ORCID Profile
0000-0003-4200-431X
Current Organisations
Flinders University
,
University of South Australia
,
University of Adelaide
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Publisher: Oxford University Press (OUP)
Date: 02-08-2018
DOI: 10.1093/CVR/CVY199
Publisher: American Medical Association (AMA)
Date: 09-2019
Publisher: Wiley
Date: 11-02-2015
DOI: 10.1002/EJHF.242
Abstract: The release of the B-type natriuretic peptide (BNP) is increased in heart failure (HF), a condition associated with oxidative stress. BNP is known to exert anti-inflammatory effects including suppression of neutrophil superoxide (O2(-)) release. However, BNP-based restoration of homeostasis in HF is inadequate, and the equivocal clinical benefit of a recombinant BNP, nesiritide, raises the possibility of attenuated response to BNP. We therefore tested the hypothesis that BNP-induced suppression of neutrophil O2(-) generation is impaired in patients with acute HF. We have recently characterized suppression of neutrophil O2(-) generation (PMA- or fMLP-stimulated neutrophil burst) by BNP as a measure of its physiological activity. In the present study, BNP response was compared in neutrophils of healthy subjects (n = 29) and HF patients (n = 45). Effects of BNP on fMLP-induced phosphorylation of the NAD(P)H oxidase subunit p47phox were also evaluated. In acute HF patients, the suppressing effect of BNP (1 µmol/L) on O2(-) generation was attenuated relative to that in healthy subjects (P < 0.05 for both PMA and fMLP). Analogously, BNP inhibited p47phox phosphorylation in healthy subjects but not in HF patients (P < 0.05). However, O2(-)-suppressing effects of the cell-permeable cGMP analogue (8-pCPT-cGMP) were preserved in acute HF. Conventional HF treatment for 5 weeks partially restored neutrophil BNP responsiveness (n = 25, P < 0.05), despite no significant decrease in plasma NT-proBNP levels. BNP inhibits neutrophil O2(-) generation by suppressing NAD(P)H oxidase assembly. This effect is impaired in acute HF patients, with partial recovery during treatment.
Publisher: Elsevier BV
Date: 09-2017
DOI: 10.1016/J.IJCARD.2017.04.085
Abstract: Acute myocardial infarction (AMI) and other forms of myocardial acute oxidative stress are associated with variable "shedding" of the endothelial glycocalyx (GCS) which can be quantitated ex vivo by release into plasma of glycocalyx components such as Syndecan-1 (SD-1). Previous studies have implicated release of both catecholamines and BNP as potential accentuating factors in GCS: since these are prominent aspects of the pathogenesis of Takotsubo cardiomyopathy (TTC), we hypothesised that TTC is associated with increased GCS and the extent of GCS is predictable on the basis of NT-proBNP and catecholamine releases. SD-1 concentrations were measured in 48 TTC patients acutely and after 3months, and compared with those in 12 healthy controls, and 17 patients with AMI. Correlations were sought between SD-1 levels markers of severity of TTC episodes in in idual patients. Acute SD-1 concentrations in TTC patients were elevated significantly (p<0.0001, 1-way ANOVA) compared to control values. There were no significant correlations between SD-1 concentrations and any markers of severity of acute TTC episodes, such as NT-proBNP or catecholamine release. Over 3months, SD-1 concentrations fell significantly (p=0.0002) to approximately the same values as in control subjects. TTC is associated acutely with a marked increase in GCS. Potentially, GCS might contribute to increased coronary vascular permeability in TTC, thus dissociating development of myocardial oedema from severity of associated inflammation. Prevention of GCS represents a potential therapeutic option in TTC.
No related grants have been discovered for Saifei Liu.