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Apoptosis of polymorphonuclear neutrophils (PMN) is currently discussed as a key event in the control of inflammation. This study determined PMN apoptosis and its underlying mechanisms in controls (C), patients with stable (SAP) or unstable angina (UAP), and with acute myocardial infarction (AMI). Blood was drawn from 15 subjects of each C, SAP, UAP, and AMI. Apoptosis was measured by flow cytometry in isolated PMN (propidium iodide staining) and PMN from whole blood (CD16, FcγRIII). Serum cytokines were determined by enzyme‐linked immunosorbent assay. Apoptosis of isolated PMN was delayed significantly in acute coronary syndromes (ACS) as compared with SAP or C (C, 51.2±12.6%; SAP, 44.9±13.6%; UAP, 28.4±10.1%; AMI, 20.3±8.5%; AMI or UAP vs. SAP or C, P<0.001). These results were confirmed by measurement of PMN apoptosis in cultured whole blood from patients and controls. Moreover, serum of patients with ACS markedly reduced apoptosis of PMN from healthy donors. Analysis of patients’ sera revealed significantly elevated concentrations of tumor necrosis factor α, interferon‐γ (IFN‐γ), granulocyte macrophage‐colony stimulating factor (GM‐CSF), and interleukin (IL)‐1β in ACS (vs. C and SAP). IFN‐γ, GM‐CSF, and IL‐1β significantly delayed PMN apoptosis in vitro. Furthermore, coincubation of PMN with adenosine 5′‐diphosphate‐activated platelets significantly inhibited PMN apoptosis as compared with coculture with unstimulated platelets. This study demonstrates a pronounced delay of PMN apoptosis in UAP and AMI, which may result from increased serum levels of IFN‐γ, GM‐CSF, and IL‐1β and from enhanced platelet activation. Therapeutical modulation of these determinants of PMN lifespan may provide a new concept for the control of inflammation in ACS.

AbstractBackground and Objectives: To evaluate the rheological properties and the oxidative susceptibility of γ-ray-irradiated red blood cells (RBCs). Materials and Methods: RBCs in mannitol-adenine-phosphate (MAP) medium were irradiated with 35 Gy and stored at 4°C for 4 weeks. The deformability of the RBCs was examined under shear flow in relation to the morphological and biochemical changes. The RBCs were further exposed to 1 mM FeSO4 and 5 mM ascorbate to examine the oxidative susceptibility. Results: The RBC deformability was decreased during storage, and the impairment was further enhanced by the irradiation, which promoted cell shrinkage and intracellular hemoglobin condensation accompanying potassium loss. Lipid peroxidation and protein aggregation of the RBC membrane as well as echinocytosis were not enhanced by the irradiation. The exposure to free iron did not stimulate the oxidation of the irradiated RBC membrane. Conclusion: The decreased deformability of γ-ray-irradiated RBCs in MAP medium was mainly induced by dehydration due to potassium loss, and the membrane lipids and proteins were stably preserved against oxidative stress.Copyright © 2000 S. Karger AG, Basel