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Liver Diseases Contribute to Functional Platelet Aggregation Defects
Author(s) -
Bacher Cassandra,
Farooqui Ambar,
Siddiqui Fakiha,
Daravath Bharathi,
Hoppensteadt Debra,
Iqbal Omer,
Fareed Jawed,
George Magdalena,
Van Thiel David
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03485
Subject(s) - platelet , adenosine diphosphate , epinephrine , arachidonic acid , platelet rich plasma , chemistry , hemostasis , thromboxane a2 , thromboxane b2 , whole blood , platelet aggregation , medicine , pharmacology , endocrinology , biochemistry , enzyme
The role of platelets in hemostasis involves their adherence to sites of vessel injury, aggregation to form plugs. Agents that physiologically activate platelets in vivo include adenosine diphosphate (ADP), epinephrine, collagen, thromboxane A2 (TxA2) and serotonin. Vascular and platelet dysfunction represent complications of hepatic disease. The purpose of this study is to investigate the effect of various agonists on platelet aggregation profile of patient with hepatic disease. Materials and Methods Icteric Samples from the clinical lab from Loyola University medical center were randomly selected for this study (n=25). Blood samples from the healthy donors were included to prepare platelet rich plasma (PRP) and platelet poor plasma (PPP). PRP and PPP from various donors were separated to make pools. Four different pools were made namely Normal PRP, Icteric PRP, Icteric PRP + Normal PPP 1:1, Normal PRP + Icteric PPP1:1. Agonists such as ADP, arachidonic acid (AA), epinephrine and collagen were used to activate the platelets. The final assay concentration for ADP is 20 uM, AA is 500 ug/ml, collagen is 190 ug/ml and epinephrine is 10 ug/ml. Results All results were compiled in terms of percent aggregation of platelets and represented as mean ± standard deviation. Normal PRP showed platelet aggregation response reaching a peak aggregation of 93.± 27.70 with ADP agonist. Icteric PRP, and two different pools did not show any significant platelet aggregation with ADP. Varying degrees of the inhibition of platelet aggregation was noted with epinephrine, collagen and arachidonic acid in comparison to normal PRP. Discussion On the basis of these results it is concluded that while the normal PRP showed platelet aggregation responses to various agonists’ icteric plasma, when mixed with normal PRP produced inhibition of platelet aggregation. This data suggests that the icteric plasma contains an endogenous substance which produces the inhibitory effect on agonist induced platelet aggregation.