[Show abstract][Hide abstract] ABSTRACT: The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twenty-two New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI + single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI + 1 microg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.
European Spine Journal 02/2009; 18(3):336-44. DOI:10.1007/s00586-008-0872-x · 2.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of this experimental study was to investigate pathological signs of lung damages caused by acute organophosphate (OP) poisoning by using Tc-99m DTPA radioaerosol scintigraphy and histopathological investigation.
Fourteen rabbits were divided into two equal groups (n = 7). Group 1 (control group) received normal saline (same volume of fenthion, 2 ml/kg) via orogastric tube. Group 2 (OP toxicity group) received 150 mg/kg of fenthion (diluted fenthion, 2 ml/kg) via orogastric tube. Six hours later, Tc-99m-DTPA aerosol inhalation lung scintigraphy was performed in both groups. Then all rabbits were anesthetized with ketamine hydrochloride (35 mg/kg, i.p.) and xysilazine (5 mg/kg, i.p.), and sacrificed by intracardiac blood discharge. The lungs were then removed.
There was a significant difference in T1/2 values of Tc-99m DTPA clearance between control group and OP toxicity group (p = 0.04). Intraparenchymal vascular congestion and thrombosis, intraparenchymal hemorrhage, respiratory epithelial proliferation, number of macrophages in the alveolar, and bronchial lumen, alveolar destruction, emphysematous changes, and bronchoalveolar hemorrhage scores were significantly higher in the rabbits exposed to OP compared with the control group (p < 0.05).
This study showed that OP toxicity caused a decrease in the alveolar clearance. Tc-99m DTPA radioaerosol inhalation lung scintigraphy was found to be a sensitive determination of acute lung damage in OP poisoning.
[Show abstract][Hide abstract] ABSTRACT: In our study, we evaluated the neuroprotective effects of dexmedetomidine on oxidant-antioxidant systems, pro-inflammatory cytokine TNF-alpha and number of apoptotic neurons on hippocampus and dentate gyrus after transient global cerebral I/R injury. Eighteen rats divided into 3 groups, equally. Group I rats were used as shams. For group II and III rats, they were prepared for transient global cerebral ischemia using a four-vessel-occlusion model. 5 mL/kg/h 0.9% sodium chloride was infused to the Group II and 3 microg/kg/h/5 ml dexmedetomidine was infused to the Group III for 2 h after I/R injury. The levels of MDA and NO and activities of SOD and CAT were measured in the left hippocampus tissue. The levels of TNF-alpha concentration were measured in the plasma. The number of apoptotic neurons was counted by TUNNEL method in histological samples of right hippocampus tissue. MDA and NO levels increased in Group II compared with Group I rats (p=0.002, p=0.002, respectively). In group III, MDA and NO levels decreased as compared to Group II (p=0.015, p=0.002, respectively). SOD and CAT activities increased in Group III as compared to Group II rats (p=0.002, p=0.002, respectively). The decrease in TNF-alpha levels of group III was significant as compared to group II (p=0.016). The number of apoptotic neurons in group III was lower than Group II rats. Our study showed that dexmedetomidine has a neuroprotective effect on hippocampus and dentate gyrus of rats after transient global cerebral I/R injury.
Brain Research 08/2008; 1218:250-6. DOI:10.1016/j.brainres.2008.04.045 · 2.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study presents neuroprotective effects of fish n-3 EFA on the prefrontal cortex after cerebral ischemia and reperfusion. Eighteen rats divided into three groups. Group A rats were used as control. Cerebral ischemia and reperfusion was produced in rats either on a standard diet (Group B) or a standard diet plus fish n-3 EFA for 14 days (Group C). The malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were measured and the number of apoptotic neurons was counted. The levels of MDA and activities of SOD increased in Group B rats as compared to Group A rats, and decreased in Group C rats as compared to Group B rats. The activities of CAT increased in Group C as compared to Group B rats. The number of apoptotic neurons in the prefrontal cortex was lower in Group C as compared to Group B rats.
[Show abstract][Hide abstract] ABSTRACT: We searched the influence of dose and timing of atropine therapy in fenthion-induced pancreatitis model.
All rats were intoxicated with fenthion except the control group. Two milligrams of atropine was administered for 24 hours in a high dose atropine group while a low dose atropine group received 100 micrograms of atropine for 24 hours. One group received 2 milligrams of atropine in the first four hours of intoxication while the other group received 2 milligrams of atropine in the last four hours before sacrifice. All rats were sacrificed 24 hours after intoxication. Pseudo-cholinesterase and lipase concentrations and histopathological markers of pancreatitis were studied.
