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(Circulation. 2000;102:452.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Involvement of Cytokines in the Mechanism of Whole-Body Hyperthermia-Induced Cardioprotection
From the First Department of Medicine (N.Y., S.H., K.O., T.K., M.H.), Department of Pathophysiology (T.K.), and Department of Biochemistry (N.T.), Osaka University Medical School, and the Cardiovascular Division, Osaka Rosai Hospital (S.H.), Osaka, Japan.
Correspondence to Shiro Hoshida, MD, PhD, Cardiovascular Division, Osaka Rosai Hospital, 1179-3 Nagasone-cho, Sakai, Osaka 591-8025, Japan. E-mail hoshidas{at}orh.go.jp
Background—Hyperthermia increases
cardiac tolerance to ischemia/reperfusion injury and
activates manganese superoxide dismutase (Mn-SOD), an intrinsic
radical scavenger, in myocardium in a biphasic manner.
Tumor necrosis factor-
(TNF-) and interleukin-1ß (IL-1ß)
induced a biphasic cardioprotection that corresponded to the activation
of Mn-SOD. However, a direct association between Mn-SOD activation in
myocardium and the acquisition of tolerance to
ischemia/reperfusion injury induced by hyperthermia and the
involvement of the cytokines in the signal transduction pathway
for the hyperthermia-induced cardioprotection have not yet been
elucidated.
Methods and Results—Hyperthermia was induced in
anesthetized rats by placement in a temperature-controlled
water bath. At 0.5 and 72 hours after hyperthermia, ischemia
was induced by occlusion of the left coronary artery for 20
minutes, followed by reperfusion for 48 hours. Inhibition of the
increases in Mn-SOD content and activity 72 hours after hyperthermia by
the administration of antisense oligodeoxynucleotides to
Mn-SOD abolished the expected decrease in myocardial infarct size. The
simultaneous administration of neutralizing antibodies to
TNF- and IL-1ß before hyperthermia abolished the biphasic
cardioprotection and increase in Mn-SOD activity.
Conclusions—The increase in Mn-SOD activity mediated through the
production of TNF- and IL-1ß by whole-body hyperthermia is
important in the acquisition of early- and late-phase cardioprotection
against ischemia/reperfusion injury in rats.
Key Words: enzymes • hormones • interleukins • hyperthermia • genes
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