The relationship between blood lactate, carboxy-hemoglobin and clinical status in CO poisoning.

AIM: We aimed to determine the relationship between blood lactate, carboxy-hemoglobin (COHb) levels and the severity of clinical findings in patients with CO poisoning. MATERIALS AND METHODS: Patients over 18 years old and of both gender who were admitted to Emergency Department with the diagnosis of CO poisoning between 10.02.2008 and 17.03.20011 were enrolled in this study. Detailed physical examination of each patient was performed, patients and their relatives were informed about the study and written consents were noted. The levels of consciousness, physical examination findings, electrocardiographic findings, Glasgow Coma Scale (GCS) scores, laboratory results (lactate, COHb, CK-MB, Troponin-I levels) and applied treatments [normobaric oxygen therapy (NBOT), hyperbaric oxygen therapy (HBOT)] were recorded to standart data entry form for each patient. "SPSS for Windows version 18″ package program was used for statistical analysis of the data. RESULTS: Total 201 patients were included in this study. Thirty five patients (17.4%) received HBOT and lactate, COHb, CKMB, Troponin-I levels of this group were higher than the other patients. Lactate and COHb levels were statistically significantly higher in patients with GCS < 15 than the ones with GCS = 15 (p < 0.01). The patients whose both Troponin-I and CK-MB levels increased have higher lactate levels (p = 0.038), but COHb levels of these patients did not change (p = 0.495). CONCLUSIONS: According to our study, blood lactate and COHb levels were both correlated with the changes of consciousness in CO poisoning. Blood lactate levels together with COHb in defining indications for HBO treatment might be suggested.

The effects of glycyrrhizin on experimental acute pancreatitis in rats.

INTRODUCTION: Although physiopathology of acute pancreatitis (AP) is not fully understood, the roles of reactive oxygen species (ROS) and changes of cytokines have been determined. AIM: To investigate anti-inflammatory and anti-oxidant effects of glycyrrhizin (GL) on taurocholate-induced AP in rats. MATERIALS AND METHODS: Thirty six rats were randomly divided into three groups as sham, AP and AP+GL (n=12 per group). AP was induced by 1 ml/kg body weight using 5% taurocholate injection into the biliopancreatic duct in groups II and III after clamping the hepatic duct. In groups III, GL (20 mg/kg) was given by oral gavage twice daily for 4 days. Group I and II did not receive any treatment. After the rats were killed; blood samples were taken to measure amylase, lipase, calcium, albumin, urea, glucose, AST and LDH assays before killing. Pancreatic tissue samples were also taken for biochemical analyses and histopathology. RESULTS: Amylase, lipase, AST and urea levels were significantly lower in the AP+GL group than in the AP group. Cytokines including IL-6, TNF-α and MPO levels were significantly lower in the AP+GL group than in the AP group. Even so there is no statistically difference between in the AP+GL group and the AP group in terms of pancreatic tissue IL-1ß, IL-6 and TNF-α levels. DISCUSSION: GL treatment significantly decreased pancreatic tissue MPO activities and MDA levels in the AP+GL group compared with the other groups (p = 0.001 and p = 0.05, respectively). Acinar cell necrosis, hemorrhage, and edema determined that were significantly lower in the AP+GL group than in the AP group (p < 0.001). CONCLUSIONS: GL treatment for acute necrotizing pancreatitis in rats suppressed the levels of pro-inflammatory cytokines, and caused a clear recovery of histological changes.

Hyperbaric oxygen treatment and N-acetylcysteine ameliorate acetaminophen-induced liver injury in a rat model.

An overdose of acetaminophen (APAP) produces centrilobular hepatocellular necrosis. We aimed to investigate the hepatoprotective effects of N-acetylcysteine (NAC) only and hyperbaric oxygen (O(2)) treatment (HBOT) combined with NAC, and their anti-inflammatory properties in liver tissue. In the current study, a total of 32 male Sprague Dawley rats were divided into 4 groups: sham, APAP, NAC, and NAC + HBOT. In the APAP, NAC, and NAC + HBOT groups, liver injury was induced by oral administration of 1 g/kg APAP. The NAC group received 100 mg/kg NAC per day. NAC + HBOT group received intraperitoneal injection of 100 mg/kg/day NAC and were given HBOT at 2.8 ATA pressure with 100% O(2) inhalation for 90 min every 12 h for 5 days. Rats in the sham group received distilled water only by gastric tube. All animals were killed on day 6 after APAP or distilled water administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, hepatic neopterin, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) levels were measured. There was a significant increase in serum AST and ALT activities in the APAP group compared with the sham group (in both p = 0.001). NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-α, and IL-6 levels compared with the APAP group. APAP administration caused extensive hepatic necrosis. NAC and NAC + HBO treatments significantly reduced APAP-induced liver injury. Our results showed that the liver damage in APAP toxicity was attenuated by NAC and NAC + HBO treatments. NAC + HBOT exhibit hepatoprotective activity against APAP-induced liver injury in rats.

The protective effects of taurine on experimental acute pancreatitis in a rat model.

The aim of this study was to investigate the protective effects of taurine (Tau) on experimental acute pancreatitis (AP) in a rat model by measuring cytokines and oxidant stress markers. Forty rats were randomly divided into four groups: sham, AP, Tau and AP + Tau. AP was induced with sodium taurocholate. No treatment was given to the AP. All rats were killed 5 days later. Pancreatic tissues of rats and blood samples were obtained. Tau treatment significantly decreased serum amylase activity (p < 0.001), total injury score (p < 0.001), malondialdehyde levels (p < 0.001) and myeloperoxidase (MPO) activity (p < 0.001). There was no significant difference between the Tau and AP + Tau groups in serum and pancreatic tumor necrosis factor-α, interleukin (IL)-1ß and IL-6 levels (p = 1.000). Histopathologic scores in the AP + Tau and Tau groups were significantly lower compared with the AP group (both p < 0.001). These results showed that Tau reduces lipid peroxidation, amylase and MPO activities and the concentrations of proinflammatory cytokines secondary to AP and also increases superoxide dismutase and glutathione peroxidase activities in rats with sodium taurocholate-induced AP. It also has a marked ameliorative effect at histopathologic lesions. With these effects, Tau protects the cells from oxidative damage, reduces inflammation and promotes regression of pancreatic damage.