Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart

Y. F. Ding, Yulong Li, S. Y. Ho

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The effects of NO donor - L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-reperfusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min) -reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 ± 2.4% of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 ± 2.2% (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor - Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 ± 2.1% (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfusion myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP.

Original languageEnglish (US)
Pages (from-to)564-570
Number of pages7
JournalActa Physiologica Sinica
Volume48
Issue number6
StatePublished - Dec 1 1996

Fingerprint

Ischemic Preconditioning
Arginine
Rabbits
Myocardial Infarction
Reperfusion
Ischemia
Myocardial Reperfusion
Oxygen Consumption
Heart Ventricles
Myocardial Ischemia
Myocardium
Heart Rate
Hemodynamics
Blood Pressure

Keywords

  • L-arginine
  • ischemia-reperfusion
  • ischemic preconditioning
  • myocardial infarct size
  • nitro-L-arginine

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart. / Ding, Y. F.; Li, Yulong; Ho, S. Y.

In: Acta Physiologica Sinica, Vol. 48, No. 6, 01.12.1996, p. 564-570.

Research output: Contribution to journalArticle

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abstract = "The effects of NO donor - L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-reperfusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min) -reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 ± 2.4{\%} of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 ± 2.2{\%} (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor - Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 ± 2.1{\%} (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfusion myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP.",
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