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J Thorac Cardiovasc Surg 2003;125:650-660
© 2003 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Hyperoxia elicits myocardial protection through a nuclear factor {kappa}B-dependent mechanism in the rat heart

Peeter Tähepõld, MD, PhDa, Jarle Vaage, MD, PhDb, Joel Starkopf, MD, PhDc, Guro Valen, MD, PhDa,b

From the Crafoord Laboratory of Experimental Surgerya and the Department of Thoracic Surgery,b Karolinska Hospital, Stockholm, Sweden, and the Institute of Biochemistry and Clinic of Anesthesiology and Intensive Care,c University of Tartu, Tartu, Estonia.

Grants were received from the Swedish Medical Research Council (11235 and 12665), The Swedish Heart-Lung Foundation, the Foundations Fredrik o Ingrid Thuring, Tore Nilsson, Åke Wiberg, The Laerdahl Foundation for Acute Medicine, Sigurd and Elsa Goljes Memory, AGA Gas, Gösta Franckel's Foundation, and the Karolinska Institutet. P.T. has been recipient of a grant from Karolinska Institutet.

Received for publication Nov 29, 2001. Revisions requested Jan 8, 2002; revisions received July 28, 2002. Accepted for publication Aug 6, 2002. Address for reprints: Guro Valen, MD, PhD, Crafoord Laboratory of Experimental Surgery, L6:00, Karolinska Hospital, S-171 76 Stockholm, Sweden (E-mail: Guro.Valen{at}cmm.ki.se).

Objective: Hyperoxia has been previously shown to protect the heart from ischemia-reperfusion injury. In the present study we investigated whether the cardioprotective effects of hyperoxia were dependent on the redox-sensitive transcription factor nuclear factor {kappa}B.
Methods: Rats were kept in a hyperoxic (>=95% O2) environment for 60 minutes. Their hearts were isolated immediately afterward, buffer perfused in a Langendorff apparatus, and subjected to 25 minutes of global ischemia and 60 minutes of reperfusion. Cardiac pressures and coronary flow were measured, and infarct size was determined by means of triphenyl tetrazolium chloride staining. Activation of nuclear factor {kappa}B was assessed by means of the electrophoretic mobility shift assay, whereas the inhibitor I{kappa}B{alpha} was evaluated by means of immunoblotting. Pharmacologic inhibition of nuclear factor {kappa}B was achieved with 2 different agents, SN50 and pyrrolidine dithiocarbamate.
Results: Preischemic exposure to hyperoxia improved postischemic recovery of myocardial contractile function and coronary flow and reduced infarct size. Hyperoxia activated pulmonary and myocardial nuclear factor {kappa}B. Pretreatment with SN50 (400 µg/kg administered intraperitoneally) or pyrrolidine dithiocarbamate (100 mg/kg administered intraperitoneally) before hyperoxia abolished the functional and infarct-limiting protection. Hyperoxia reduced nuclear factor {kappa}B activation in the heart during sustained ischemia and reperfusion and increased the cytoplasmatic inhibitory factor I{kappa}B{alpha}. Administration of pyrrolidine dithiocarbamate or SN50 during ischemia and reperfusion to isolated hearts from normoxic control animals improved postischemic contractile function and coronary flow and reduced infarct size.
Conclusions: Hyperoxia protects the rat heart against ischemia-reperfusion injury. The cardioprotection depends on myocardial activation of the transcription factor nuclear factor {kappa}B. Our results support evidence for a dual role of nuclear factor {kappa}B in the heart.




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