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|Title:||The effects of gynaecological surgery on coagulation activation, fibrinolysis and fibrinolytic inhibitor in patients with and without ketorolac infusion|
|Authors:||Koh, S.C.L. |
Plasminogen activators and inhibitor (PAI-1)
|Citation:||Koh, S.C.L., Pua, H.L., Tay, D.H.B., Ratnam, S.S. (1995). The effects of gynaecological surgery on coagulation activation, fibrinolysis and fibrinolytic inhibitor in patients with and without ketorolac infusion. Thrombosis Research 79 (5-6) : 501-514. ScholarBank@NUS Repository.|
|Abstract:||The effects of gynaecological surgery on the fibrinolytic and inhibitor mechanisms were followed up for 24 h post-operatively in patients receiving a single dose of ketorolac infusion (n = 18) as compared with those not receiving ketorolac infusion (n = 11). A pre-operative state of lower mean t-PA activity and higher PAI-1 levels with increased platelet activation than that reported in normal subjects were observed in both groups of patients. Increased t-PA activity upon anaesthetic induction together with a decreased level at 24 h post-operation was seen in both groups. However, fibrinolytic 'shut-down' was not evident as significant increase in D-dimer levels was observed post-operatively, suggesting an enhanced lytic state concurrent with an enhanced activation of coagulation and diminished platelet activation although β-TG remained above the normal level; plasmin from this enhanced lytic state affects platelet adhesion and cleaves platelet glycoprotein Ib thus inhibit release reaction. Ketorolac infusion elicited a significant response in PAI-1 activity within 24 h post-operation and this was not seen in the non-ketorolac group. in spite of the rising trend by 24 h post-operation which did not achieve statistical significance. There were no statistical significant differences in blood loss and duration of surgery between the two groups of patients. Overall, both groups of patients showed similar haemostatic changes post-operatively for 24 h, a longer duration of post-operative study would have revealed any subtle changes in the molecular markers of thrombosis which was not the objective of this study.|
|Source Title:||Thrombosis Research|
|Appears in Collections:||Staff Publications|
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