Previous Heat Shock Treatment Attenuates Lipopolysaccharide-Induced Hyporesponsiveness of Platelets in Rats

Abstract

Several studies demonstrated that previous heat shock treatment caused expression of heat shock proteins (HSPs) and reduced organ dysfunction and mortality in experimentally induced severe sepsis. However, the protective mechanism on platelet function remains unclear. The aim of this study was to investigate the effect of heat shock treatment on platelet aggregation ex vivo in endotoxin-induced rats with sepsis. Rats of the heated group were heated by whole-body hyperthermia 18 h before lipopolysaccharide (LPS) injection. Blood samples were obtained from the carotid artery 90 min after LPS injection. Platelet aggregation ability was measured by aggregometer. Results revealed that platelet aggregation ex vivo was significantly inhibited in LPS-induced rats in a manner of dose dependence. Previous heat shock treatment caused overexpression of HSPs and significantly attenuated the LPS-induced platelet hyporesponsiveness. This attenuation disappeared in accordance with absence of HSP72 at 7 days after heat shock treatment. Aggregation of normal platelets was also inhibited by incubating with plasma obtained from endotoxemic rats but not from preheated endotoxemic rats. Furthermore, no significant hyporesponsiveness was found in endotoxemic platelets in addition to preheated endotoxemic plasma. The addition of H2O2 scavenger catalase diminished the platelet hyporesponsiveness significantly only in nonheated endotoxemic rats. Moreover, the plasma nitrite and nitrate levels were significantly attenuated in preheated endotoxemic rats. These results revealed that previous heat shock treatment might attenuate LPS-induced hyporesponsiveness of platelets by changing the plasma components possibly through altering H2O2 and nitric oxide concentrations.

Changes in cell culture temperature alter release of inflammatory mediators in murine macrophagic RAW264.7 cells

“…Moderate fever enhances a patient's defenses, increasing the chance of survival and shortening the disease's duration [10]. The heat shock protein (HSP) response is a highly conserved cellular defense mechanism, and in mild hyperthermia, activation of the HSP response allows cells to withstand a subsequent metabolic insult that would otherwise be lethal [11].…”

Inhibitory effects of staphylococcal enterotoxin type B on human platelet adhesionin vitro

“…There are increasing evidences showing that H 2 O 2 can be generated by sources other than xanthine oxidase/ superoxide dismutase pathway. Accordingly, recent studies have implicated mitochondria as a source of ROS (mainly H 2 O 2 ) responsible for mediating flow-induced dilatation in coronary arteries [47] and intercellular communication in vascular smooth muscle cells subjected to stretch [48]. Moreover, the inhibition of platelet aggregation in response to NO and S-nitrosoglutathione has been shown to be strongly enhanced by H 2 O 2 [46].…”

Alterações morfológicas de tecido laminar do casco e parâmetros clínicos e laboratoriais de equinos com síndrome cólica letal

“…A contagem de plaquetas foi inferior ao valor normal em um animal e próxima ao valor inferior em outros dois equinos, achado que se relaciona ao agravamento do quadro clínico e morte (Koury et al 2006, Silva et al 2007). Por esse fato sugere-se que os animais poderiam desenvolver tromboembolia e diátese hemorrágica, como nos quadros terminais de endotoxemia (Dong et al 2005). A trombocitopenia também foi observada em equinos com laminite induzida por sobrecarga de carboidratos (Moore et al 1981).…”

“…As alterações de parâme-tros laboratoriais são descritas na ativação inflamatória sistêmica presente na endotoxemia e estão relacionadas ao agravamento do quadro clínico, como trombocitopenia e leucocitose ou leucopenia. A trombocitopenia relaciona-se com o aparecimento de tromboembolia e com a diátese hemorrágica presente na sepse (Dong et al 2005, Koury et al 2006, Campebell et al 2007), sendo identificada também em animais durante a indução de laminite (Moore et al 1981). A leucopenia, causada pela migração e ativação de leucócitos nos tecidos, pode levar a liberação de metaloproteinases que causam lesão tecidual (Zerpa et al 2005).…”