None of the models in this study completely prevented pancreatitis, however high dose atropine that is administered for 24 hours or the first four hours after intoxication prevented severe pancreatitis.
Atropine administration influence on fenthion-induced pancreatitis should be studied for other organophosphates in animals and humans.
[Show abstract][Hide abstract] ABSTRACT: Subarachnoid hemorrhage is a serious condition, often accompanied by cerebral vasospasm, which may lead to brain ischemia and neurologic deterioration. We evaluated if dexmedetomidine has neuroprotective effects in the hippocampus of vasospastic SAH rabbits or not.
Eighteen New Zealand rabbits were taken. An experimental SAH model was formed by injecting 0.9 mL of autologous arterial blood per 1 kg of body weight to the cisterna magna of 12 rabbits. Craniotomy was performed in the control group (n = 6) except performing experimental SAH. Rabbits in the SAH-alone (n = 6) group were infused with 5 mL.kg(-1).h(-1) 0.9% sodium chloride, and rabbits (n = 6) in the SAH-dexmedetomidine group were infused with 5 microg.kg(-1).h(-1) dexmedetomidine for 2 hours, 48 hours after SAH was established. Rabbits of all groups were sacrificed via penthotal 24 hours after dexmedetomidine administration. Brains were removed immediately, and hippocampal tissues were blocked from the right hemisphere for histopathologic study. In addition to this, hippocampal tissues of left hemispheres were dissected for biochemical analyses to evaluate MDA levels, activity of XO, and SOD.
The histopathologic study showed that dexmedetomidine may have a neuroprotective effect in SAH-induced hippocampal injuries. The biochemical parameters support the neuroprotective effect of dexmedetomidine (P < .05).
Our study showed that dexmedetomidine may have a neuroprotective effect in the hippocampus of vasospastic SAH rabbits.
[Show abstract][Hide abstract] ABSTRACT: Sepsis and ensuing multiorgan failure continue to be the major causes of mortality in intensive care units. Nuclear factor (NF)-kappaB activation is supposed to be one of the targets in the treatment of sepsis. We studied the effectiveness of caffeic phenethyl ester (CAPE), a known NF-kappaB inhibitor, in cecal ligation and puncture (CLP)-induced sepsis and lung injury.
Randomized, controlled animal study.
Research laboratory of an academic institution.
Female Sprague-Dawley rats.
CLP was performed in all rats except the rats in control and sham+CAPE groups. CAPE was administered to rats at the time of operation in sham+CAPE and CAPE+sepsis 0 groups. CAPE was administered to rats in the CAPE+sepsis12 group 12 hrs after CLP. Eight rats from each group were killed 24 hrs after CLP. Blood was taken for assessment of interleukin-1, interleukin-6, interleukin-10, and tumor necrosis factor-alpha; the right lung was removed for histopathologic examination and the left lung for biochemical examination. Apoptosis, inducible nitric oxide synthase, heat shock protein 70, malondialdehyde, catalase, superoxide dismutase, and glutathione peroxidase were studied. The rest of the rats were observed for mortality.
Mortality was significantly decreased in groups that received CAPE compared with the sepsis group. All cytokine levels were similar to control levels only in the CAPE+sepsis12 group. Apoptosis, inducible nitric oxide synthase, and heat shock protein 70 evaluation were significantly changed between all groups in the following order: control < sham+CAPE< CAPE+sepsis12 < CAPE+sepsis 0 < sepsis. Malondialdehyde and catalase were increased in the sepsis group.
CAPE reduced mortality in sepsis and improved histopathologic variables best when it was administered after the onset of sepsis.
Critical Care Medicine 01/2008; 35(12):2822-9. DOI:10.1097/01.CCM.0000295588.86982.7D · 6.31 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The pneumoperitoneum (Pp) is associated with ischemia and reperfusion (I/R) injury and oxidative stress. Various ischemic-preconditioning (IP) methods were used to reduce ischemic injury in intra-abdominal organs. In this experimental, randomized, controlled trial with a blind assessment of the outcome, we evaluated the effects of a new IP method, stepwise rising CO(2) insufflation, on oxidative stress and inflammatory cytokine response.
Twenty-one rats were divided into three groups. Rats in the control group were subjected to general anesthesia for only 60 minutes. The stepwise group was subjected to 5 mm Hg for 10 minutes, 10 mm Hg for 10 minutes, and 15 mm Hg of CO(2) insufflation for 60 minutes without deflation. In the Pp15 group, the pressure of CO(2) insufflation was fixed at 15 mm Hg for 60 minutes without deflation. Liver and blood samples were examined to determine malondialdehyde (MDA), the antioxidant, superoxide dismutase (SOD), and inflammatory cytokine (tumor necrosis factor-alpha [TNF-alpha], interleukin-6 [IL-6]) levels. Histopathologic scores of liver tissue were examined in all groups.
