased significantly in the T/D group and decreased significantly in the T/D+RSV group. In the contralateral testis, apoptosis increased significantly in the T/D group. It decreased significantly in the T/D+RSV group. ConclusionsOur findings show that RSV had a protective effect against oxidative damage induced with a testicular T/D model, especially at the antiapoptotic and histopathological level. OSI may be a good guide to the clinical status of testicular T/D.

Pancreatic Injury Secondary to Renal Ischemia/Reperfusion (I/R) Injury: Possible Role of Oxidative Stress

Recent studies demonstrated remote effects of renal ischemia/reperfusion (I/R) injury on some organs such as brain, liver, and lungs. We investigated the effects of renal I-R injury on function, histology and oxidative stress state of pancreas. Twenty-four male adult Sprague-Dawley rats were divided equally into 2 groups; sham group: rats underwent midline laparotomy and dissection of renal pedicles without renal ischemia, and ischemic group: rats underwent bilateral renal ischemia for 45 min. Renal functions (serum creatinine and BUN), pancreatic functions (serum amylase, lipase and insulin) and fasting blood glucose were measured at 2 h, 1 day, 3 days and 7 days after ischemia. Also, pancreatic histology and malondialdehyde (MDA), catalase and reduced glutathione (GSH) were examined at 2 h and 7 days after ischemia. The ischemic rats showed significant increase in serum creatinine and BUN with significant increase in serum amylase and lipase at 2 h, 1 day and 3 days after ischemia. Blood glucose and fasting insulin showed no significant change apart from significant increase in insulin in sham group at 1 day after ischemia. Pancreas isolated from ischemic rats showed significant increase in histopathological damage score and significant increase in MDA and catalase enzyme with decrease in GSH. In conclusion, bilateral renal ischemia for 45 min caused significant impairment of pancreatic functions and histology. This might be due to deficiency of antioxidant and increased lipid peroxidations in pancreatic tissues.

Protective effects of melatonin and quercetin on experimental lung injury induced by carbon tetrachloride in rats

ABSTRACTIntroduction: Exposure to carbon tetrachloride (CCl4), a well-known toxicant, causes tissue damage by inducing oxidative stress via formation of free radicals. The fundamental structure of the organs of rats and humans is similar, so administration of CCl4 to rats is an accepted experimental model to produce oxidative damage to various tissues including pulmonary tissue. In this study, we evaluated the protective capacity of melatonin and quercetin against CCl4-induced oxidative lung damage in rats. Material-Metods: Rats were divided into five groups each containing seven rats as follows: Control group, Olive oil group CCl4 group, CCl4+Melatonin, and CCl4+Quercetin group. The tissue samples were processed by routine histological and biochemical procedures. Sections were stained with Hematoxylin-eosin and Masson's trichrome. Histopathologic damage score was calculated. Malondialdehyde (MDA) and glutathione (GSH) levels and catalase (CAT) activities were assayed. Results: The lung sections of control groups showed normal histological characteristics. Fibrosis, interstitial hemorrhage, epithelial desquamation in bronchiole and alveoli, intra-alveolar edema, leukocyte, and macrophage infiltration were observed in lung sections of rats exposed to CCl4 alone. The findings were reduced in the treatments groups. The MDA level in the CCI4 group were significantly higher than in the other groups (p < .001), and the CAT and GSH levels in the CCI4+Mel and CCI4+Quer groups were significantly higher than in the CCI4 group (p < .05). Conclusion: In conclusion, we suggest that agents with antioxidant properties such as melatonin and quercetin may have positive effects in the treatment of pulmonary diseases characterized by especially edema, inflammation, and fibrosis.

Protective effects of pretreatment with neurotrophin-3 on intrathecal ropivacaine in rats

To investigate the effect of pretreatment with neurotrophin-3 (NT-3) on intrathecal ropivacaine in rats. A total of 144 male Sprague Dawley rats weighing 280-320 g were successfully implanted with microspinal cather following the improved methods of Yaksh. The rats were randomly divided into 4 groups and given saline (Group NS, n=36), 0.5% ropivacaine (Group M, n=36), 1% ropivacaine (Group R, n=36), and ropivacaine+NT-3 (Group T, n=36). The rats received 0.12 mL/ kg body weight of ropivacaine at 0.5% or 1%, or normal saline only, via an implanted intrathecal catheter at 90-min interval for 12 h in Group NS, M, R and T. In the meantime the rats also received NT-3 0.1 mg/kg in group T. On days 1, 3, 5, 7, 14 and 28, we assessed the paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL), behavioural change and histopathological damage score changed for possible neuronal injury within the spinal cord. Compared with Group NS and Group M, the PWMT and PWTL were significantly higher on 1, 3, 5 d and the histopathological damage score was significantly higher on 1, 3, 5, 7, 14 d in Group R (P<0.05). Compared with Group T, the PWMT and PWTL in Group R were significantly higher on 1, 3, 5 d and histopathological damage score was significantly higher on 5, 7, 14 d (P<0.05). NT-3 pretreatment in mice has obvious protective effect against repeated intrathecal injection of 1% ropivacaine in the spinal nerve.

