کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9296394 | 1233529 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid
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کلمات کلیدی
NSAIDTXB2TEGPrPADPNDGAOPAPPPadenosine diphosphate - آدنوزین دی فسفاتArachidonic acid - اسید آراشیدونیکnordihydroguaiaretic acid - اسید نوردی هیدروگالیارتیstandard deviation - انحراف معیارthromboxane B2 - ترومبوکسی B2Maximum amplitude - حداکثر دامنهnonsteroidal anti-inflammatory drug - داروهای ضد التهابی غیر استروئیدیplatelet-poor plasma - پلاسمای خون پلاکتیplatelet-rich plasma - پلاسمای غنی از پلاکت، PRP، پی آر پی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid](/preview/png/9296394.png)
چکیده انگلیسی
Optical platelet aggregation (OPA) with platelet-rich plasma (PRP) was compared with a Thrombelastograph (TEG) whole blood assay for monitoring arachidonic acid (AA)-induced platelet activation. Assays were performed on 47 interventional cardiology and 24 general surgery patients receiving aspirin therapy for cardiovascular disease, as well as 48 volunteers asked to take nonsteroidal anti-inflammatory drugs (NSAIDs) or 12 volunteers on chronic NSAID therapy unrelated to diagnosed cardiovascular disease. Whole blood TEG monitoring of NSAID inhibition detected NSAID-insensitive AA activation of platelets in a significantly higher number of cardiology (23%) and surgery (25%) patients and normal volunteers on chronic NSAID (25%) therapy relative to normal subjects not on chronic NSAID therapy (0%). Whole blood NSAID insensitivity was observed with cyclooxygenase-I inhibitors, such as aspirin and ibuprofen; was not affected by Celebrex, a cyclooxygenase-II inhibitor; but was completely inhibited by thromboxane-receptor antagonists. This was not due to platelet NSAID insensitivity, because complete inhibition of AA-activation responses in PRP was observed with either TEG or OPA assays. We confirmed that thromboxane B2 formation in PRP from NSAID-insensitive subjects was completely inhibited by NSAIDs. However, significant amounts were formed in whole blood from NSAID-insensitive subjects, but not in whole blood from NSAID-sensitive subjects. Thromboxane formation after AA addition was not found in washed blood cells with 90% reduced platelet counts or in leukocyte-rich buffy coat fractions, but could be restored by addition of PRP. NSAID-insensitive activation was inhibited by nordihydroguaiaretic acid, with an IC50 of 30 μmol, implicating 12- and/or 15-lipoxygenases in this transcellular pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Laboratory and Clinical Medicine - Volume 146, Issue 1, July 2005, Pages 30-35
Journal: Journal of Laboratory and Clinical Medicine - Volume 146, Issue 1, July 2005, Pages 30-35
نویسندگان
Roger C. Carroll, Robert M. Craft, Jack J. Chavez, Carolyn C. Snider, Stuart J. Bresee, Eli Cohen,