The effects of transport by car on coagulation tests.

BACKGROUND: This research investigated the effects of the transport of blood samples between centers/laboratories by car on coagulation tests. METHODS: Five tubes of blood samples were taken from 20 healthy volunteers. The samples consisted of a baseline (control) group, centrifuged and noncentrifuged transported samples; centrifuged and noncentrifuged untransported samples. The groups of centrifuged and noncentrifuged samples were transported by car for 2 h. The centrifuged and noncentrifuged untransported samples were incubated in the laboratory until the transported samples arrived. Prothrombin time (PT) and activated partial thromboplastin time (APTT) tests were conducted for all samples. RESULTS: Significant differences between the baseline group and the centrifuged and noncentrifuged transported samples and the noncentrifuged untransported samples were found for APTT levels (p<0.05, for all). In addition, significant mean percentage differences in PT values were found between the baseline group and the noncentrifuged transported samples (p<0.001) and the noncentrifuged untransported samples (p=0.005). The mean level of PT in the noncentrifuged transported samples was outside the upper limit of the clinical decision level. CONCLUSIONS: Noncentrifuged transported samples showed clinically significant differences in PT test results that may have stemmed from mechanical agitation during transportation. Therefore, we recommend not transporting noncentrifuged specimens for PT testing by car.

Disulfide stress in carbon monoxide poisoning.

OBJECTIVES: Carbon monoxide (CO) remains the most common cause of lethal poisoning around the world. The purpose of this study was to investigate the homeostasis between thiol-disulfide couples and to evaluate oxidative status comprehensively in acute CO poisoning, using new parameters along with other well-known oxidant-antioxidant molecules. DESIGN AND METHODS: This case study consisted of 43 subjects who were diagnosed with carbon monoxide poisoning and 35 healthy individuals who were used as controls. Thiol-disulfide paired tests were examined in both groups using the method developed recently. RESULTS: Patients with CO poisoning had significantly higher levels of serum disulfide than the control patients (20.7±5.03 versus 16.43±3.97, p=0.001). Native thiol and total thiol levels were lower in the CO patient group than in the control group (p<0.001, for each variable). The disulfide/native thiol ratios and disulfide/total thiol ratios were significantly higher, while native thiol/total thiol ratios were significantly lower, in patients with acute CO poisoning than in the healthy controls (p<0.001, for all ratios). The disulfide/native ratios were negatively correlated with both total antioxidant response and paraoxonase and arylesterase values and were positively correlated with total oxidant status and ceruloplasmin values (p<0.05, for all correlations). CONCLUSIONS: Excessive disulfide levels and their related ratios were found in CO poisoning patients. In particular, the disulfide/native thiol ratio was identified as an indicator for overall oxidative status. Among CO poisoning patients, the thiol-disulfide balance was found to be impaired. Therefore, the disruption of thiol-disulfide homeostasis might be involved in CO toxicity.

Effect of probiotics on aspirin-induced gastric mucosal lesions.

BACKGROUND/AIMS: We aimed to investigate the role of a probiotic mixture, including 13 different bacteria, in the prevention of aspirin-induced gastric mucosal injury. METHODS: Forty rats were allocated into 4 groups: normal control, aspirin, probiotic control, and probiotic plus aspirin. Normal control and aspirin groups received 0.2 ml of skim milk by daily gavage for 14 days. Probiotic control and probiotic plus aspirin groups were administered 0.2 ml/day of probiotic mixture (1.3 x 10(10) cfu/ml) suspended in skim milk by daily gavage for 14 days. On day 15, gastric lesions were induced by administration of aspirin (200 mg/kg) in the aspirin and probiotic plus aspirin groups. Normal control and probiotic control groups were given saline. RESULTS: Pretreatment with probiotic mixture reduced aspirin-induced gastric damage scores (4.50 ± 0.43 and 2.60 ± 0.40, p<0.01) and exerted tendency of downregulation of proinflammatory cytokines elicited by aspirin (p>0.05). We also found that the probiotic mixture increased sIgA production approximately 7.5-fold in the stomach, and significantly reduced the malondialdehyde (MDA) increase in the gastric mucosa elicited by aspirin (p<0.001). Additionally, pretreatment with the probiotic mixture alleviated aspirin-induced reduction of mast cell count in the gastric mucosa. CONCLUSIONS: Probiotic mixture pretreatment attenuates the aspirin-induced gastric lesions by reducing the lipid peroxidation, enhancing mucosal sIgA production, and stabilizing mucosal mast cell degranulation into the gastric mucosa.