Possible role of nitric oxide in hepatic injury secondary to renal ischemia-reperfusion (I/R) injury.

Hepatic injury secondary to renal I/R injury has been documented in several studies. This study aimed to investigate the role of NO in hepatic injury secondary to renal I/R in rat model. Sprague-Dawley rats (n = 48) were divided into 4 equal groups; sham-operated, I/R injury group (45 min of bilateral renal ischemia), L-arginine group (I/R with 300 mg/kg L-arginine, 20 min before ischemia), L-NAME group (I/R with 50 mg/kg L-NAME, 20 min before ischemia). L-NAME (NO synthase inhibitor) caused significant elevation in serum creatinine, BUN, liver enzymes, liver histopathological damage score (p ≤ 0.05) and MDA production (p ≤ 0.001); on the other hand significantly decreased NO and GSH levels (p ≤ 0.05). L-arginine significantly decreased serum creatinine, BUN and GSH (p ≤ 0.05) and caused significant elevation in liver enzymes and NO (p ≤ 0.05), and also in MDA levels (p ≤ 0.001) in liver tissues. We conclude that endogenous NO might have protective effect against hepatic injury induced by renal I/R injury and inhibition of this endogenous NO by L-NAME or exogenous administration of NO (by L-arginine) might be harmful.

Melatonin is effective in reducing stress-induced organ damage in Wistar albino rats

In the present study, we tried to investigate the effects of melatonin, a novel antioxidant and a potent free radical scavenger, in stress-induced cerebral, cerebellar, cardiac, and hepatic oxidative damage using microscopic and biochemical analysis. A total of 32 male Wistar albino rats were divided into control, stress, stress + saline, and stress + melatonin groups. The rats from the stress groups were exposed to high stress conditions of starvation, immobilization, and cold exposure. The rats from the stress + melatonin group received melatonin daily at 20 mg/kg body weight intraperitoneally for 7 days. At the end of the experiment, the brain, cerebellum, heart, and liver were rapidly removed. The main histopathological damage scores (MHDSs) of the stress and stress + saline groups were higher than those of control group for all of the organs. The MHDSs of melatonin-administered group were lower than those of stress and stress + saline groups. The main tissue superoxide dismutase activities of the stress + melatonin group were even higher than those of the control group in the cerebellum and liver, and main tissue catalase activities of the stress + melatonin group were even higher than those of control group in all of the organs. As a conclusion, we found melatonin very effective in reducing stress-induced organ damage by inhibiting lipid peroxidation and supporting the cellular antioxidant defense system.

Protective effect of infliximab on ischemia/reperfusion injury in a rat ovary model: biochemical and histopathologic evaluation

ObjectiveThe aim of this study was to investigate the effect of infliximab on experimentally induced ovarian ischemia/reperfusion injury (IRi). Study designA total of 42 female rats were equally divided into 6 experimental groups; group 1: sham operation, group 2: 3-h ischemia, group 3 and 4: 3-h ischemia, 3-h reperfusion, group 5 and 6: 3-h ischemia, 24h reperfusion. In group 4 and group 6, 30min before reperfusion, infliximab was administered intraperitoneally at a dose of 5mg/kg. Bilateral ovaries were removed for histopathologic and biochemical analysis. Serum MDA (sMDA), tissue MDA (tMDA), serum NO (sNO), tissue NO (tNO) and serum catalase concentrations were analyzed. Tissue damage of ovarian tissue was scored by histological examination. ResultsThe infliximab administration significantly lowered the sNO, tNO and sMDA concentrations in group 4 compared to group 3 (p=0.041, p=0.025 and p=0.035, respectively). sNO, tNO and sMDA concentrations were also lower in group 6 when compared to group 5, but this differences were not significant (p>0.05). On the other hand, tMDA concentrations were lower in infliximab-applied groups when compared to ischemia/reperfusion groups (group 3 vs. 4 and 5 vs. 6) (p=0.045 and p=0.048, respectively). Moreover, histopathologic tissue damage scores in infliximab administration groups were significantly lower than in ischemia/reperfusion groups (p<0.001). ConclusionInfliximab attenuates I/R-induced ovarian tissue injury in rats subjected to ischemia/reperfusion.

