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Expired Breath Oxidant Activity during Haemodialysis
Author(s) -
E.R. Maker,
D. G. Wickens,
J R Curtis,
T. L. Dormandy
Publication year - 1989
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000185633
Subject(s) - medicine , intensive care medicine
Dr. E.R. Maher, Department of Nephrology, Royal Free Hospital, Pond Street, Hampstead, London NW3 2QG (UK) Dear Sir, Complement activation during haemodialysis with a cuprophan membrane produces a severe transient neu-tropenia caused by sequestration of activated neutrophils in the pulmonary microcirculation [1]. Coincident with this hypoxaemia develops, but the relationship of pulmonary leucosequestration to pulmonary dysfunction during haemodialysis is controversial [1]. Animal and in vitro experiments have suggested that pulmonary dysfunction during early haemodialysis is mediated by free radicals released from activated neutrophils within the pulmonary microcirculation [2–5]. However, in contrast to animal models of systemic complement activation [5], we have been unable to demonstrate increased free radical release during haemodialysis by measuring plasma free radical reaction products [6], and were unable to detect any evidence of haemodialysis-induced pulmonary vascular injury in vivo [7]. Hydrogen peroxide is a volatile oxygen species which is released (along with oxygen radicals) by activated neutrophils, and can enter the gas phase at physiological temperatures. Spontaneous chemiluminescence in human breath has been shown to correlate with hydrogen peroxide content [8], and in the adult respiratory distress syndrome (ARDS), a condition in which free radicals released from activated neutrophils are thought to be important in the pathogenesis of pulmonary injury, an increased concentration of hydrogen peroxide in expired breath condensate has been reported [9]. Plasma free radical reaction products are not increased in patients with ARDS [10], suggesting that breath hydrogen peroxide content is a more sensitive index of oxygen radical generation in the lung. We therefore investigated the effect of haemodialysis on expired breath hydrogen peroxide concentration. Five patients with end-stage renal failure (aged 34–60 years) were studied during a routine haemodialysis session with a cuprophan membrane (Lundia Plate, Gam-bro, Sweden). Breath condensate was collected before and serially during the first 2 h of haemodialysis, by passing expired breath through an 80-cm plastic tubing (internal diameter 15 mm) submerged in an ice-water bath. Expired air was collected until about 1 ml of breath condensate had pooled in the tubing, which was usually accomplished within 10 min. Hydrogen peroxide was measured in the condensate by the scopoletin/horserad-ish peroxidase method [11]. Studies in normal subjects demonstrated that hydrogen peroxide concentration in the breath condensate remained constant over a 2-hour

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