The effect of Nomega-nitro-L-arginine methyl ester and L-arginine on lung injury induced by abdominal aortic occlusion-reperfusion.

PURPOSE: The aim of this study was to examine the effects of Nomega-nitro-L-arginine methyl ester (L-NAME) and L-arginine on lung injury after aortic ischemia-reperfusion (IR). METHODS: Twenty-four Wistar-Albino rats were randomized into four groups (n = 6) as follows: Control (sham laparotomy), Aortic IR (30 min ischemia and 120 min reperfusion), L-Arginine (intraperitoneal 100 mg kg(-1) live weight)+aortic IR, and L: -NAME (intraperitoneal 10 mg kg(-1) live weight)+aortic IR. In the lung specimens, the tissue levels of malondialdehyde (MDA), vascular endothelial growth factor (VEGF), and nitric oxide (NO) were measured and a histological examination was done. RESULTS: Aortic IR increased MDA, VEGF, and NO. L-Arginine further significantly increased MDA and NO, and decreased VEGF (P < 0.05 vs aortic IR). L-NAME significantly decreased MDA and NO (P < 0.05 vs L-arginine+aortic IR) and increased VEGF (P < 0.05 vs other groups). A histological examination showed the aortic IR to significantly increase (P < 0.05 vs control) while L-arginine also further increased (P > 0.05 vs aortic IR), whereas L-NAME caused a significant decrease in pulmonary leukocyte infiltration (P < 0.05 vs aortic IR). CONCLUSIONS: Our results indicate that L-arginine aggravates the lung injury induced by aortic IR, while L-NAME attenuates it.

Inflammatory markers according to types of atrial fibrillation.

BACKGROUND: There is an increasing evidence linking inflammation to some cardiovascular conditions, such as coronary artery disease and hypertension. Similarly, there is emerging data to support the association between inflammation and atrial fibrillation (AF). We also investigated the role of systemic inflammation in different categories of AF. METHODS: Eighty five consecutive patients with AF were enrolled in this study. AF was categorized as new onset, chronic (persistent and permanent) and lone. Age- and sex-matched 30 healthy people consisted of control group. Serum level of high sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6) was measured. RESULTS: Serum hs-CRP level was higher in overall AF patients than in controls (0.63+/-0.57 vs 0.23+/-0.1 mg/dL, p=0.001). Similarly, IL-6 level was also higher in all AF patients compared with controls (29+/-36 vs 11.6+/-9.7 pg/mL, p=0.008). In subgroup analysis, hs-CRP and IL-6 levels were significantly higher in both chronic (0.69+/-0.62 vs 0.23+/-0.1 mg/dL, p=0.001; 30+/-39 vs 11.6+/-9.7 pg/mL, p=0.001, respectively) and new onset AF patients (0.51+/-0.46 vs 0.23+/-0.1 mg/dL, p=0.003; 28.4+/-31 vs 11.6+/-9.7 pg/mL, p=0.009, respectively) compared with controls. These markers were not different in new onset and chronic AF subgroups. On the other hand, hs-CRP and IL-6 levels tended to be high in lone AF patients (p=0.06). The presence of AF was an independent factor for hs-CRP (OR=0.35, 95%CI=0.1-0.61, p=0.005) and IL-6 (OR=17, 95%CI=1-37, p=0.037). CONCLUSIONS: Our results support that inflammation may have an important role in the AF pathogenesis.

Pentoxifylline, a methyl xanthine derivative, reduces peritoneal adhesions and increases peritoneal fibrinolysis in rats.

