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Biomedical subjects

B Dupuis

Publications and source records attributed to B Dupuis.

96 records · Page 6Linked to original sources
PubMedDate not supplied

[Arterial wall: a new pharmacological and therapeutic target?].

In recent years, endothelial dysfunction and arterial remodelling in various cardiovascular diseases have emerged as two key concepts, with numerous interrelationships. Both endothelial dysfunction and arterial remodelling occur in various pathologies including heart failure, atherosclerosis, restenosis after angioplasty, and pulmonary hypertension, and have modified the therapeutic approach by offering new pharmacological targets: specific receptors not only at the site of the vascular smooth muscle cells but also on the endothelial cells, growth factors that stimulate proliferation of smooth muscle, and receptors and enzymes of the extracellular matrix. Among the various substances under research, the present review will discuss angiotensin II receptor antagonists, endothelin receptor antagonists, nitrates-NO donors, potassium channel activators, and substances interfering with proteoglycans and other components of the extracellular matrix.

Animals↗
PubMedDate not supplied

[Progressive muscular dystrophies and drug risks].

Many therapeutic agents are necessary during the evolution of progressive muscular dystrophy to cure intercurrent diseases. Some of them may impair muscular structure and induce rhabdomyolysis, toxic or inflammatory myopathy. Other treatments may produce metabolic and functional alterations or impair cardiac and respiratory functions, yet endanged in progressive muscular dystrophy. They must be contra-indicated or used carefully during progressive muscular dystrophy.

Humans↗
PubMedDate not supplied

[Pre-clinical and clinical electrophysiological studies for the prediction of iatrogenic proarrhythmic effect (torsade de pointes)].

The risk of drug-induced torsade de pointes, a potentially lethal ventricular arrhythmia, raises the problem of the early detection of the effects of any new chemical entity (NCE) on ventricular repolarization since prolongation of myocardial repolarization is a major trigger among others (hypokalaemia, bradycardia, congenital abnormalities in cellular ionic channels) for this arrhythmia. During pre-clinical studies, the effects of a range of concentrations (10(-9) M to 10(-4) M) of NCE on the duration of the action potential of Purkinje and left ventricular myocardial cells (guinea-pig and rabbit) have to be measured. If these effects are present, the duration of QT interval on ECG recorded in animal studies (dogs) has to be carefully measured and correlated with plasma concentrations of NCE and/or its metabolite(s). During clinical trials, additional studies have to be performed in order to document QT interval-plasma concentration relationships and the influence of heart rate on QT interval duration. Ambulatory ECG recordings will attest to the safety of the NCE and precautions for use of the drug will be established according to our knowledge of predisposing factors for a proarrhythmic effect. Should there be a notification of a case of torsade de points after a new drug has been launched, urgent consultations with the drug file will be necessary in order to assess which pre-clinical and clinical studies may be needed for a better evaluation of the benefit/risk ratio of the new drug.

Animals↗