Alcohol induces profuse reversible decrease in platelet function and delayed initiation of co-agulation

Schramko, Alexey; Niemi, Tomi

doi:10.7243/2052-6229-2-4

Cited by 2 publications

(1 citation statement)

References 6 publications

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“…Alcohol is known to have in vivo and ex vivo platelet aggregation inhibitory effects [119][120][121], related to alteration of blood osmolality, lactate, and acidosis [122]. Conversely, bidirectional effects termed rebound effects [121] composed of initial decreased aggregation followed by hyperaggregation have been shown [123]. The mechanism for increased aggregation appears to be erythrocyte release of ADP [124] and fibrinolytic shutdown [125,126].…”

Section: Alcohol and Toxinsmentioning

confidence: 99%

Interplay between Platelet Dysfunction and Vascular Thrombosis in Traumatic Injury

Ogweno¹,

Murungi²

2023

Microcirculation - Updates in the Next Frontier of Vascular Disease

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Platelets halt bleeding accompanying traumatic injury by performing primary hemostasis to repair vascular leakage at injury sites. In trauma individuals, ex vivo platelet function tests often indicate impairment despite normal count. Moreover, incubation of platelets from normal non-traumatized individuals with plasma from trauma victims demonstrates impairment suggesting association with factors in circulation. Notably, not all trauma victims die from hemorrhage. Despite laboratory evidence of dysfunction, thrombotic vascular occlusions are persistent in trauma survivors as corroborated by postmortem findings from victims who die. The time course of platelet reactions post-traumatic injury, that is, the transition from states favoring bleeding to those that facilitate thrombosis is still unclear. Of the several terminologies describing platelet behavior with regards to injury, including hyporeactivity, anergy, exhaustion, and maladaptive states, few have focused on platelet-platelet interactions. It is increasingly becoming clear that platelet interaction with injured endothelium is a probable missing link in the mechanistic explanation of vascular thrombosis post-traumatic injury. This postulate is supported by evidence of increased adhesive protein, von Willebrand factor, and released from injured endothelium. In all, this potentially explains the suboptimal response to anticoagulants or antiplatelets post-trauma. This chapter will review current knowledge on platelet functions in relation to vascular thrombosis post-trauma, the time course, mechanistic hypothesis, and response to therapeutic interventions and clinical outcomes.

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