[EDRF/NO and endothelial functions]. / EDRF/NO et fonctions endothéliales.

Our appreciation of the vascular endothelium has changed considerably over the last decade. This organ, finally recognized as such, participates actively in vasomotor regulation and haemostasis. It secretes several relaxing and contracting factors which act locally to determine resting vascular tone. One of the relaxing factors, EDRF/NO plays an important physiological role as it contributes to the rapid adaptation of blood flow to various pharmacological and mechanical stimuli, thereby ensuring maintenance of adequate tissue perfusion. Nitric oxide (NO) is an ubiquitous factor which was crowned "molecule of the year 1992" by the scientific review Science. Its effects extend well beyond those on the cardiovascular system. Endothelial dysfunction is observed in many pathological states such as atherosclerosis, reperfusion injury, postangioplasty endothelial regeneration, degeneration of venous bypass grafts, pure spastic angina, hypertension and diabetes. It is associated with decreased production of EDRF/NO, which probably contributes significantly to the aggravation of endothelial and parietal lesions and to the natural progression of atherosclerotic disease in general. This article describes the principal vasoactive factors secreted by the endothelium and goes on to list the physiologic cardiovascular effects of EDRF/NO in detail, and to review the different pathologies associated with a disorder of secretion of this factor.

[Effects of an anti-inflammatory agent of benzamide structure, dexamethasone and indomethacin on experimental cerebral edema induced by phospholipase 2 in rats]. / Effets d'un anti-inflammatoire à structure benzamide, de la déxaméthasone et de l'indométacine sur l'oedème cérébral expérimental à la phospholipase A2 chez le rat.

Only a few molecules show any efficacy against brain edema. Different methods such as brain copper-wire implantation or arachidonic acid injection are used in the research of active drugs. A new model, involving injection of phospholipase A2, is described. The effect of an anti-inflammatory compound, N-(4,6-dimethyl 2-pyridinyl) benzamide, was evaluated on the three different experimental brain edemas mentioned above; dexamethasone and indomethacin were used as reference drugs. The studied molecule is, like dexamethasone, active on the three brain edema models. It has no direct inhibitory effect on phospholipase A2, cannot block cyclooxygenase activity but does reduce prostaglandin biosynthesis. Other factors, such as dopaminergic and alpha 2-adrenergic agonist activities, could also interfere.