Stress and Platelet Activation

Andrén, Lennart; Wadenvik, Hans; Kutti, Jack; Hansson, Lennart

doi:10.1159/000206759

Cited by 16 publications

(5 citation statements)

References 6 publications

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“…It should be noted that 30% of the control group showed also hyperaggre-gation in response to ADP. It is known that individuals subjected to stress show enhanced platelet functions [3], possibly as a result of increased endogenous adrenaline release, producing a synergistic effect with ADP on platelets [6]. Blood sampling is a stressful experience to children and this may account for the enhanced aggregation responses to ADP seen in the control group.…”

Section: Discussionmentioning

confidence: 99%

Haemostatic measurements in childhood nephrotic syndrome

et al. 1991

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Blood coagulation and platelet aggregation were assessed in children with nephrotic syndrome who were divided into the following groups: (1) relapse without treatment: (2) relapse on steroids; (3) early remission; (4) late remission and (5) steroid resistant. The renal histological findings were also recorded. Plasma anti-thrombin III (ATIII) levels were markedly reduced in groups 1 and 2, below normal in group 3 and were normal in groups 4 and 5. There was significant urinary loss of ATIII in groups 1 and 2 as well as in group 5. Plasma fibrinogen fluctuations exhibited the expected negative correlations with plasma ATIII. Reptilase time showed significant prolongation in groups 1, 2 and 3, and was near normal in groups 4 and 5. Platelet aggregation in response to arachidonic acid exhibited aggregation followed by disaggregation in groups 1, 2, 4 and 5, and was normal in group 3. Hyperaggregation in response to decreasing doses of ADP was noted in all patient groups as well as controls with no relationship to serum albumin levels. Aggregation responses to collagen and ristocetin were normal. It is concluded that: 1. The fluctuations in ATIII levels in childhood nephrotic syndrome are determined by the response to steroids and not by the renal histology per se. 2. An acquired fibrin polymerization defect (dysfibrinogenaemia) and an abnormality of the prostaglandin pathway of platelet activation, both reversible, are yet other haemostatic abnormalities in childhood nephrosis. 3. The discrepancies in the literature on haemostatic parameters, specially ATIII in childhood nephrosis, would not have arisen if their fluctuation in relation to steroid therapy as well as the renal histological features of nephrotic syndrome had been documented simultaneously.

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Section: Discussionmentioning

confidence: 99%

Haemostatic measurements in childhood nephrotic syndrome

et al. 1991

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“…Andren et al (34) reported increased PF4 levels after exposure to noise stress in healthy subjects. Andren et al (34) reported increased PF4 levels after exposure to noise stress in healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Muscle Contraction Headache and Migraine: Platelet Activation and Plasma Norepinephrine during the Cold Pressor Test

Takeshima¹,

Takao²,

Urakami³

et al. 1989

Cephalalgia

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For clarification of possible platelet activation in migraine and chronic muscle contraction headache (MCH) under stress, plasma platelet factor 4 (PF4), norepinephrine (NE), and free fatty acids (FFA) were investigated during the cold pressor test. Both PF4 and NE increased significantly, whereas FFA showed no remarkable changes. The increases of PF4 in MCH and migraine during this test were significantly greater than in healthy controls. The increase of PF4, however, was independent of NE increase and FFA changes. On the other hand, we observed decreased NE levels in both MCH and migraine, which might suggest peripheral sympathetic hypofunction. The platelets of MCH or migraine patients seem to be impaired, and the impairment may be caused by continuous sympathetic hypofunction. The behaviour of the above three substances in MCH was similar to that in migraine throughout the present study.

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“…During the early stages of sepsis, the levels of cortisol, catecholamines, and other substances are elevated in response to severe stress. Several years ago, researchers proposed that increased adrenaline secretion in response to severe stress could result in increased platelet activation [ 115 , 116 ]. In addition, a study conducted on trauma patients showed that short-term co-incubation of platelets with epinephrine enhanced platelet aggregation, adhesion, and activation of GpIIb/IIIa.…”

Section: Platelets and Endocrine Systemmentioning

confidence: 99%

The role of platelets in sepsis: A review

Xu,

Wang,

Tao

et al. 2024

Biomol Biomed

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Sepsis, a life-threatening condition characterized by organ dysfunction, results from a complex series of pathophysiological mechanisms including immune dysfunction, an uncontrolled inflammatory response, and coagulation abnormalities. It is a major contributor to global mortality and severe disease development. Platelets, abundant in the circulatory system, are sensitive to changes in the body's internal environment and are among the first cells to respond to dysregulated pro-inflammatory and pro-coagulant reactions at the onset of sepsis. In the initial stages of sepsis, the coagulation cascade, inflammatory response, and endothelial tissue damage, perpetually trigger platelet activation. These activated platelets then engage in complex inflammatory and immune reactions, potentially leading to organ dysfunction. Therefore, further research is essential to fully understand the role of platelets in sepsis pathology and to develop effective therapeutic strategies targeting the associated pathogenic pathways. This review delves into the involvement of platelets in sepsis and briefly outlines the clinical applications of associated biomarkers.

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Stress and Platelet Activation

Cited by 16 publications

References 6 publications

Haemostatic measurements in childhood nephrotic syndrome

Haemostatic measurements in childhood nephrotic syndrome

Muscle Contraction Headache and Migraine: Platelet Activation and Plasma Norepinephrine during the Cold Pressor Test

The role of platelets in sepsis: A review

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