Acute carbon monoxide (CO) poisoning may cause cardiotoxicity. The natriuretic peptides, including atrial natriuretic peptide, brain natriuretic peptide (BNP), N-BNP, and NT-proBNP (N-terminal pro brain natriuretic peptide), are endogenous cardiac hormones that may be secreted upon myocardial stress. The aim of this study was to assess the plasma NT-proBNP level in acute CO poisoning and to compare it with healthy control. After approval by the ethical committee, 15 healthy controls and 15 patients admitted to the Gaziantep University Hospital (Gaziantep, Turkey) between January 2005 and July 2005 with the diagnosis of carbon monoxide poisoning were studied. Echocardiography was performed to all patients. Serum NT-proBNP, creatine kinase (CK), creatine kinase-MB (CK-MB), and troponin-T were also analyzed, along with the carboxyhemoglobin (COHb) level. The correlation between serum NT-proBNP and COHb level was investigated. Electrocardiography (ECG) was performed to all patients and healthy controls, and the results were compared. Differences in troponin, CK, and CK-MB levels were not statistically significant between groups (p > 0.05). The level of NT-proBNP and COHb were found to be increased in the study group. There was a positive correlation between the COHb and the NT-proBNP (r = 0.829, p < 0.01), and between the COHb and the CK (r = 0.394, p < 0.01). There was no difference between groups in other parameters, all of which were within normal range. Thus, in this study we showed that the plasma NT-proBNP level may contribute to the early diagnosis of cardiotoxicity in patients with carbon monoxide poisoning.

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This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30 mg kg(-1) i.p.), 1 and 10 mg kg(-1) Y-27632 + dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats.

Although atropine and oximes are traditionally used in the management of organophosphate poisoning, investigations have been directed to finding additional therapeutic approaches. Thus, the aim of this study was to evaluate the cardiac effects of magnesium sulfate pretreatment on dichlorvos intoxication in rats. Rats were randomly divided into three groups as control, dichlorvos, and magnesium sulfate groups. After 6 h of dichlorvos or corn oil (as a vehicle) injection, venous blood samples were collected, and cardiac tissue samples were obtained. Biochemical analyses were performed to measure some parameters on serum and cardiac tissue. Immunohistochemical analyses of apoptosis and inducible nitric oxide (NO) synthase showed no change in cardiac tissue. Serum cholinesterase levels were markedly depressed with dichlorvos, and further suppressed markedly with magnesium sulfate pretreatment. Although we have demonstrated that serum NO levels in dichlorvos and magnesium sulfate groups were lower than the control group, cardiac tissue NO levels in magnesium sulfate group were higher than the other two groups. Mortality was not significantly affected with magnesium sulfate pretreatment. Uncertainty still persists on the right strategies for the treatment of organophosphate acute poisoning; however, it was concluded that our results do not suggest that magnesium sulfate therapy is beneficial in the management of acute dichlorvos-induced organophosphate poisoning, and also further studies are required.

Background:Free radical damage is known to occur during liver regeneration. The Ginkgo biloba extract EGb761 has antioxidant properties due to its ability to scavenge free radicals. FK506 has been widely used as an immunosuppressant that stimulates hepatocyte proliferation following partial hepatectomy.Aims:To explore whether EGb761 enhances liver regeneration after hepatectomy in rats, we investigated the effects of EGb761 alone and in combination with FK506 on the liver regenerative process.Study Design:Animal experimentation.Methods:A total of 75 Wistar albino rats weighing 340.08±11.66 g were randomly divided into five experimental groups: sham, control, FK506, EGb761, and FK506 + EGb761. According to the study groups, rats were administered FK506 at a dose of 0.1 mg/kg/day and EGb761 at 25 mg/kg/day three times via the intraperitoneal route. Then, two-thirds hepatectomy was performed according to the Higgins and Anderson technique in all the rats. At postoperative 48 h, 53 surviving rats were sacrificed. Serum and plasma samples were collected for analyzing thymidine kinase and oxidative stress marker levels. The regenerated liver was entirely resected, weighed, and sectioned. The mitotic index was assessed using hematoxylin-eosin staining. The extent of liver regeneration was calculated using the Child’s formula. The data were statistically analyzed using ANOVA, with a significance level of 5% (p<0.05).Results:Rats who received EGb761 showed significantly higher levels of liver regeneration than those who received FK506 or FK506 + EGb761 (p<0.01). Thymidine kinase level and mitotic index were significantly higher in the EGb761 (p<0.005) and FK506 (p<0.05) groups than in the control and sham groups. In addition, the liver regeneration percentage was significantly higher in the EGb761 group than in the FK506 group (p<0.01). Myeloperoxidase and malondialdehyde levels were significantly correlated between the EGb761 and FK506 groups, even at lower levels in the EGb761 group (p<0.001).Conclusion:EGb761, which is an antioxidant, reduces liver damage and stimulates liver regeneration following partial hepatectomy in rats through its anti-inflammatory and antioxidative effects.