Modulation of disseminated intravascular coagulation (DIC) by steroidal and non-steroidal anti-inflammatory drugs.
Activation of the coagulation systems by endotoxin and release of vasoactive agents are both essential for the production of microthrombosis. Glucocorticoids prevent activation of factor XII by endotoxin in vivo and decrease production of tissue factor by macrophages. NSAID do not interfere with factor XII activation and increase the severity and risks of microthrombosis by inhibiting synthesis and release of protective prostaglandins. On the other hand, prolonged administration of glucocorticoids results in the reduction of the immune defence and fibrinolysis, increases the alpha-adrenergic response to endotoxin and sensitizes to endotoxin-induced intravascular coagulation like NSAID.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001777:Blood Coagulation / Q000187:drug effects; D002395:Catecholamines / Q000502:physiology; D002462:Cell Membrane / Q000187:drug effects; D003167:Complement Activation / Q000187:drug effects; D004211:Disseminated Intravascular Coagulation / Q000517:prevention & control*; D004727:Endothelium / Q000166:cytology; D005174:Factor XII / Q000502:physiology; D005342:Fibrinolysis / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology*; D006728:Hormones / Q000378:metabolism; D006801:Humans; D007705:Kinins / Q000502:physiology; D012157:Mononuclear Phagocyte System / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D010741:Phospholipases A / Q000037:antagonists & inhibitors; D010974:Platelet Aggregation / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D002395:Catecholamines; D005938:Glucocorticoids; D006728:Hormones; D007705:Kinins; D005174:Factor XII; D010741:Phospholipases A