What question did this study set out to answer?

To determine whether the cardioprotective preconditioning effect of isoflurane is mediated through adenosine triphosphate-sensitive potassium channels and adenosine receptors in rabbits.

March 1, 1999AnesthesiologyOpen Access

Mechanisms of Isoflurane-induced Myocardial Preconditioning in Rabbits

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Why the study?

Does isoflurane preconditioning reduce myocardial infarct size in rabbits, and is this mediated by ATP-sensitive potassium channels and adenosine receptors?

Population

Propofol-anesthetized rabbits subjected to 30 min of anterolateral coronary occlusion followed by 3 h of…

Comparison

Isoflurane preconditioning, with or without… vs No pretreatment, ischemia preconditioning…

Design

Preclinical

Follow-up

3 hours of reperfusion

Authors

MIMohamed S. IsmaeilCairo University ITI. I. TkachenkoUniversity of California, San Francisco KGKurt GamperlMemorial University of Newfoundland

Discussion

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Implication

Isoflurane preconditioning may reduce infarct size via KATP/adenosine pathways in rabbits; leaves open translation to clinical cardioprotection.

Key Points

To determine whether the cardioprotective preconditioning effect of isoflurane is mediated through adenosine triphosphate-sensitive potassium channels and adenosine receptors in rabbits.
Propofol-anesthetized rabbits across seven experimental groups underwent 30 minutes of anterolateral coronary occlusion followed by 3 hours of reperfusion.
Pretreatments included ischemic preconditioning, 1.1% end-tidal isoflurane, isoflurane preceded by the K_ATP channel blocker glyburide (0.33 mg/kg IV) or the adenosine receptor antagonist SPT (7.5 mg/kg IV), and blocker-only controls.
Myocardial infarct size and area at risk were determined by histological staining and compared using analysis of variance or covariance.
Ischemic preconditioning and isoflurane preconditioning significantly reduced infarct size as a percentage of the area at risk to 8.3 ± 5% and 13.4 ± 8.2%, respectively, compared to 30.2 ± 11% in controls (P < 0.05).
Pretreatment with either glyburide or SPT eliminated the cardioprotective effect of isoflurane, producing infarct sizes of 30.0 ± 9.1% and 29.2 ± 12.6% (P = not significant vs. control).
Administration of glyburide alone (33.9 ± 7.6%) or SPT alone (31.8 ± 12.7%) did not significantly alter infarct size compared to control hearts.

Structured PICO

Does isoflurane preconditioning reduce myocardial infarct size in rabbits, and is this mediated by ATP-sensitive potassium channels and adenosine receptors?

Population

Propofol-anesthetized rabbits subjected to 30 min of anterolateral coronary occlusion followed by 3 h of reperfusion

Intervention

Isoflurane preconditioning (15 min end-tidal isoflurane, 1.1%, then 15 min washout), with or without glyburide (0.33 mg/kg IV) or 8-(p-sulfophenyl)-theophylline (SPT) (7.5 mg/kg IV)

Comparator

No pretreatment (control), ischemia preconditioning (5 min occlusion, 15 min reperfusion), glyburide alone, or SPT alone

Outcome

Myocardial infarct size expressed as a percentage of the area at risk (IS:AR)surrogate

Isoflurane-induced myocardial preconditioning in rabbits is mediated by activation of ATP-sensitive potassium channels and adenosine receptors.

Cite This Study

Ismaeil et al. (1999) studied this question.

synapsesocial.com/papers/6a8535a9dc9e7acb57f247a2 https://doi.org/10.1097/00000542-199903000-00024

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Implication

Isoflurane preconditioning may reduce infarct size via KATP/adenosine pathways in rabbits; leaves open translation to clinical cardioprotection.

Mechanisms of Isoflurane-induced Myocardial Preconditioning in Rabbits

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Mechanisms of Isoflurane-induced Myocardial Preconditioning in Rabbits

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider