White blood cells and clinical - therapeutic parameters in coronary artery disease.

1999 ◽  
Vol 12 (4) ◽  
pp. 183
Author(s):  
RESTORI
2015 ◽  
Vol 40 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Alon Schaffer ◽  
Monica Verdoia ◽  
Ettore Cassetti ◽  
Lucia Barbieri ◽  
Pasquale Perrone-Filardi ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e66945 ◽  
Author(s):  
Sonia Eligini ◽  
Benedetta Porro ◽  
Alessandro Lualdi ◽  
Isabella Squellerio ◽  
Fabrizio Veglia ◽  
...  

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 435
Author(s):  
Ivan Melnikov ◽  
Sergey Kozlov ◽  
Olga Saburova ◽  
Ekaterina Zubkova ◽  
Olga Guseva ◽  
...  

The objective of this work was to study the ability of blood cells and their microparticles to transport monomeric and pentameric forms of C-reactive protein (mCRP and pCRP) in the blood of patients with coronary artery disease (CAD). Blood was obtained from 14 patients with CAD 46 ± 13 years old and 8 healthy volunteers 49 ± 13.6 years old. Blood cells and microparticles with mCRP and pCRP on their surface were detected by flow cytometry. Messenger RNA (mRNA) of CRP was extracted from peripheral blood monocytes stimulated with lipopolysaccharide (LPS) and granulocyte-macrophage colony-stimulating factor (GM-CSF). mRNA of CRP in monocytes was detected with PCR. Monocytes were predominantly pCRP-positive (92.9 ± 6.8%). mCRP was present on 22.0 ± 9.6% of monocyte-derived exosomes. mCRP-positive leukocyte-derived microparticle counts were significantly higher (8764 ± 2876/µL) in the blood of patients with CAD than in healthy volunteers (1472 ± 307/µL). LPS and GM-CSF stimulated monocytes expressed CRP mRNA transcripts levels (0.79 ± 0.73-fold), slightly lower relative to unstimulated hepatocytes of the HepG2 cell line (1.0 ± 0.6-fold), but still detectable. The ability of monocytes to transport pCRP in blood flow, and monocyte-derived exosomes to transmit mCRP, may contribute to the maintenance of chronic inflammation in CAD.


2018 ◽  
Vol 12 (4) ◽  
pp. 354-359
Author(s):  
Mingshan Lin ◽  
Yuan Zhang ◽  
Zhaozhuo Niu ◽  
Yifan Chi ◽  
Qiang Huang

2021 ◽  
Vol 26 (6) ◽  
pp. 4532
Author(s):  
O. V. Romashchenko

Aim. To develop a personalized approach to the trimetazidine use in patients with coronary artery disease (CAD) based on the criteria for predicting the cytoprotective activity tested in vitro.Material and methods. We examined 30 patients with class I-III stable effort angina with concomitant hypertension and heart failure. The patients underwent echocardiography, complete blood count, biochemical tests with determination of the lipid profile, creatine phosphokinase (CPK), CPK-MB, renal and hepatic parameters. To determine the cytoprotective activity of trimetazidine, white blood cells (WBCs) of patients were examined in vitro using an Eclipse Ti-U inverted fluorescence microscope (Nikon, Japan). Living and dead cells were determined by staining WBCs with fluorescent dyes (Calcein AM, Ethidium bromide). Cell viability index (CVI) was calculated. The statistical processing was carried out. The criteria for predicting the trimetazidine cytoprotective effect were determined using Wald statistics.Results. When trimetazidine was injected into a WBC suspension sample, two types of cell viability changes were observed: in 60% of patients, CVI increased, on average, by 37% (from 23% to 60%, p<0,001) and in 40% of patients, CVI decreased, on average, by 30% (from 54% to 24%, p<0,05).A number of conditions of the patient initial status were identified for the manifestation of trimetazidine cytoprotective activity: grade 1 hypertension; right ventricular end diastolic dimension up to 30 mm according to echocardiography; normal lipid profile with a total cholesterol <5,3 mmol/L, very-low-density lipoproteins <1 mmol/L and an atherogenic coefficient up to 3 CU, myocyte and cardiomyocyte destruction (total CPK >100 U/L and CPK-MB >15 U/L), normal liver function (alanine aminotransferase <25 U/L), renal dysfunction (total protein <75 g/L, urea >8 mmol/L and blood creatinine >100 pmol/L), normal thrombopoiesis (immature platelet fraction <5%) and the state of functional adaptive system resistance (blood lymphocytes <30% and neutrophils >4x109/L).Conclusion. According to this in vitro analysis, the trimetazidine significantly increases (by an average of 37%) the cell (WBC) viability in 60% of patients with CAD. There are conditions of patient initial status, which specifies an individual pharmacodynamic target for the cytoprotective action of the drug.


Blood ◽  
2012 ◽  
Vol 120 (20) ◽  
pp. 4229-4237 ◽  
Author(s):  
Miriam M. Cortese-Krott ◽  
Ana Rodriguez-Mateos ◽  
Roberto Sansone ◽  
Gunter G. C. Kuhnle ◽  
Sivatharsini Thasian-Sivarajah ◽  
...  

Abstract A nitric oxide synthase (NOS)–like activity has been demonstrated in human red blood cells (RBCs), but doubts about its functional significance, isoform identity and disease relevance remain. Using flow cytometry in combination with the nitric oxide (NO)–imaging probe DAF-FM we find that all blood cells form NO intracellularly, with a rank order of monocytes > neutrophils > lymphocytes > RBCs > platelets. The observation of a NO-related fluorescence within RBCs was unexpected given the abundance of the NO-scavenger oxyhemoglobin. Constitutive normoxic NO formation was abolished by NOS inhibition and intracellular NO scavenging, confirmed by laser-scanning microscopy and unequivocally validated by detection of the DAF-FM reaction product with NO using HPLC and LC-MS/MS. Using immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-3H-arginine to L-3H-citrulline in a Ca2+/calmodulin-dependent fashion. Moreover, in patients with coronary artery disease, red cell eNOS expression and activity are both lower than in age-matched healthy individuals and correlate with the degree of endothelial dysfunction. Thus, human RBCs constitutively produce NO under normoxic conditions via an active eNOS isoform, the activity of which is compromised in patients with coronary artery disease.


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