Sevoflurane preconditions stunned myocardium in septic but not healthy isolated rat hearts

R. Serita, Hiroshi Morisaki, K. Ai, Y. Morita, Y. Innami, T. Satoh, Shizuko Kosugi, Y. Kotake, J. Takeda

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background. Recent evidence indicates that sevoflurane treatment before prolonged ischaemia reduces infarct size in normal hearts, mimicking ischaemic preconditioning. We examined whether exposure to sevoflurane before brief ischaemia, inducing a 'stunned myocardium', provided such protective effects in an isolated working heart from normal or septic rats. Methods. With institutional approval, 91 rats were randomly allocated into one of either caecal-ligation and perforation (CLP: n=50) or sham (Sham: n=41) procedure groups 24 h before the study. After determination of baseline measurements, including cardiac output (CO), myocardial oxygen consumption (mVO2) and cardiac efficiency (CE; COpeak systolic pressure/mVO2), each isolated heart was perfused with or without 2% sevoflurane for 15 min before global ischaemia (pre-ischaemia). After 15 min ischaemia and 30 min reperfusion, all hearts were assessed for functional recovery of myocardium (post-reperfusion). Results. During the pre-ischaemia period, 2% sevoflurane caused a significant reduction of CO in the CLP group compared with the Sham group. During the post-reperfusion period, both CO (16.9 vs 11.0 ml min-1) and CE (11.2 vs 7.7 mm Hg ml-1 (μI O2)-1) was higher in the sevoflurane-treated vs -untreated hearts from CLP rats, and was accompanied by lower incidence of reperfusion arrhythmia compared with control hearts (8 vs 32%). In contrast, 2% sevoflurane did not provide cardioprotective effects in normal rats. Conclusions. The current study demonstrates that pre-treatment with sevoflurane minimizes myocardial dysfunction and the incidence of reperfusion arrhythmia after brief ischaemic insults in septic hearts.

Original languageEnglish
Pages (from-to)896-903
Number of pages8
JournalBritish Journal of Anaesthesia
Volume89
Issue number6
DOIs
Publication statusPublished - 2002 Dec 1

Fingerprint

Myocardial Stunning
Ischemia
Reperfusion
Cardiac Output
Cardiac Arrhythmias
Ischemic Preconditioning
Incidence
sevoflurane
Oxygen Consumption
Ligation
Myocardium
Blood Pressure
Therapeutics

Keywords

  • Anaesthetics volatile, sevoflurane
  • Heart, reperfusion arrhythmia
  • Infection, sepsis

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Sevoflurane preconditions stunned myocardium in septic but not healthy isolated rat hearts. / Serita, R.; Morisaki, Hiroshi; Ai, K.; Morita, Y.; Innami, Y.; Satoh, T.; Kosugi, Shizuko; Kotake, Y.; Takeda, J.

In: British Journal of Anaesthesia, Vol. 89, No. 6, 01.12.2002, p. 896-903.

Research output: Contribution to journalArticle

Serita, R. ; Morisaki, Hiroshi ; Ai, K. ; Morita, Y. ; Innami, Y. ; Satoh, T. ; Kosugi, Shizuko ; Kotake, Y. ; Takeda, J. / Sevoflurane preconditions stunned myocardium in septic but not healthy isolated rat hearts. In: British Journal of Anaesthesia. 2002 ; Vol. 89, No. 6. pp. 896-903.
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T1 - Sevoflurane preconditions stunned myocardium in septic but not healthy isolated rat hearts

AU - Serita, R.

AU - Morisaki, Hiroshi

AU - Ai, K.

AU - Morita, Y.

AU - Innami, Y.

AU - Satoh, T.

AU - Kosugi, Shizuko

AU - Kotake, Y.

AU - Takeda, J.

PY - 2002/12/1

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N2 - Background. Recent evidence indicates that sevoflurane treatment before prolonged ischaemia reduces infarct size in normal hearts, mimicking ischaemic preconditioning. We examined whether exposure to sevoflurane before brief ischaemia, inducing a 'stunned myocardium', provided such protective effects in an isolated working heart from normal or septic rats. Methods. With institutional approval, 91 rats were randomly allocated into one of either caecal-ligation and perforation (CLP: n=50) or sham (Sham: n=41) procedure groups 24 h before the study. After determination of baseline measurements, including cardiac output (CO), myocardial oxygen consumption (mVO2) and cardiac efficiency (CE; COpeak systolic pressure/mVO2), each isolated heart was perfused with or without 2% sevoflurane for 15 min before global ischaemia (pre-ischaemia). After 15 min ischaemia and 30 min reperfusion, all hearts were assessed for functional recovery of myocardium (post-reperfusion). Results. During the pre-ischaemia period, 2% sevoflurane caused a significant reduction of CO in the CLP group compared with the Sham group. During the post-reperfusion period, both CO (16.9 vs 11.0 ml min-1) and CE (11.2 vs 7.7 mm Hg ml-1 (μI O2)-1) was higher in the sevoflurane-treated vs -untreated hearts from CLP rats, and was accompanied by lower incidence of reperfusion arrhythmia compared with control hearts (8 vs 32%). In contrast, 2% sevoflurane did not provide cardioprotective effects in normal rats. Conclusions. The current study demonstrates that pre-treatment with sevoflurane minimizes myocardial dysfunction and the incidence of reperfusion arrhythmia after brief ischaemic insults in septic hearts.

AB - Background. Recent evidence indicates that sevoflurane treatment before prolonged ischaemia reduces infarct size in normal hearts, mimicking ischaemic preconditioning. We examined whether exposure to sevoflurane before brief ischaemia, inducing a 'stunned myocardium', provided such protective effects in an isolated working heart from normal or septic rats. Methods. With institutional approval, 91 rats were randomly allocated into one of either caecal-ligation and perforation (CLP: n=50) or sham (Sham: n=41) procedure groups 24 h before the study. After determination of baseline measurements, including cardiac output (CO), myocardial oxygen consumption (mVO2) and cardiac efficiency (CE; COpeak systolic pressure/mVO2), each isolated heart was perfused with or without 2% sevoflurane for 15 min before global ischaemia (pre-ischaemia). After 15 min ischaemia and 30 min reperfusion, all hearts were assessed for functional recovery of myocardium (post-reperfusion). Results. During the pre-ischaemia period, 2% sevoflurane caused a significant reduction of CO in the CLP group compared with the Sham group. During the post-reperfusion period, both CO (16.9 vs 11.0 ml min-1) and CE (11.2 vs 7.7 mm Hg ml-1 (μI O2)-1) was higher in the sevoflurane-treated vs -untreated hearts from CLP rats, and was accompanied by lower incidence of reperfusion arrhythmia compared with control hearts (8 vs 32%). In contrast, 2% sevoflurane did not provide cardioprotective effects in normal rats. Conclusions. The current study demonstrates that pre-treatment with sevoflurane minimizes myocardial dysfunction and the incidence of reperfusion arrhythmia after brief ischaemic insults in septic hearts.

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