Intracellular Ca2+ homeostasis and aggregation in platelets are impaired by ethanol through the generation of H2O2 and oxidation of sulphydryl groups

Rosado, Juan A.; Núñez, Ana M.; López, José J.; Pariente, José A.; Salido, Ginés M.

doi:10.1016/j.abb.2006.05.011

Cited by 13 publications

(7 citation statements)

References 47 publications

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“…Some in vitro studies have found no influence [8,23,25,31], others a decreased platelet aggregation after 2 drinks in vivo [48] or under certain conditions in vitro [23,28,37,44], while others described a platelet activation in vivo [5,20,21,32] or even both platelet activation and inhibition [40]. The divergence of results suggests among others a strong dependence on methodology.…”

Section: Discussionmentioning

confidence: 99%

Influence of acute alcohol exposure on hemorheological parameters and platelet function in vivo and in vitro

Fehr¹,

Galliard-Grigioni²,

Reinhart³

2008

Clinical Hemorheology and Microcirculation

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We have analysed the influence of acute alcohol exposure in vivo and in vitro on blood flow properties and platelet function. 12 healthy male volunteers drank either 4.36 ml red wine/kg body weight (=0.5 g ethanol/kg) or water at 06.00 p.m. under fasting conditions. Blood was drawn immediately before, and 1, 2, 4 and 13 h after alcohol ingestion. Alcohol had a detectable osmotic effect on erythrocytes; the mean cellular volume (MCV) was significantly smaller 1-4 h after ingestion. Whole blood viscosity remained unaffected, but blood viscosity at a standardized Hct of 45% measured at a high shear rate (94.5 s −1 ) was increased 2 h after wine ingestion. In the morning, 13 h after wine drinking, platelet aggregation measured with a platelet function analyser PFA-100 ® was increased to a greater extent than after water drinking. In vitro, no effect was seen when blood was incubated with 0, 12.5, 25, 50 and 100 mmol/l ethanol for 1 h at 37 • C. We conclude that an acute exposure to alcohol has only modest effects on hemorheological parameters and platelet aggregation in vivo and no effect in vitro, which suggests that other factors must be involved in both beneficial and harmful effects of wine drinking.

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Section: Discussionmentioning

confidence: 99%

Influence of acute alcohol exposure on hemorheological parameters and platelet function in vivo and in vitro

Fehr¹,

Galliard-Grigioni²,

Reinhart³

2008

Clinical Hemorheology and Microcirculation

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“…The protective effects of resveratrol against heart diseases are thought to stem from its ability to decrease platelet aggregation [29,54], promote vasorelaxation [55,56], reduce lipid peroxidation [22,24], improve serum cholesterol and triglyceride concentrations [57], and reduce procoagulant tissue factor [31,58]. The beneficial effects of red wine are possibly not only mediated through the phenolics, but also ethanol, as it was shown to modulate various biological activities including inhibition of platelet aggregation [59] and tissue factor expression in monocytes [60]. In the present study, we identified an additional potential mechanism by which resveratrol and other wine phenolics could provide protection against atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Effect of wine phenolics on cytokine‐induced C‐reactive protein expression

Kaur

Rao

Agrawal

et al. 2007

Journal of Thrombosis and Haemostasis

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Summary. Background: Elevation of C-reactive protein (CRP) levels in blood was recognized as one of the cardiac disease risk factors. Consumption of wine is shown to reduce the risk from heart disease and improve longevity. Objectives: In the present study, we evaluated the effect of various wine polyphenolic compounds and several active synthetic derivatives of resveratrol on the inflammatory cytokines (IL-1ß + IL-6)-induced CRP expression in Hep3B cells. Results: Among the wine phenolics tested, quercetin and resveratrol, in a dose-dependent manner, suppressed cytokine-induced CRP expression. Two of the synthetic derivatives of resveratrol, R3 and 7b, elicited a fiftyfold higher suppressive effect compared with resveratrol. The inhibitory effects of resveratrol and its derivatives on CRP expression were at the level of mRNA production. Investigation of signaling pathways showed that the cytokines induced the phosphorylation of p38 and p44/42 MAP kinases. Inhibitors of p38 and p44/42 mitogen-activated protein kinase (MAPK) activation inhibited CRP expression, implicating the involvement of both pathways in cytokine-induced CRP expression. These data revealed a previously unrecognized role of the p44/ 42 MAPK signaling pathway in CRP expression. Wine polyphenolics or the synthetic compounds of resveratrol did not affect cytokine-activated phosphorylation of these MAPKs. Conclusions: Wine phenolics inhibit CRP expression; however, to do so, they do not utilize the MAPK pathways.

