Changes in platelet Bax levels contribute to impaired platelet response to thrombin after cardiopulmonary bypass: prospective observational clinical and laboratory investigations

Murase, Masanori; Nakayama, Yushi; Sessler, Daniel I.; Mukai, Nobuhiro; Ogawa, Satoshi; Nakajima, Yasufumi

doi:10.1093/bja/aex349

Cited by 11 publications

(10 citation statements)

References 31 publications

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“…A recent clinical study confirmed a decrease in platelet GPIb surface expression after adult CPB. 122 Our results also showed CPBassociated platelet activation and concomitant receptor shedding in pediatric patients with CPB. 123 Similarly, increased platelet GPIba and GPVI shedding is already present in patients before ECMO placement and remain significantly elevated after on ECMO support.…”

Section: Shear-induced Platelet Receptor Sheddingsupporting

confidence: 72%

Device-Induced Hemostatic Disorders in Mechanically Assisted Circulation

Wang

Griffith

2021

Clin Appl Thromb Hemost

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Mechanically assisted circulation (MAC) sustains the blood circulation in the body of a patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) or on ventricular assistance with a ventricular assist device (VAD) or on extracorporeal membrane oxygenation (ECMO) with a pump-oxygenator system. While MAC provides short-term (days to weeks) support and long-term (months to years) for the heart and/or lungs, the blood is inevitably exposed to non-physiological shear stress (NPSS) due to mechanical pumping action and in contact with artificial surfaces. NPSS is well known to cause blood damage and functional alterations of blood cells. In this review, we discussed shear-induced platelet adhesion, platelet aggregation, platelet receptor shedding, and platelet apoptosis, shear-induced acquired von Willebrand syndrome (AVWS), shear-induced hemolysis and microparticle formation during MAC. These alterations are associated with perioperative bleeding and thrombotic events, morbidity and mortality, and quality of life in MCS patients. Understanding the mechanism of shear-induce hemostatic disorders will help us develop low-shear-stress devices and select more effective treatments for better clinical outcomes.

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Section: Shear-induced Platelet Receptor Sheddingsupporting

confidence: 72%

Device-Induced Hemostatic Disorders in Mechanically Assisted Circulation

Wang

Griffith

2021

Clin Appl Thromb Hemost

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“…An imbalance between antioxidants and oxidants following reperfusion induces oxidative stress followed by mitochondrial dysfunction, because rapid oxygen accumulation following reperfusion causes excessive production of reactive oxygen species [7]. Next, cardiomyocyte death is induced by the mitochondrial pathway [8,9]. Increased permeability of the mitochondrial inner membrane leads to release of cytochrome c and other activating factors, which induce apoptosis by promoting activation of caspase.…”

Section: Introductionmentioning

confidence: 99%

“…Increased permeability of the mitochondrial inner membrane leads to release of cytochrome c and other activating factors, which induce apoptosis by promoting activation of caspase. It has been proved that permeability transition, which occurs during the IR process, is induced by increased ROS production, insufficiency of antioxidants, changes in pyridine nucleotide ratios, and calcium overload [8,9]. Clinically, the incidence of systemic inflammatory response syndrome is 2-10% because cardiopulmonary bypass induces a systemic inflammatory response due to contact between peripheral blood and artificial tube material used for the operation, which can aggravate the local inflammatory response in myocardial IRI [10,11].…”

Section: Introductionmentioning

confidence: 99%

Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass

Luo

Xie

et al. 2020

Med Sci Monit

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Background: Interleukin-36 has been demonstrated to be involved in inflammatory responses. Inflammatory responses due to ischemia-reperfusion injury following cardiopulmonary bypass (CPB) can cause heart dysfunction or damage. Material/Methods: The CPB models were constructed in IL-36R-/-, IL-36RN-/-, and wild-type SD rats. Ultrasonic cardiography and ELISA were used to evaluate the cardiac function and measuring myocardial biomarker levels in different groups. TUNEL assay was used to evaluate apoptosis. Western blot assays and RT-PCR were performed to measure the expression of chemokines and secondary inflammatory cytokines in the heart. Oxidative stress in tissue and cultured cells was assessed using a DCFH-DA fluorescence probe and quantification of superoxide dismutase activity. Results: Improved systolic function and decreased serum levels of myocardial damage biomarkers were found in IL-36R-/-rats compared to WT rats, while worse cardiac function and cardiomyocyte IR injury were observed in IL-36RN-/-rats compared to WT rats. TUNEL staining and Western blot analyses found that cardiomyocyte apoptosis and inflammation were significantly lower in the hearts of IL-36R-/-rats compared with that of WT rats. Oxidative stress was significantly lower in IL-36R-/-rats compared to WT rats. iNOS expression was significantly reduced, while eNOS expression was increased in the hearts of IL-36R-/-rats. Silencing of IL-36R expression in vitro activated SIRT1/FOXO1/p53 signaling in cardiomyocytes. Conclusions: IL-36R deficiency in cardiomyocytes repressed infiltration of bone marrow-derived inflammatory cells and oxidative stress dependent on SIRT1-FOXO1 signaling, thus protecting cardiomyocytes and improving cardiac function in CPB model rats.

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“…Platelet protein expression impairment may further contribute to postoperative platelet dysfunction. A platelet qualitative impairment such as a reduced surface GPIb expression was found to be associated with the overexpression of some miRNAs (i.e., mir-10b and mir-96) and also with enhanced platelet Bax apoptotic signaling in cardiac surgery cohorts [38,39]. Microcirculatory impairment is another factor associated with platelet dysfunction following heart procedures.…”

Section: Platelets Cardiac Surgery and Extracorporeal Circulation: Tmentioning

confidence: 99%

Quantitative and Qualitative Platelet Derangements in Cardiac Surgery and Extracorporeal Life Support

Squiccimarro

Jiritano

Serraino

et al. 2021

JCM

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Thrombocytopenia and impaired platelet function are known as intrinsic drawbacks of cardiac surgery and extracorporeal life supports (ECLS). A number of different factors influence platelet count and function including the inflammatory response to a cardiopulmonary bypass (CPB) or to ECLS, hemodilution, hypothermia, mechanical damage and preoperative treatment with platelet-inhibiting agents. Moreover, although underestimated, heparin-induced thrombocytopenia is still a hiccup in the perioperative management of cardiac surgical and, above all, ECLS patients. Moreover, recent investigations have highlighted how platelet disorders also affect patients undergoing biological prosthesis implantation. Though many hypotheses have been suggested, the mechanism underlying thrombocytopenia and platelet disorders is still to be cleared. This narrative review aims to offer clinicians a summary of their major causes in the cardiac surgery setting.

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Changes in platelet Bax levels contribute to impaired platelet response to thrombin after cardiopulmonary bypass: prospective observational clinical and laboratory investigations

Abstract: UMIN Clinical Trials Registry (number UMIN000006033).

Cited by 11 publications

References 31 publications

Device-Induced Hemostatic Disorders in Mechanically Assisted Circulation

Device-Induced Hemostatic Disorders in Mechanically Assisted Circulation

Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass

Quantitative and Qualitative Platelet Derangements in Cardiac Surgery and Extracorporeal Life Support

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