Peritoneum has an intrinsic fibrinolytic activity that breaks the peritoneal adhesions. Peritoneal injuries with ischemia interfere this fibrinolytic activity and cause adhesions. Pentoxifylline, a methyl xanthine derivative, improves blood flow by decreasing its viscosity and also increases fibrinolytic activity in plasma. We hypothesized that pentoxifylline would increase peritoneal fibrinolysis and ameliorate adhesions. A rat model of peritoneal adhesion (cecal abrasion with gauze, n = 15 for each group) was used to test this hypothesis and cardinal parameters of peritoneal fibrinolysis were measured in peritoneal samples. No medication was given in control animals, while pentoxifylline was administered intraperitonealy (IP) (25 mg/kg, before abdominal closure to whole abdomen) or intravenously (IV) (25 mg/kg, for 9 days after operation) in the experimental groups. At postoperative day 10, peritoneal biopsies were obtained and adhesions were graded qualitatively. Activities and concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), tPA/PAI-1 complex and hydroxyproline contents were determined. Total adhesion scores were decreased in both treated groups. Mean levels of tPA concentration and tPA activity were increased in the treated groups compared to controls (p < 0.001 and p = 0.001, respectively). The tPA/PAI-1 complex levels were similar among the three groups. PAI-1 levels were lower in animals receiving IP pentoxifylline compared to control animals and those treated with IV pentoxifylline (p = 0.048, p = 0.015, respectively). Peritoneal hydroxyproline levels were similar among the three groups. Our results suggest that pentoxifylline administration either through IV or IP may reduce peritoneal adhesion formation probably by altering peritoneal fibrinolytic activity.

Lithium-induced renal toxicity in rats: protection by a novel antioxidant caffeic acid phenethyl ester.

Lithium carbonate used in the long-term treatment of manic-depressive illness has been reported to lead to progressive renal impairment in rats and humans. Caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, protects tissues from reactive oxygene species mediated oxidative stress in ischemia-reperfusion and toxic injuries. The beneficial effect CAPE on lithium-induced nephrotoxicity has not been reported yet. The purpose of this study was to examine a possible renoprotective effect of CAPE against lithium-induced nephrotoxicity in a rat model. Twenty-two adult male rats were randomly divided into three experimental groups, as follows: control group, lithium-treated group (Li), and lithium plus CAPE-treated group (Li+CAPE). Li were treated intraperitoneally (i.p.) with 25 mg/kg Li2CO3 solution in 0.9% NaCl twice daily for 4 weeks. CAPE was co-administered i.p. with a dose of 10 microM/kg/day for 4 weeks. Serum Li, blood urea nitrogen and plasma creatinine, urinary N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular injury), and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of oxidative stress-induced renal impairment in Li-treated rats. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in renal tissue. Serum Li levels were found high in the Li and Li+CAPE groups. In Li-administrated rats, urinary NAG and renal MDA levels were increased according to control and Li+CAPE groups (p < 0.05). CAPE caused a significant reduction in the levels of these parameters. Likewise, renal SOD, CAT and GSH-Px activities were decreased in Li-administrated animals; CAPE caused a significant increase in the activities of these antioxidant enzymes. In conclusion, CAPE treatment has a protective effect against Li-induced renal tubular damage and oxidative stress in a rat model.

Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented by melatonin.

Most mobile phones emit 900 MHz of radiation that is mainly absorbed by the external organs. The effects of 900 MHz of radiation on fibrosis, lipid peroxidation, and anti-oxidant enzymes and the ameliorating effects of melatonin (Mel) were evaluated in rat skin. Thirty Wistar-Albino rats were used in the study. The experimental groups were the control group, the irradiated group (IR), and the irradiated+Mel treated group (IR+Mel). A dose of 900 MHz, 2 W radiation was applied to the IR group every day for 10 days (30 min/day). The IR+Mel group received 10 mg/kg/day melatonin in tap water for 10 days before the irradiation. At the end of the 10th day, a skin specimen was excised from the thoracoabdominal area. The levels of malondialdehyde (MDA) and hydroxypyroline and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were studied in the skin samples. MDA and hydroxyproline levels and activities of CAT and GSH-Px were increased significantly in the IR group compared to the control group (p<0.05) and decreased significantly in the IR+Mel group (p<0.05). SOD activity was decreased significantly in the IR group and this decrease was not prevented by the Mel treatment. These results suggest that rats irradiated with 900 MHz suffer from increased fibrosis and lipid peroxidation (LPO). Mel treatment can reduce the fibrosis and LPO caused by radiation.