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“…11,18,28,30 Newer molecular studies have identified impaired calcium entry into platelets as the mechanism by which ethanol prevents platelet aggregation, rendering them dysfunctional. 9,26,34 For these reasons, the effects of ethanol on platelet function must be considered when patients present with clinically significant hemorrhage. Here, differences in the mean BAL did not reach significance in patients with HPC compared with those with no HPC (Table 2), although there was a nonsignificant correlation between higher BAL and hemorrhagic progression.…”

Section: Blood Alcohol Levelmentioning

confidence: 99%

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

Carnevale

Segar

Powers

et al. 2018

Journal of Neurosurgery

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OBJECTIVE Traumatic brain injury (TBI) remains a significant cause of neurological morbidity and mortality. Each year, more than 1.7 million patients present to the emergency department with TBI. The goal of this study was to evaluate the prognosis of traumatic cerebral intraparenchymal hemorrhage (tIPH), to develop subclassifications of these injuries that relate to prognosis, and to provide a more comprehensive assessment of hemorrhagic progression contusion (HPC) by analyzing the rate at which tIPH "blossom" (i.e., expansion), depending on a variety of intrinsic and modifiable factors. METHODS In this retrospective study, 726 patients (age range 0-100 years) were admitted to a level 1 trauma center with tIPH during an 8-year period (2005-2013). Of these patients, 491 underwent both admission and follow-up head CT (HCT) within 72 hours. The change in tIPH volume over time, the expansion rate, was recorded for all 491 patients. Effects of prehospital and in-hospital variables were examined using ordinal response logistic regression analyses. These variables were further examined using multivariate linear regression analysis to accurately predict the extent to which a hemorrhage will progress. RESULTS Of the 491 (67.6%) patients who underwent both admission and follow-up HCT, 368 (74.9%) patients experienced HPC. These hemorrhages expanded on average by 61.6% (4.76 ml) with an average expansion rate of 0.71 ml per hour. On univariate analysis, certain patient characteristics were significantly (p < 0.05) related to HPC, including age (> 60 years), admission Glasgow Coma Scale score, blood alcohol level, international normalized ratio, absolute platelet count, transfusion of platelets, concomitant anticoagulation and antiplatelet medication, the initial tIPH volume on admission HCT, and ventriculostomy. Increased expansion rate was significantly associated with patient disposition to hospice or death (p < 0.001). To determine which factors most accurately predict overall patient disposition, an ordinal-response logistic regression identified systolic blood pressure, Injury Severity Score, admission Glasgow Coma Scale score, follow-up scan volume, transfusion of platelets, and ventriculostomy as predictors of patient discharge disposition following tIPH. A multivariate logistic regression identified several prehospital and in-hospital variables (age, Injury Severity Score, blood alcohol level, initial scan volume, concomitant epidural hematoma, presence of subarachnoid hemorrhage, transfusion of platelets, and ventriculostomy) that predicted the volumetric expansion of tIPH. Among these variables, the admission tIPH volume by HCT proved to be the factor most predictive of HPC. CONCLUSIONS Several factors contribute to the rate at which traumatic cerebral contusions blossom in the acute posttraumatic period. Identifying the intrinsic and modifiable aspects of cerebral contusions can help predict the rate of expansion and highlight potential therapeutic interventions to improve TBI-associated morbidity and mortality.

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Intracellular Ca2+ homeostasis and aggregation in platelets are impaired by ethanol through the generation of H2O2 and oxidation of sulphydryl groups

Cited by 13 publications

References 47 publications

Influence of acute alcohol exposure on hemorheological parameters and platelet function in vivo and in vitro

Influence of acute alcohol exposure on hemorheological parameters and platelet function in vivo and in vitro

Effect of wine phenolics on cytokine‐induced C‐reactive protein expression

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

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