The highest plasma and liver MDA, TNF-alpha, and IL-6 values were in the Pp15 group, followed by the stepwise and control groups. However, plasma and liver SOD levels determined in the control group were significantly higher, compared to stepwise and Pp15 groups. The lowest plasma and liver levels of SOD were in the Pp15 group, followed by the stepwise and control groups. Significantly higher histopathologic scores were found in the Pp15 group, followed by the stepwise and control groups, as well as MDA and inflammatory cytokine (TNF-alpha, IL-6) levels.
We concluded that the stepwise rising CO(2) insufflation method may be an alternative IP method that may lead to a reduction in I/R injury.
[Show abstract][Hide abstract] ABSTRACT: The beneficial effects of avocado/soybean unsaponifiables (ASU) are known as an antiarthritic agent. This experimental study presents the effects of ASU on oxidant/antioxidant systems and the number of apoptotic neurons of hippocampal formation after ischemia and reperfusion.
Eighteen rats were divided into three equal groups: group I rats were used as controls; group II rats were fed with standard diet and group III rats were fed with standard diet plus ASU pills for 10 days. One day after electrocauterization of bilateral vertebral arteries for groups II and III, bilateral common carotid arteries were occluded for 30 min and then reperfused for 30 min. After these procedures, rats of all groups were sacrificed. The levels of malondialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in the left hippocampus. The number of apoptotic neurons was counted by Tunel method in histological samples of right hippocampus.
MDA and NO levels increased in group II compared with group I rats (p = 0.002, p = 0.015). In group III, MDA and NO levels decreased as compared to group II (p = 0.041, p = 0.002). SOD and CAT activities increased in group III as compared to group II rats (p = 0.002, p = 0.002). The number of apoptotic neurons was lower in group III as compared to group II rats.
The present findings suggest that ASU could decrease oxidative stress and apoptotic changes in ischemic rat hippocampus. Dietary supplementation of ASU may be beneficial to prevent or ameliorate ischemic cerebral vascular disease.
Archives of Medical Research 08/2007; 38(5):489-94. DOI:10.1016/j.arcmed.2007.01.008 · 2.65 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We studied the influence of dose and timing of atropine therapy on fenthion-induced organ dysfunction. Thirty-six rats were randomized into six groups. All rats in the five groups except the control group were intoxicated with fenthion. The high-dose atropine group received 2 mg/kg of atropine, whereas the low-dose group received 100 microg/kg of atropine every hour for 24 hr. One group received 2 mg/kg of atropine in the first 4 hr of intoxication while the other group received 2 mg/kg of atropine in the last 4 hr before killed, which for all rats was 24 hr after intoxication. Pseudocholinesterase and aspartate aminotransferase and alanine aminotransferase levels and histopathological markers of lung, brain and liver were studied. None of our atropine therapy strategies in this study totally prevented harm on the three organs. Although the high dose of atropine administered for 24 hr had the least harmful markers for lung, it also had the most harmful markers for brain and liver. We did not succeed in finding a unique therapy strategy in our models beneficial for all studied organs in fenthion intoxication in rats. Atropine administration strategy should be oriented for the most affected organ pathology in fenthion intoxication.
[Show abstract][Hide abstract] ABSTRACT: Reactive oxygen species (ROS) have been implicated in the pathogenesis of cerebral injury after ischemia-reperfusion (I/R). Fish n-3 essential fatty acids (EFA), contain eicosapentaenoic acids (EPA) and docosahexoenoic acids (DHA), exhibit antioxidant properties. DHA is an important component of brain membrane phospholipids and is necessary for the continuity of neuronal functions. EPA prevents platelet aggregation and inhibits the conversion of arachidonic acid into thromboxane A(2) and prostaglandins. They have been suggested to be protective agents against neurological and neuropsychiatric disorders. In this study, the neuroprotective effects of fish n-3 EFA on oxidant-antioxidant systems and number of apoptotic neurons of the hippocampal formation (HF) subjected to cerebral I/R injury was investigated in Sprague-Dawley rats. Six rats were used as control (Group I). Cerebral ischemia was produced by occlusion of both the common carotid arteries combined with hypotension for 45 min, followed by reperfusion for 30 min, in rats either on a standard diet (Group II) or a standard diet plus fish n-3 EFA (Marincap((R)), 0.4 g/kg/day, by gavage) for 14 days (Group III). At the end of procedures, the rats were sacrificed and their brains were removed immediately. The levels of malonedialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in left HF. In addition, the number of apoptotic neurons was counted by terminal transferase dUTP nick end labelling (TUNEL) assay in histological samples of the right HF. We found that SOD activities and MDA levels increased in Group III rats compared with Group II rats. On the other hand, CAT activities and NO levels were found to be decreased in Group III rats compared with Group II rats. Additionally, the number of apoptotic neurons was lower in Group III in comparison with Group II rats. The present findings suggest that fish n-3 EFA could decrease the oxidative status and apoptotic changes in ischemic rat hippocampal formation. Dietary supplementation of n-3 EFA may be beneficial to preserve or ameliorate ischemic cerebral vascular disease.
