Comparison Of Endothelin And Nitric Oxide Synthase Blockers On Hemorheological Parameters In Endotoxemic Rats

Background/aim: Septic shock is an important health problem that vastly alters cardiovascular and hemodynamic status. Increased production of nitric oxide (NO) and endothelin is a counterpart of this endotoxemic state. This study was conducted to test the hypothesis that nonselective NO synthesis blocker (L-NAME), inducible NO synthesis blocker (L-canavanine), or endothelin receptor antagonist (bosentan) will reverse the effects of sepsis on hemorheological parameters. Materials and methods: Forty-eight male Sprague-Dawley rats were used in 8 groups: saline (control), endotoxin, bosentan, L-NAME, L-canavanine, endotoxin + bosentan, endotoxin + L-NAME, and endotoxin + L-canavanine. Blood was withdrawn at the 4th hour of endotoxemic state. Erythrocyte deformability and erythrocyte aggregation were determined by laser-assisted optical rotational cell analyzer at 37 degrees C. Plasma viscosity (mPa.s) was measured by a cone-plate viscometer with 0.5 mL of plasma. Results: Endotoxin administration significantly increased aggregation half-time and lowered erythrocyte aggregation amplitude and aggregation index compared to the control, indicating a slower and weaker aggregation pattern. L-NAME and L-canavanine alleviated the effects of endotoxin on erythrocyte aggregation without altering the values in the control animals. However, bosentan did not perform such a restoration. Conclusion: This finding suggests that these restoration effects of the blockers occur via their modulation of nitric oxide synthesis rather than through the endothelin pathway.WoSScopu

Acute carbon monoxide poisoning alters hemorheological parameters in human

Acute carbon monoxide (CO) poisoning seriously hinders oxygen delivery to tissues. This harmful effect of CO may be aggravated by accompanying changes in the viscosity of blood. We had previously reported increased plasma viscosity in people chronically exposed to CO. This study was planned to test our hypothesis that acute CO poisoning increases blood viscosity. For this purpose four main parameters contributing to blood viscosity -hematocrit, erythrocyte deformability, erythrocyte aggregation and plasma viscosity - were determined in patients with acute CO poisoning and compared with healthy controls. Plasma viscosity and erythrocyte aggregation tendency were lower in the CO group (p < 0.05). Erythrocyte deformability was also lower in CO group (p < 0.05). Our results indicate that acute CO poisoning has diverse effects on hemorheological parameters such as attenuating hematocrit value, plasma viscosity, erythrocyte aggregation tendency and erythrocyte deformability

Theophylline attenuates bleomycin-induced oxidative stress in rats: The role of IL-6, NF-κB, and antioxidant enzymes

The purpose of this study was to evaluate the antifibrotic and antioxidant roles of theophylline (Theo), a bioactive compound, in bleomycin (BLM)-induced pulmonary fibrosis in Wistar albino rats. Assigned into 4 groups were 32 Wistar albino rats, comprising the control group (administered 0.9% isotonic saline), BLM group (treated with BLM at a dose of 2.5 mg/kg), BLM+Theo group (treated with Theo at a dose of 75 mg/kg + BLM at a dose of 2.5 mg/kg), and Theo group (treated with Theo at a dose of 75 mg/kg). In the BLM group, a significant decrease was observed in the catalase and glutathione peroxidase enzyme activities, and reduced glutathione (GSH) (p &lt; 0.05, p&lt; 0.05, p&lt; 0.001, respectively), while the malondialdehyde (MDA) levels (p&lt; 0.001) were significantly elevated when compared to the control group. However, the MDA levels in the BLM+Theo group were also significantly higher than in the control group (p&lt; 0.01). Similarly, the GSH levels were significantly higher in the BLM+Theo group than in the BLM group (p&lt; 0.05). The results indicated that Theo reduced the BLM-induced activation of nuclear factor-kappaB (NF-κB) and decreased interleukin-6 (IL-6) levels, together with significant amelioration of the immunohistochemical and histopathological architecture in the lung tissues. It was concluded that the administration of Theo had a positive effect on the GSH level, and activation of NF-κB and IL-6 expression, which were significant proinflammatory markers in the BLM-treated rats

Blood Urea Nitrogen (BUN) is independently associated with mortality in critically ill patients admitted to ICU.

Blood urea nitrogen (BUN) was reported to be associated with mortality in heart failure patients. We aimed to evaluate admission BUN concentration in a heterogeneous critically ill patient collective admitted to an intensive care unit (ICU) for prognostic relevance.A total of 4176 medical patients (67±13 years) admitted to a German ICU between 2004 and 2009 were included. Follow-up of patients was performed retrospectively between May 2013 and November 2013. Association of admission BUN and both intra-hospital and long-term mortality were investigated by Cox regression. An optimal cut-off was calculated by means of the Youden-Index.Patients with higher admission BUN concentration were older, clinically sicker and had more pronounced laboratory signs of multi-organ failure including kidney failure. Admission BUN was associated with adverse long-term mortality (HR 1.013; 95%CI 1.012-1.014; p28 mg/dL to case-controls ≤ 28mg/dL corrected for APACHE2 scores: BUN above 28 mg/dL remained associated with adverse outcome in a paired analysis with the difference being 5.85% (95%CI 1.23-10.47%; p = 0.02).High BUN concentration at admission was robustly associated with adverse outcome in critically ill patients admitted to an ICU, even after correction for co-founders including renal failure. BUN might constitute an independent, easily available and important parameter for risk stratification in the critically ill

Higher admission BUN levels are associated with adverse in-hospital outcome.

<p>Hazard ratios (HR) were obtained by logistic regression analysis.</p

An admission BUN concentration above 28mg/dL is associated with mortality after correction for several cofounders in a multivariate analysis.

<p>Hazard ratios (HR) were obtained by Cox regression analysis, for the multivariate regression models, a backward variable elimination was performed. Elimination criterion was a p-value of more than 0.10.</p

An admission BUN concentration above 28mg/dL is associated with long-term mortality regardless of admission diagnosis [pneumonia (n = 533), pulmonary embolism (n = 153), acute coronary syndrome (ACS; n = 1909), sepsis (n = 544) and heart failure (AHF, n = 611)].

<p>Hazard ratios (HR) were obtained by Cox regression analysis.</p

Laboratory and clinical baseline characteristics.

<p>4176 medical patients were split in three cohorts according to their BUN concentration at admission, comparison of means by ANOVA.</p

An admission BUN concentration above 28mg/dL, the optimal cut-off calculated by Youden Index, is associated with long term mortality in a matched-control analysis of 614 patients matched on APACHE2 scores, depicted as Kaplan-Meier curve, group comparison by log-rank test, p-value <0.001.

<p>An admission BUN concentration above 28mg/dL, the optimal cut-off calculated by Youden Index, is associated with long term mortality in a matched-control analysis of 614 patients matched on APACHE2 scores, depicted as Kaplan-Meier curve, group comparison by log-rank test, p-value <0.001.</p