1996
DOI: 10.1097/00003643-199609000-00007
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Evaluation of the anticoagulant properties of aprotinin in vitro

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“…Thrombelastography is often utilized to monitor coagulation in the settings of cardiopulmonary bypass (4) and liver transplantation (5), which led several investigators to assess the effects of aprotinin on thrombelastographic data in whole blood (6–9) and plasma (10). The fairly uniform finding of these investigations was that aprotinin activities between 100 and 800 kallikrein inhibitory units (KIU) prolonged the time to clot initiation, denoted as the reaction time ( R ) (6, 8–10) via thrombelastography, following contact system activation via exposure to the plastic surfaces of the thrombelastographic reaction cup or to celite. Activation of samples with tissue factor (tissue factor‐Factor VII system) eliminated the aprotinin‐mediated prolongation of clot initiation (9, 10).…”
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confidence: 99%
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“…Thrombelastography is often utilized to monitor coagulation in the settings of cardiopulmonary bypass (4) and liver transplantation (5), which led several investigators to assess the effects of aprotinin on thrombelastographic data in whole blood (6–9) and plasma (10). The fairly uniform finding of these investigations was that aprotinin activities between 100 and 800 kallikrein inhibitory units (KIU) prolonged the time to clot initiation, denoted as the reaction time ( R ) (6, 8–10) via thrombelastography, following contact system activation via exposure to the plastic surfaces of the thrombelastographic reaction cup or to celite. Activation of samples with tissue factor (tissue factor‐Factor VII system) eliminated the aprotinin‐mediated prolongation of clot initiation (9, 10).…”
mentioning
confidence: 99%
“…Activation of samples with tissue factor (tissue factor‐Factor VII system) eliminated the aprotinin‐mediated prolongation of clot initiation (9, 10). Of interest, clot propagation (angle, α ) has been demonstrated to increase (7), not change (8) or decrease (9), in response to aprotinin, whereas clot strength (amplitude, A ) has been found not to change (7, 8) or to decrease in the presence of aprotinin (9). Thus, it was posited that kallikrein inhibition was the primary mechanism by which aprotinin delayed clot initiation as determined by thrombelastography.…”
mentioning
confidence: 99%