Effects of desmopressin on thrombogenesis in aspirin-induced platelet dysfunction.

Aspirin causes a coagulation disorder. Desmopressin has haemostatic effects by increasing the plasma levels of coagulation factor VIII and von Willebrand factor. The precise effects of desmopressin on thrombogenesis are not known. In an in vivo model, we investigated the effect of the drug on thrombus formation and platelet function after aspirin use. Male Lewis rats weighing 250-300 g were used. Four groups with 10 animals each were formed: control, aspirin, desmopressin and aspirin + desmopressin. In each animal, the femoral artery was dissected. A thrombogenic vessel injury was created by inverting a full thickness portion of the proximal edge of the incised artery into the lumen. The following parameters were measured: maximum thrombus size, time period until maximum thrombus size was reached and overall platelet function. In addition, the thrombi generated were investigated histologically. Thrombus formation time was significantly shorter with desmopressin compared with the animals treated with aspirin (P < 0.0001) and controls (P = 0.008). Maximum thrombus size was larger in the desmopressin and desmopressin + aspirin groups when compared with the group treated with aspirin only. Overall platelet function was significantly enhanced with desmopressin compared with controls (P = 0.025) and with aspirin (P < 0.0001). The differences were confirmed histologically. In conclusion, desmopressin significantly accelerates thrombus formation in aspirin-treated animals. It can also re-establish thrombus size after the use of aspirin. Overall platelet function is significantly increased by desmopressin.

Sources of gram-negative bacilli colonizing the tracheae of intubated patients.

Twenty acutely ill patients requiring prolonged orotracheal intubation were studied to determine the source and progression of gram-negative bacilli colonizing the trachea. Organisms recovered from daily tracheal, hypopharyngeal, and rectal cultures were typed and speciated to identify identical strains at the three sites. All patients acquired gram-negative bacilli in the trachea by day 3 after intubation. Thirty organisms that were not recovered from the tracheal aspirate immediately following intubation were isolated for at least two days some time thereafter. Nine of the 30 colonizing bacteria were Enterobacteriaceae, and all were found in another culture site, usually the hypopharynx, before isolation from the trachea. In contrast, only four of the 21 non-Enterobacteriaceae that colonized the trachea were recovered previously from either the hypopharynx or rectum, a finding which represents a significant difference (P = 0.0002). Quantitation of isolates from the hypopharynx was of no value in predicting subsequent acquisition in the trachea, and the numbers of bacteria recovered from the first positive tracheal specimen were not predictive of subsequent persistence in the trachea.