The effect of prenatal exposure to 900-MHz electromagnetic field on the 21-old-day rat testicle

The aim of this study was to investigate the effect of exposure to a 900-MHz electromagnetic field (EMF) in the prenatal term on the 21-old-day rat testicle. Pregnant rats were divided into control (CG) and EMF (EMFG) groups. EMFG was exposed to 900-MHz EMF during days 13–21 of pregnancy. Newborn CG rats were obtained from the CG and newborn EMFG (NEMFG) rats from the EMFG. Testicles were extracted at postnatal day 21. Lipid peroxidation and DNA oxidation levels, apoptotic index and histopathological damage scores were compared. NEMFG rats exhibited irregularities in seminiferous tubule basal membrane and epithelium, immature germ cells in the lumen, and a decreased diameter in seminiferous tubules and thickness of epithelium. Apoptotic index, lipid peroxidation and DNA oxidation were higher in NEMFG rats than in NCG. 21-day-old rat testicles exposed to 900-MHz EMF in the prenatal term may be adversely affected, and this effect persists after birth.

Protective Effect of Dimethyl Sulfoxide on Stricture Formation in Corrosive Esophageal Burns in Rats

The aim of this study was to investigate the effects of dimethyl sulfoxide (DMSO) on stricture formation in corrosive esophageal burns. A total of 21 male rats were divided equally into three groups. In Group 1 (burn) and Group 2 (burn + DMSO) burns were induced in the distal esophagi with a 30% NaOH solution. In Group 3 (control), a saline solution was applied to the esophageal lumen. In Group 2, DMSO was administered intraperitoneally (3 mg/kg) 15 minutes after the burn was induced and then every 24 hours for 7 days. All rats were humanely killed at the end of Day 22. Distal esophagi were harvested for analysis. The stenosis index (SI) and histopathologic damage score were evaluated in addition to malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels. DMSO significantly decreased the levels of MDA, NO, TNF-α, and IL-6 in the rats with burned esophagi. Furthermore, the SI and histopathologic scores decreased significantly in the burn + DMSO group relative to the burn group (p < 0.05). Our results suggest that DMSO can decrease the occurrence of stricture formation and could represent a beneficial alternative therapy for the treatment of corrosive esophagitis.

The Diagnostic Value of Serum Ischemia-modified Albumin Levels in Experimentally Induced Carbon Monoxide Poisoning and Their Correlation With Poisoning Severity

The objectives were to determine the diagnostic value of blood ischemia-modified albumin (IMA) levels in experimentally induced carbon monoxide (CO) poisoning and to analyze their correlation with poisoning severity. Thirty-six female rats were randomly assigned to one of three groups: I (control group), II (low-dose CO poisoning group), and III (high-dose CO poisoning group). The control group was kept in room air, while groups II and III were exposed to 3 L/min of 3,000 ppm and 3 L/min of 5,000 ppm CO gas for 30 minutes, respectively. Serum carboxyhemoglobin (COHb), IMA, and malondialdehyde (MDA) levels; brain, heart, lung, liver, and kidney tissue MDA measurements; and histopathologic damage scores were then compared. IMA levels were significantly higher in groups II and III than in group I. A moderate positive correlation was observed between COHb and IMA levels. There was a strong positive correlation between COHb levels and degree of damage in all organs, but IMA and MDA levels did not reflect a similar correlation. Ischemia-modified albumin levels are higher in rats exposed to CO. This indicates that IMA levels can potentially be important in the diagnosis of exposure to CO or of CO poisoning. However, IMA levels are not a good biochemical marker in terms of determining the severity of poisoning.

Evaluation of histological damage of solid organs after donor preconditioning with thymoglobulin in an experimental rat model

Rabbit anti-rat thymoglobulin (rATG) administered to donors with brain death (BD) may improve organs quality. We explored the effects of rATG administered to BD donors in the histology of heart, lungs and small bowel in a rat experimental model. Animals were randomly assigned to 3 groups: V (n=5) no BD, 2h ventilation; BD (n=5) BD and 2h ventilation; BD and rATG: BD, 2h ventilation, rATG (10mg/kg) after BD diagnosis. Histopathological damage scores were based on neutrophil infiltration, airway epithelial cell damage, interstitial edema, hyaline membrane formation, and pulmonary hemorrhage (lungs); neutrophil infiltration and interstitial edema (heart); Park score (bowel). Lung damage was significantly lower in BD+rATG group: V 5±1.6; BD 11.25±0.5, BD+rATG 6.5±1.9 (p<0.01). Heart: V 2.0±0.81; BD 4.75±1.25 and BD+rATG 3.5±1.7 (p>0.05). Small bowel: BD 2.25±0.96 vs. BD+rATG 1.00±1.15 (n.s.). Histological damage amelioration in lung and attenuation tendency in heart and small bowel encourages research of cytoprotective strategies to improve organ viability.