Neurochemistry International 03/2007; 50(3):548-54. DOI:10.1016/j.neuint.2006.11.005 · 3.09 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Reperfusion injury is a perplexing cause of early graft failure after lung transplantation and today we know that reperfusion may be more harmful to tissues than the preceding ischemia. We hypothesized that administration of the nitric oxide donor nitroglycerin (NTG) during flush perfusion and reperfusion periods would ameliorate reperfusion-induced lung injury.
Using an IN SITU normothermic ischemic lung rabbit model, three groups were studied (n = 7/group): (1) NTG given during flush perfusion (ischemia group); (2) NTG given in the flush perfusion and the reperfusion period (reperfusion group); and (3) no NTG (control group). All groups were flushed with low potassium dextran glucose solution. Blood gas analysis, tissue nitrite (nitric oxide metabolite) level analysis, bronchoalveolar lavage (BAL) fluid examination and morphological examinations were performed.
Compared with the ischemia group, the reperfusion group had significantly improved arterial oxygenation (318 +/- 31.4 mmHg vs. 180 +/- 14.7 mmHg, P < 0.05), decreased BAL fluid neutrophil percentage (21 +/- 1.9 % vs. 30 +/- 5.6 %, P < 0.05), increased tissue nitrite level (32.55 +/- 4.12 nmol/g vs. 27.81 +/- 1.05 nmol/g, P < 0.05), and decreased tissue histopathological lesion scores (0.42 +/- 0.53 vs. 1.14 +/- 0.37, P < 0.05).
This study suggests that nitric oxide donors supplemented during flush perfusion and reperfusion have more beneficial effects on lung functions against reperfusion injury than any other treatment modalities during IN SITU normothermic ischemic lung model.
The Thoracic and Cardiovascular Surgeon 11/2006; 54(7):477-83. DOI:10.1055/s-2006-923978 · 0.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Obstructive sleep apnoea (OSA) is defined as episodes of obstructive apnoeas and hypopnoeas during sleep with daytime somnolence. The gold standard in diagnostic tool patients with these symptoms is polisomnography. The goals of this study were to determine the frequency of OSA symptoms and the prevalence of OSA in patients undergoing operation. Patients were asked questions pertaining to symptoms of sleep apnoea. The patients who had two major symptoms or one major and two minor symptoms were invited to undergo a sleep study. Patients were diagnosed as OSA when they had apnoea-hypopnoea index higher than five. Forty-one patients with two major or one major and two minor symptoms of 433 patients were referred to the sleep laboratory. The most frequent major symptom was snoring, and the most frequent minor symptom was morning tiredness. In this connection, 18 (43.9%) patients accepted to be studied in the sleep laboratory (14 with two major, 4 with one major and two minor symptoms). Obstructive sleep apnoea was finally diagnosed in 14 patients or 3.2% of the initial entire population. Thirteen of them had two major symptoms, and only one of the 14 had one major and two minor symptoms. Six of the OSA patients were women. High percentage of OSA focus attention on anaesthesiology concerns of OSA. The exact management of each sleep apnoea patient with regard to intubation, extubation and pain control requires judgement and is a function of many anaesthesia, medical and surgical considerations. Therefore, we suggest that all patients should be asked for OSA symptoms, and patients with two major OSA symptoms must be evaluated with polisomnography.
Sleep And Breathing 10/2006; 10(3):161-5. DOI:10.1007/s11325-006-0067-9 · 2.48 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: BackgroundHydatid disease is the most severe helminthic zoonosis, with an important public health problem especially in rural areas
in Turkey. The aim of this study was to review the problems and advantages encountered in surgical treatment of 43 patients
who were ventilated with one-lung ventilation during last four years.
MethodsPatients, operated with one-lung ventilation, constitute the study group. Data related to symptoms, radiographic findings,
performed surgical procedures, perioperative and postoperative morbidity, hospitalization time, and cyst recurrence were collected
from each individual's records.
