Free Radical Biology & Medicine, Vol. 14, pp. 643-647, 1993 0891-5849/93 $6.00 + .00 Printed in the USA. All rights reserved. Copyright © 1993 Pergamon Press Ltd. Brief Communication ELEVATED BREATH PENTANE IN HEART FAILURE FREE RADICAL SCAVENGER REDUCED BY PAUL A. SOBOTKA,* MICHAEL D. BROTTMAN,* ZE'EV WEITZ, t ALAN J. BIRNBAUM, t JOHN L. SKOSEY, I and EDWIN J. ZARLING* *Department of Medicine, Loyola University of Chicago, Maywood, IL 60153, USA; and +The Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA (Received 14 September 1992; Revised 1 December 1992; Accepted 17 December 1992) Abstract--Pentane, a product of lipid peroxidation, has been detected in situations involving ischemic injury. Such injury may be limited if lipid peroxidation can be controlled by antioxidants. The role of lipid peroxidation in chronic heart failure (CHF) was assessed by measuring breath pentane in patients with CHF vs. age matched controls. The effect of a free radical scavenger on pentane released during CHF was also measured. Pentane levels were correlated with the daily dose of captopril, a sulfhydril- containing drug used to treat CHF, which is an angiotensin converting enzyme inhibitor. To separate the scavenging effects of captopril from the pharmacologic effects of converting enzyme inhibitors, a crossover study using a nonsulfhydril inhibitor was used. Patients with CHF excreted (p < 0.005) high concentrations ofpentane (5.7 _+2.1 vs. control 3.6 _+ 1.2 nmol/1). Patients treated with captopril also had significantly higher (p < 0.05) excretion of pentane than the control patients (4.7 +_ 1.3 vs. 3.6 + 1.2 nmol/l). The dose of captopril was inversely proportional to the concentration of pentane excreted (r = 0.55, p < 0.05). Pentane excretion during captopril therapy was significantly lower before (p < 0.01 ) and after (p < 0.02) nonsulfhydril inhibitor therapy. Conclusion: breath pentane is elevated in CHF and it can be reduced by a free radical scavenger. This reduction of pentane excretion is not a converting enzyme inhibitor class effect. Keywords--Pentane, Lipid peroxidation, Congestive heart failure, Ischemia, Antioxidant, Free Radicals INTRODUCTION Oxygen free radicals induce cellular damage by at- tacking membrane lipids, as well as nucleic acids and proteins. The peroxidation of various cellular polyun- saturated lipids produces short chain alkanes, with the most common being pentane. Pentane, evolved from the reaction of free radicals with omega-six fatty acids (linoleic acid family), is readily excreted through the lungsJ Thus, pulmonary pentane excretion serves as a reliable noninvasive index of lipid peroxidation. 2 Other byproducts of peroxidation include hydroper- oxides2 and malondialdehyde.3 The latter compound has been noted to be elevated in patients with chronic heart failure (CHF); 3 however its presence is not spe- Funded, in part, by an American Heart Association, Metropoli- tan Chicago Grant to P. A. Sobotka. Presented, in part, at the American Heart Association Scientific Session in November, 1990. Address correspondence to: Edwin J. Zarling, Loyola University at Chicago, Department of Medicine, 2160 South First Avenue, Maywood, IL 60153. cific for lipid peroxidation. 4,5 This observation, how- ever, opens the question of whether lipid peroxidation has a role in the tissue damage associated with CHF. In order to more deafly define the role of lipid peroxidation in CHF, we measured breath pentane excretion in CHF patients. In addition, the role of radical scavenging medication in reducing the excre- tion ofpentane was explored. This was accomplished by comparing pentane excretion in stable CHF pa- tients while crossing over between two drugs (angio- tensin converting enzyme inhibitors) commonly used to treat CHF, which differ only by the presence of a radical scavenging sulfhydryl group. MATERIAL AND METHODS Patients with CHF were recruited from inpatient and outpatient services at Loyola University. Normal, healthy, age-matched control subjects were recruited from the hospital staff. The diagnosis of heart failure required a history of breathlessness and a physical ex- 643