fibrin and Carbon-Monoxide-Poisoning

Carbon monoxide (CO) poisoning is a leading cause of unintentional poisoning deaths in many countries. In ex vivo studies, CO released from carbon monoxide-releasing molecules has been shown to attenuate fibrinolysis via increased alpha-2-antiplasmin activity. Hypofibrinolysis is associated with coronary ischaemia, which is also commonly observed in CO poisoning. We examined fibrin clot properties in acutely poisoned CO patients. Ex vivo plasma fibrin clot permeability, turbidimetry and efficiency of fibrinolysis were investigated in 48 patients and controls matched for age and sex. CO-poisoned patients had 11.6% longer clot lysis time than the controls (p < 0.0001). No intergroup differences in clot permeability or turbidimetric variables were observed. Plasma tissue-type plasminogen antigen (tPA), plasminogen activator inhibitor-1 (PAI-1) antigen and activity and F1.2 prothrombin fragments were higher in the patients than in the controls (all p < 0.0001). Plasma tPA activity was lower in the CO-poisoned group. Multiple linear regression showed that a thrombin generation marker, F1.2, is the strongest predictor of clot lysis time, followed by PAI-1 activity and carboxyhaemoglobin levels. In conclusion, this report is the first to demonstrate that acute CO poisoning in human beings is linked to increased thrombin generation and impaired fibrinolysis, which might contribute to ischaemic complications.

Topics: Acute Disease; Adult; Blood Coagulation Tests; Carbon Monoxide Poisoning; Female; Fibrin; Fibrinolysis; Humans; Male; Peptide Fragments; Permeability; Plasminogen Activator Inhibitor 1; Prothrombin; Thrombin; Tissue Plasminogen Activator

In order to study the fibrinolytic activity of vein walls in smokers and nonsmokers, 71 randomly selected heavy smokers, i.e., smoking more than 15 g tobacco per day, and 41 nonsmokers from the population group "Men born in 1914 residing in Malmo" were invited to undergo a health examination. When examined after 12 hours' abstention from tobacco, the smokers were found to have the same fibrinolytic activity as nonsmokers. Out of the 71 heavy smokers, 31 refrained from smoking during 8-9 weeks (as monitored with questionaire and COHb-determinations). Neither in those who had abstained from smoking nor in the controls did the fibrinolytic activity differ from that initially recorded. In a randomly selected subsample of 19 individuals examined after only one week's abstention from tobacco, the fibrinolytic activity, after venous occlusion of forearms, tended to be lower in the blood as well as in superficial hand veins, but the difference was not significant. The effect of smoking six cigarettes during three hours was measured. This level of smoking was associated with an increased fibrinolytic activity in blood, measured as euglobulin clot lysis time, and in superficial hand veins. This increase is probably due to the combined effects of nicotine and carbon monoxide.

Topics: Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Carbon Monoxide Poisoning; Factor VIII; Fibrin; Fibrinogen; Fibrinolysis; Humans; Male; Middle Aged; Nicotine; Platelet Adhesiveness; Smoking; Statistics as Topic; Time Factors; Veins