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(Circulation Research. 1996;78:573-580.)
© 1996 American Heart Association, Inc.

Articles

Transient Ischemia Reduces Norepinephrine Release During Sustained Ischemia

Neural Preconditioning in Isolated Rat Heart

Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994.

Melchior Seyfarth, Gert Richardt, Anna Mizsnyak, Thomas Kurz, Albert Schömig

From I. Medizinische Klinik, Technische Universität München (Germany).

Correspondence to Dr M. Seyfarth, I. Medizinische Klinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Str. 22, 81675 München, Germany. E-mail seyfarth@med1.med.tu-muenchen.de.

Abstract Endogenous catecholamine release may play a role in ischemic preconditioning either as a trigger or as a target within the process of myocardial preconditioning. Therefore, we investigated the effect of transient ischemia (TI) on norepinephrine release during sustained ischemia in isolated rat hearts. TI was induced by multiple cycles of global ischemia followed by reperfusion with a duration of 5 minutes each, comparable to ischemic preconditioning protocols. After TI, norepinephrine release was evoked by either sustained global ischemia, anoxia, cyanide intoxication, tyramine, or electrical stimulation. During TI, no washout of norepinephrine was observed, and tissue concentrations of norepinephrine were not changed. TI, however, reduced norepinephrine overflow after 20 minutes of sustained ischemia from 239±26 pmol/g (control) to 79±8 pmol/g (67% reduction, P<.01). A similar reduction of ischemia-induced norepinephrine release from 192±22 pmol/g (control) to 90±15 pmol/g was observed when hearts underwent transient anoxia without glucose (P<.05). When reperfusion between TI and sustained ischemia was prolonged from 5 to 90 minutes, the inhibitory effect of TI on norepinephrine release was gradually lost. Susceptibility to TI was a unique feature of norepinephrine release induced by sustained ischemia, since release of norepinephrine evoked by anoxia, cyanide intoxication, tyramine, or electrical stimulation remained unaffected by TI. We propose a protective effect of TI on neural tissue, which may reduce norepinephrine-induced damage during prolonged myocardial ischemia.

Key Words: norepinephrine release • preconditioning • myocardial ischemia • rat hearts • anoxia

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