[Hepatonephritis during the treatment of malaria by the therapeutic combinations from a pharmacovigilance database].

Introduction: Prior studies have shown an association between the onset of hepatonephritis and the use of arteminisin-based combination therapy (ACT) during the treatment of uncomplicated malaria. The objective of this study was to identify the risk factors of hepatonephritis occurrence because of the uncertainty regarding the appearance and the aggravation of this syndrome.

Methods: A case-non case study was carried out on 428 notifications of pharmacovigilance extracted from the database of the clinical pharmacology department of the teaching hospital of Cocody from 2008 to 2012.

Sodium and blood pressure in Africa.

In the pathophysiology of hypertension, the profile hemodynamic is modified by the relation between the increased sodium intake and blood pressure (BP) level. An increased sodium diet is related not only on the amount of fluid volume within the organism but also to the elasticity of the cardiovascular system. In humans, age and salt excess reduced elasticity is linked to BP level and to stiffness material within the vascular wall of larges arteries.

Comparison of the effects of semicarbazide and beta-aminopropionitrile on the arterial extracellular matrix in the Brown Norway rat.

To investigate a putative role for semicarbazide-sensitive amine oxidase (SSAO) in arterial extracellular matrix (ECM) organization, we compared arteries of growing Brown Norway (BN) rats after chronic administration of semicarbazide (SCZ) and beta-aminopropionitrile (BAPN), two inhibitors with different properties and relative specificities for SSAO and lysyl oxidase (LOX). The BN model is particularly well adapted to evaluating effects of toxic compounds on the arterial elastic network. We measured aortic LOX and SSAO activities and quantified several ECM parameters.

Selective reduction of central pulse pressure under angiotensin blockage in SHR: role of the fibronectin-alpha5beta1 integrin complex.

Background: Meta-analyses of antihypertensive therapy suggest that, independently of blood pressure (BP) level, stroke prevention is influenced mainly by calcium-entry blockers (CEB) and cardiac risk prevention by angiotensin-converting enzyme inhibitors (ACEIs). The possibility that central systolic and pulse pressure (PP) reduction differs between the two drug classes for the same mean BP (MBP) has never been explored. Our aim was to compare carotid PP at the same MBP obtained with the CEB, amlodipine, and the ACEI, trandolapril, in spontaneously hypertensive rats (SHR), and to evaluate the resulting changes of fibronectin (Fn) and its integrin alpha5beta1 receptor on central PP and arterial stiffness.

Role of alpha1beta1-integrin in arterial stiffness and angiotensin-induced arterial wall hypertrophy in mice.

We examined the arterial phenotype of mice lacking alpha(1)-integrin (alpha(1)(-/-)) at baseline and after 4 wk of ANG II or norepinephrine (NE) administration. Arterial mechanical properties were determined in the carotid artery (CA). Integrin expression, MAPK kinases, and focal adhesion kinase (FAK) were assessed in the aorta.

Correlation between arterial mechanical properties, vascular biomaterial and tissue engineering.

This review presents some of the recent technological developments in biomaterials used for the construction of synthetic cardiovascular vessels that are capable of simulating specific biological responses. However, with respect to the problems of stiffness, a major hypertensive risk factor, it is necessary to underline the important role of mechanical properties, such as vessel strength and composition, in vascular reconstructive surgery. Biomaterials occupy a central place in many cardiovascular disease treatments and they depend on the chemical nature of the polymers, on the biotechnology used, and also on cellular and gene therapy.

Carotid arterial stiffness, elastic fibre network and vasoreactivity in semicarbazide-sensitive amine-oxidase null mouse.

Objective: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO -/-) using various techniques including high resolution echotracking.

Methods And Results: SSAO -/- mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO -/- than in SSAO +/+ animals.

Pathophysiology, genetic, and therapy of arterial stiffness.

Stiffening of large arteries is considered as an independent predictor of cardiovascular events. This article summarizes recent theories on the mechanisms contributing to arterial stiffness involving extracellular matrix proteins, endothelial and smooth muscle cells, cell-matrix interactions, and genetic background. Despite the important role of genetic factors in essential hypertension, little is known about the genetic of arterial stiffness.

Early activation of internal medial smooth muscle cells in the rabbit aorta after mechanical injury: relationship with intimal thickening and pharmacological applications.

1. Smooth muscle cells (SMC) participate in both inflammatory and dedifferentiation processes during atherosclerosis, as well as during mechanical injury following angioplasty. In the latter, we studied medial SMC differentiation and inflammation processes implicated early after de-endothelialization in relation to mechanical stresses.

Selective reduction of heart rate by ivabradine: effect on the visco-elastic arterial properties in rats.

Background: The heart rate (HR) reduction obtained by ivabradine is associated in rats with a decrease in diastolic blood pressure (DBP) and mean blood pressure (MBP), and with an increased pulsatile carotid arterial diameter.

Objective: To determine, in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, whether acute reductions of the HR in response to ivabradine induced changes in the carotid visco-elastic behavior, as assessed by echo-tracking techniques.

Methods: The hysteresis of the carotid diameter/pressure curve was used to determine the dissipated energy per cardiac cycle, a classical index of arterial viscosity.