ResultsCystotomy and capitonnage were performed in all cases. Perioperative complications were seen in 5 patients. Four of these
5 patients had double-lumen endotracheal tube malpositioning. In one patient hypoxemia developed. The most common postoperative
complication was atelectasis. One patient had recurrent cysts. There was no perioperative or postoperative death.
ConclusionsWe prefer cystotomy and capitonnage because it is a fast and effective technique with limited postoperative complications.
One-lung ventilation prevents the exposure of lower lung areas from massive aspiration, which may cause acute obstruction
of airways, and contamination by cyst contents from the operative part of the lung that causes recurrent disease. One-lung
ventilation in pulmonary hydatid cyst surgery may be preferred owing to lower mortality and morbidity rates.
Indian Journal of Thoracic and Cardiovascular Surgery 04/2006; 22(2):137-140. DOI:10.1007/s12055-006-0022-1
[Show abstract][Hide abstract] ABSTRACT: Ischemia-reperfusion injury induces a systemic inflammatory response and production of reactive oxygen species, which potentially can be more detrimental than its local effects. Although the lung injury that is formed by the effects of ischemia-reperfusion injury on remote organs has been previously studied, no previous study that investigated the effects of pulmonary ischemia-reperfusion injury on remote organs has been considered. We hypothesized that the lung ischemia-reperfusion injury may cause the spread of inflammation to remote organs such as liver and heart.
Thirty New Zealand white rabbits were subjected to either sham operation or lung ischemia-reperfusion injury in various periods of time (60 min ischemia-60 min reperfusion and 120 min ischemia-60 min reperfusion, respectively). Pulmonary, myocardial and hepatic myeloperoxidase, protein sulfhydryl, thiobarbituric acid-reactive substances, and protein carbonyl levels were evaluated to show pulmonary, hepatic, and myocardial responses to lung ischemia-reperfusion injury.
Reperfusion after 60 min of lung ischemia led to increased myeloperoxidase and protein carbonyl levels and decreased protein sulfhydryl groups in pulmonary tissue, increased myeloperoxidase and decreased protein sulfhydryl groups in hepatic tissue, and increased myeloperoxidase, thiobarbituric acid-reactive substances and protein carbonyl levels in myocardial tissue. Reperfusion after 120 min of lung ischemia led to increased thiobarbituric acid-reactive substance levels in pulmonary tissue, increased protein carbonyl and thiobarbituric acid-reactive substance levels in hepatic tissue, and decreased protein sulfhydryl groups in myocardial tissue.
The data of the present study suggests that pulmonary ischemia-reperfusion induces liver and heart injury characterized by activated neutrophil sequestration and release of significant amounts of reactive oxygen species. The remote organ injury has to be kept in mind when performing a lung intervention or surgery and care should be taken to protect other organs remote from ischemia-reperfusion site.
European Journal of Cardio-Thoracic Surgery 04/2006; 29(3):294-8. DOI:10.1016/j.ejcts.2005.12.008 · 3.30 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background: This study was undertaken to examine the possible neuroprotective effect of dexmedetomidine in the prefrontal cortex of vasospastic subarachnoid hemorrhage (SAH) rabbits. Materials and Methods: Experimental SAH was performed to the 12 of 18 New Zealand rabbits by injecting 0.9 ml of autologous arterial blood/1 kg of body weight to cisterna magna. Craniotomy procedure was performed to the rest 6 rabbits (control group) (Group A) except performing experimental SAH. Forty eight hours after SAH was established, 5 mL/kg/hour 0.9 % sodium chloride were infused to the SAH-alone group (n=6) (Group B) and 5 μg/kg/h dexmedetomidine were infused to the SAH-dexmedetomidine group (n=6) (Group C) for 2 hours. Rabbits of all groups were sacrificed via penthotal after 24 hours following this drug administration processes. Brains were removed from the skull totally, prefrontal cortices were blocked from the right hemisphere for histopathological study, and prefrontal cortex of left hemispheres were dissected for biochemical analyses. So, malondialdehyde levels, activities of xantine oxidase, and superoxide dismutase were studied from the left prefrontal cortex. Results: The histopathological results showed that dexmedetomidine has neuroprotective effect in SAH induced prefrontal cortex injuries. The antioxidant parameters also supported the neuroprotective effect of dexmedetomidine. Conclusion: The present study showed the neuroprotective effect of dexmedetomidine in the prefrontal cortex of rabbits after vasospastic subarachnoid hemorrhage.
Neurology Psychiatry and Brain Research 01/2006; 13(4):189-194. · 0.10 Impact Factor