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Acute effects of adrenaline on platelet aggregation and kinetics in vivo.

Identifieur interne : 008139 ( Main/Exploration ); précédent : 008138; suivant : 008140

Acute effects of adrenaline on platelet aggregation and kinetics in vivo.

Auteurs : RBID : pubmed:1932177

English descriptors

Abstract

The platelet (Plt) contribution to cardiovascular events triggered by adrenergic stress is supported by some experimental and necropsy data, but a cause and effect link and mechanism have not yet been clearly demonstrated. Adrenergic stress was simulated by three successive adrenaline (A) injections (80 micrograms/kg) in anesthetized dogs previously infused with indium111 labelled Plt (111In-Plt) for a gamma-camera study. Adrenaline induced an acute and significant decrease in the Plt aggregation ratio (PAR) and a parallel decrease in the Plt count as well as in the circulating 111In-Plt, mirroring a significant and persistent Plt sequestration mainly in the liver and spleen. The long-lasting and significant decrease in the circulating Plt count observed 15 min after each A injection can be explained by a persistent retention of Plt. Further studies are in progress in order to disclose if this corresponds to platelet microaggregate embolization in microvessels of the organs so far analysed. If this postulate can be confirmed the hypothesis of an adrenergic stress triggering of ischemic events will be justified.

PubMed: 1932177

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Le document en format XML

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<name sortKey="Fortunato, J S" uniqKey="Fortunato J">J S Fortunato</name>
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<nlm:affiliation>Center for the Physiology of Haemostasis (INIC), Oporto Medical School, Porto, Portugal.</nlm:affiliation>
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<name sortKey="Pinheiro, M J" uniqKey="Pinheiro M">M J Pinheiro</name>
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<name sortKey="Monteiro, M C" uniqKey="Monteiro M">M C Monteiro</name>
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<name sortKey="Rodrigues, M A" uniqKey="Rodrigues M">M A Rodrigues</name>
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<div type="abstract" xml:lang="en">The platelet (Plt) contribution to cardiovascular events triggered by adrenergic stress is supported by some experimental and necropsy data, but a cause and effect link and mechanism have not yet been clearly demonstrated. Adrenergic stress was simulated by three successive adrenaline (A) injections (80 micrograms/kg) in anesthetized dogs previously infused with indium111 labelled Plt (111In-Plt) for a gamma-camera study. Adrenaline induced an acute and significant decrease in the Plt aggregation ratio (PAR) and a parallel decrease in the Plt count as well as in the circulating 111In-Plt, mirroring a significant and persistent Plt sequestration mainly in the liver and spleen. The long-lasting and significant decrease in the circulating Plt count observed 15 min after each A injection can be explained by a persistent retention of Plt. Further studies are in progress in order to disclose if this corresponds to platelet microaggregate embolization in microvessels of the organs so far analysed. If this postulate can be confirmed the hypothesis of an adrenergic stress triggering of ischemic events will be justified.</div>
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<AbstractText>The platelet (Plt) contribution to cardiovascular events triggered by adrenergic stress is supported by some experimental and necropsy data, but a cause and effect link and mechanism have not yet been clearly demonstrated. Adrenergic stress was simulated by three successive adrenaline (A) injections (80 micrograms/kg) in anesthetized dogs previously infused with indium111 labelled Plt (111In-Plt) for a gamma-camera study. Adrenaline induced an acute and significant decrease in the Plt aggregation ratio (PAR) and a parallel decrease in the Plt count as well as in the circulating 111In-Plt, mirroring a significant and persistent Plt sequestration mainly in the liver and spleen. The long-lasting and significant decrease in the circulating Plt count observed 15 min after each A injection can be explained by a persistent retention of Plt. Further studies are in progress in order to disclose if this corresponds to platelet microaggregate embolization in microvessels of the organs so far analysed. If this postulate can be confirmed the hypothesis of an adrenergic stress triggering of ischemic events will be justified.</AbstractText>
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