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Keywords {🔍}

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Topics {✒️}

platelet-activating factor-dependent mechanism beta-adrenergic inotropic responsiveness month download article/chapter tumor necrosis factor-alpha beta-adrenergic receptor-dependent lymphocytic beta-adrenergic receptors tumour necrosis factor-alpha sepsis-induced cardiac dysfunction tnf-alpha-induced depression subsequent platelet/leukocyte interactions tpo receptor c-mpl myocardial ischemia/reperfusion injury tnf-alpha induced shedding cardiac myocyte contractility article basic research angela pucci nitric oxide-dependent human cytokines gm-csf full article pdf nos3-dependent mechanism sepsis-induced cardiomyopathy anti-inflammatory phytosterol change myocardial contractility anti-tnf therapy cytokines profile privacy choices/manage cookies recombinant human thrombopoietin della ricerca scientifica humoral growth factor hematopoietic growth factor human thrombopoietin levels human septic shock myocardial depressing activity contractile force induced vivo cardiotoxicity induced polymorphonuclear cell activation increased platelet destruction septic shock serum circulating thrombopoietin levels circulating thrombopoietin level author correspondence article lupia increase platelet activation enhance platelet activation depress cardiac function innate immune system enhanced platelet activation inhibits tissue factor tpo significantly amplified uncertain coding potential

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         headline:Thrombopoietin modulates cardiac contractility in vitro and contributes to myocardial depressing activity of septic shock serum
         description:Thrombopoietin (TPO) is a humoral growth factor that has been shown to increase platelet activation in response to several agonists. Patients with sepsis have increased circulating TPO levels, which may enhance platelet activation, potentially participating to the pathogenesis of multi-organ failure. Aim of this study was to investigate whether TPO affects myocardial contractility and participates to depress cardiac function during sepsis. We showed the expression of the TPO receptor c-Mpl on myocardial cells and tissue by RT-PCR, immunofluorescence and western blotting. We then evaluated the effect of TPO on the contractile function of rat papillary muscle and isolated heart. TPO did not change myocardial contractility in basal conditions, but, when followed by epinephrine (EPI) stimulation, it blunted the enhancement of contractile force induced by EPI both in papillary muscle and isolated heart. An inhibitor of TPO prevented TPO effect on cardiac inotropy. Treatment of papillary muscle with pharmacological inhibitors of phosphatidylinositol 3-kinase, NO synthase, and guanilyl cyclase abolished TPO effect, indicating NO as the final mediator. We finally studied the role of TPO in the negative inotropic effect exerted by human septic shock (HSS) serum and TPO cooperation with TNF-α and IL-1β. Pre-treatment with the TPO inhibitor prevented the decrease in contractile force induced by HSS serum. Moreover, TPO significantly amplified the negative inotropic effect induced by TNF-α and IL-1β in papillary muscle. In conclusion, TPO negatively modulates cardiac inotropy in vitro and contributes to the myocardial depressing activity of septic shock serum.
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      headline:Thrombopoietin modulates cardiac contractility in vitro and contributes to myocardial depressing activity of septic shock serum
      description:Thrombopoietin (TPO) is a humoral growth factor that has been shown to increase platelet activation in response to several agonists. Patients with sepsis have increased circulating TPO levels, which may enhance platelet activation, potentially participating to the pathogenesis of multi-organ failure. Aim of this study was to investigate whether TPO affects myocardial contractility and participates to depress cardiac function during sepsis. We showed the expression of the TPO receptor c-Mpl on myocardial cells and tissue by RT-PCR, immunofluorescence and western blotting. We then evaluated the effect of TPO on the contractile function of rat papillary muscle and isolated heart. TPO did not change myocardial contractility in basal conditions, but, when followed by epinephrine (EPI) stimulation, it blunted the enhancement of contractile force induced by EPI both in papillary muscle and isolated heart. An inhibitor of TPO prevented TPO effect on cardiac inotropy. Treatment of papillary muscle with pharmacological inhibitors of phosphatidylinositol 3-kinase, NO synthase, and guanilyl cyclase abolished TPO effect, indicating NO as the final mediator. We finally studied the role of TPO in the negative inotropic effect exerted by human septic shock (HSS) serum and TPO cooperation with TNF-α and IL-1β. Pre-treatment with the TPO inhibitor prevented the decrease in contractile force induced by HSS serum. Moreover, TPO significantly amplified the negative inotropic effect induced by TNF-α and IL-1β in papillary muscle. In conclusion, TPO negatively modulates cardiac inotropy in vitro and contributes to the myocardial depressing activity of septic shock serum.
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