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Montalescot G. Actions vasculaires des prostaglandines: athérome, vasoconstriction et ischémie. [Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia]. Arch Mal Coeur Vaiss. 1992;85:181-3
Montalescot, G. (1992). Actions vasculaires des prostaglandines: athérome, vasoconstriction et ischémie. [Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia]. Archives des maladies du coeur et des vaisseaux, 85181-3.
Montalescot, G. "Actions vasculaires des prostaglandines: athérome, vasoconstriction et ischémie." [Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia]. Archives des maladies du coeur et des vaisseaux vol. 85 (1992): 181-3.
Montalescot G. Actions vasculaires des prostaglandines: athérome, vasoconstriction et ischémie. [Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia]. Arch Mal Coeur Vaiss. 1992 Sep;85:181-3. French. PMID: 1285701.
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Arch Mal Coeur Vaiss. 1992 Sep;85:181-3.

[Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia].

Archives des maladies du coeur et des vaisseaux

[Article in French]
G Montalescot

Affiliations

  1. Service de cardiologie, hôpital Pitié-Salpêtrière, Paris.

PMID: 1285701

Abstract

Prostaglandins seem to be involved in all stages of the atheromatous process, especially coronary artery disease. This condition is associated with decreased prostacyclin synthesis. Prostacyclin, by the intermediary of cAMP, regulates cholesterol metabolism in the smooth muscle cell by mobilising intracellular cholesterol. Thromboxane is liberated in great quantities in acute coronary syndromes such as myocardial infarction (especially when fibrinolysis is performed) and unstable angina. It is also found in high concentrations in coronary sinus blood during stress tests inducing transient ischaemia in patients with stable angina. There is a relationship between the degree of ischaemia and plasma concentrations of thromboxane whereas prostacyclin levels remain unchanged, causing an imbalance between these two substances during ischaemia. Thromboxane is also responsible for the acute pulmonary vasoconstriction induced by the neutralisation of heparin by protamine. The introduction of molecules modifying the synthesis of these prostaglandins or inhibiting their effects by specifically blocking their receptors should open up new therapeutic possibilities.

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