Evaluation of plasma chemerin levels in patients with non-dipper blood pressure patterns.

BACKGROUND: Chemerin is a novel adipokine that plays a role in inflammation and atherosclerosis. Although there are several correlations between hypertension and the inflammatory system, there is still insufficient information about the relationship between blood pressure variability and inflammatory markers. In this study, we aimed to determine whether chemerin levels are elevated in non-dipper patients compared with dippers and healthy controls. MATERIAL AND METHODS: This study was composed of a group of 90 patients: 60 hypertensive patients and 30 healthy control subjects (12 males, mean age 53.2 ± 15.4 years). Ambulatory blood pressure monitoring devices (ABPM) were connected to all patients. Using data from the ABPM, hypertensive patients were divided into 2 groups: 30 dipper patients (12 males, mean age 52.5 ± 15.1 years) and 30 non-dipper patients (11 males, mean age 54.6 ± 13.0 years). Complete blood count and biochemistry were measured by standard methods and plasma chemerin concentrations were quantified by ELISA. RESULTS: Non-dipper patients demonstrated higher chemerin levels compared to dippers and normotensives (219.7 ± 16.3 vs. 182.4 ± 21.4 ng/ml; 219.7 ± 16.3 vs. 85.4 ± 38.1 ng/ml, respectively, p<0.001 for both comparisons). A receiver operating characteristic curve analysis revealed that the optimal cut-off value for chemerin to predict a non-dipping pattern was 201.4, with 90% sensitivity and 90% specificity. There was a positive correlation between chemerin levels and all ambulatory blood pressure values in all hypertensive patients. CONCLUSIONS: Chemerin, which plays a role in inflammation and atherosclerosis, was higher in non-dippers compared to dippers and normotensives. Additionally, chemerin shows positive correlations with blood pressure.

Can empirical hypertonic saline or sodium bicarbonate treatment prevent the development of cardiotoxicity during serious amitriptyline poisoning? Experimental research.

OBJECTIVE: The aim of this experimental study was to investigate whether hypertonic saline or sodium bicarbonate administration prevented the development of cardiotoxicity in rats that received toxic doses of amitriptyline. METHOD: Thirty-six Sprague Dawley rats were used in the study. The animals were divided into six groups. Group 1 received toxic doses of i.p. amitriptyline. Groups 2 and 3 toxic doses of i.p. amitriptyline, plus i.v. sodium bicarbonate and i.v. hypertonic saline, respectively. Group 4 received only i.v. sodium bicarbonate, group 5 received only i.v. hypertonic saline, and group 6 was the control. Electrocardiography was recorded in all rats for a maximum of 60 minutes. Blood samples were obtained to measure the serum levels of sodium and ionised calcium. RESULTS: The survival time was shorter in group 1. In this group, the animals' heart rates also decreased over time, and their QRS and QTc intervals were significantly prolonged. Groups 2 and 3 showed less severe changes in their ECGs and the rats survived for a longer period. The effects of sodium bicarbonate or hypertonic saline treatments on reducing the development of cardiotoxicity were similar. The serum sodium levels decreased in all the amitriptyline-applied groups. Reduction of serum sodium level was most pronounced in group 1. CONCLUSION: Empirical treatment with sodium bicarbonate or hypertonic saline can reduce the development of cardiotoxicity during amitriptyline intoxication. As hypertonic saline has no adverse effects on drug elimination, it should be considered as an alternative to sodium bicarbonate therapy.