[MDA formation by platelets and plasmatic BTG levels in patients suffering from acute myocardial infarction (author's transl)].
Platelets are thought to be involved in the initiation and propagation of arterial and venous thrombi. A new formation of platelet thrombus in a coronary artery has been implicated in the genesis and extension of myocardial infarction. Experimental evidence suggests that platelet aggregates may be responsible for occlusion of small coronary arteries and subsequent ischemia. Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanisms - operating at the microenvironment level from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Although myocardial infarction is usually associated with arteriographic evidence of atherosclerotic coronary obstruction, examples of infarction in the absence of coronary artery disease have been reported. ARterial thrombosis, small vessel coronary disease and arterial spasm are several possibilities that have been described. Recently in some cases of myocardial infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets during myocardial ischemia as an increase of prostaglandin synthesis, like prostacyclin, is stimulated by ischemia and hypoxia. The local release of these substance may modify the myocardial cell viability and regional blood flow. The aim of the present study was to investigate some changes in platelet function in relation to the time stimulated with thrombin. The tests showed, in the first three days, an augmented release of BTG levels with a platelet "exhaustion", demonstrated by a reduced formation of MDA by platelets changing to a state of hyperactivity, with a maximal production of MDA in 10th-15th day.
D000328:Adult; D001609:Beta-Globulins / Q000378:metabolism*; D001792:Blood Platelets / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008314:Malonates / Q000097:blood*; D008315:Malondialdehyde / Q000097:blood*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D013917:Thrombin; D013997:Time Factors; D001620:beta-Thromboglobulin / Q000378:metabolism*
D001609:Beta-Globulins; D008314:Malonates; D001620:beta-Thromboglobulin; D008315:Malondialdehyde; D013917:Thrombin
Formazione di malondialdeide piastrinica e livelli plasmatici di betatromboglobulina in pazienti con infarto miocardico acuto.