The effect of adding lactic acid to canine whole blood on platelet aggregation as measured by impedance aggregometry

Lawson, Cheryl A.; Spangler, Elizabeth

doi:10.1111/vcp.12862

Cited by 3 publications

(2 citation statements)

References 12 publications

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“…Ex vivo, addition of lactic acid to canine platelets to create academia revealed reduced platelet aggregation on MEA [104], consistent with previous studies on LTA [105,106]. The lowered platelet aggregation due to induced acidosis is linked to modification of intracellular store calcium traffic [107] and inhibition of GPIIbIIIa conformation (PAC-1) [108].…”

Section: Shock and Acidosissupporting

confidence: 88%

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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Section: Shock and Acidosissupporting

confidence: 88%

Interplay between Platelet Dysfunction and Vascular Thrombosis in Traumatic Injury

Ogweno¹,

Murungi²

2023

Microcirculation - Updates in the Next Frontier of Vascular Disease

View full text Add to dashboard Cite

show abstract

“…Although ketones contribute to acidosis in DKA, only effects of lactic acid on platelets are well studied. Lactic acid dose dependently reduces platelet secondary wave aggregation in vitro [57][58][59][60]. The effect of pH changes is on impairing intracellular Ca++ store release [61,62], thus interfering with cytoskeletal changes [63], facilitating platelet reactions [64].…”

Section: Acute Metabolic Acidosismentioning

confidence: 99%

Controversies in Platelet Functions in Diabetes Mellitus Type 1

Ogweno¹,

Murungi²

2023

Type 1 Diabetes in 2023 - From Real Practice to Open Questions

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Individuals with diabetes mellitus (DM) are at high risk of thrombosis in which hyperactive platelets are implicated. The platelet hyperactivity has been linked to hyperglycemia. This hypothesis is supported by studies in type II diabetes mellitus showing increased sensitivity of platelets to stimulating agonists in the context of tissue resistance to high-circulating insulin. However, controversy still exists regarding the altered platelet functions in type 1 diabetes mellitus (T1DM) and the link to modifying factors such as blood glucose, hyperlipidemia, metabolic acidosis and insulin treatment. Moreover, increased insulin dosage or treatment appears to have antagonistic actions: diminished functions at low doses and enhanced activation at high doses, the switch being attributable to insulin-like growth factor. The physiological role of insulin in suppressing platelet activation is lost in T1DM, a scenario that favors increased platelet sensitivity to stimulating agonists. Furthermore, the response to antiplatelet agents and statins is sub-optimal in diabetics presenting clinical and research knowledge gap regarding the ideal antiplatelet treatment in DM in general and T1DM in particular. This chapter reviews the unique characteristics of platelet functions in T1DM highlighting the controversial areas linking unique behavior of platelets and the abnormal response to therapeutic interventions.

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Complexities, Benefits, Risks, and Clinical Implications of Sodium Bicarbonate Administration in Critically Ill Patients: A State-of-the-Art Review

Eraky,

Yerramalla,

Khan

et al. 2024

JCM

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Sodium bicarbonate has been used in the treatment of different pathologies, such as hyperkalemia, cardiac arrest, tricyclic antidepressant toxicity, aspirin toxicity, acute acidosis, lactic acidosis, diabetic ketoacidosis, rhabdomyolysis, and adrenergic receptors’ resistance to catecholamine in patients with shock. An ongoing debate about bicarbonate’s efficacy and potential harm has been raised for decades because of the lack of evidence supporting its potential efficacy. Despite the guidelines’ restrictions, sodium bicarbonate has been overused in clinical practice. The overuse of sodium bicarbonate could be because of the desire to correct the arterial blood gas parameters rapidly instead of achieving homeostasis by treating the cause of the metabolic acidosis. Moreover, it is believed that sodium bicarbonate may reverse acidosis-induced myocardial depression, hemodynamic instability, ventricular arrhythmias, impaired cellular energy production, resistance to catecholamines, altered metabolism, enzyme suppression, immune dysfunction, and ineffective oxygen delivery. On the other hand, it is crucial to pay attention to the potential harm that could be caused by excessive sodium bicarbonate administration. Sodium bicarbonate may cause paradoxical respiratory acidosis, intracellular acidosis, hypokalemia, hypocalcemia, alkalosis, impaired oxygen delivery, cerebrospinal fluid acidosis, and neurologic dysfunction. In this review, we discuss the pathophysiology of sodium bicarbonate-induced adverse effects and potential benefits. We also review the most recent clinical trials, observational studies, and guidelines discussing the use of sodium bicarbonate in different pathologies.

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The effect of adding lactic acid to canine whole blood on platelet aggregation as measured by impedance aggregometry

Cited by 3 publications

References 12 publications

Interplay between Platelet Dysfunction and Vascular Thrombosis in Traumatic Injury

Interplay between Platelet Dysfunction and Vascular Thrombosis in Traumatic Injury

Controversies in Platelet Functions in Diabetes Mellitus Type 1

Complexities, Benefits, Risks, and Clinical Implications of Sodium Bicarbonate Administration in Critically Ill Patients: A State-of-the-Art Review

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