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European Journal of Anaesthesiology:
Abstracts and Programme: EUROANAESTHESIA 2011: The European Anaesthesiology Congress: ESA Best Abstract Prize Competition (BAPC)

Mild hypothermia induced cardioprotection against ischemia/reperfusion injury mediated by nitric oxide in rat isolated heart model: BAPCPC1‐5

Mochizuki, T.; Yu, S.; Katoh, T.; Aoki, K.; Sato, S.

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Hamamatsu University School of Medicine, Department of Emergency Medicine, Hamamatsu, Japan

Introduction: Hypothermia is a promising cardioprotective treatment for cardiac arrest. Previously, deep hypothermia of 32°C induced during ischemia and reperfusion exhibited a cardioprotective effect in a cardiomyocyte model of ischemia/reperfusion (I/R) injury 1). However, it remains unknown whether mild hypothermia used in the clinical setting, or late induction exhibit cardioprotective effects. We hypothesized that mild 34°C hypothermia immediately after reperfusion would be cardioprotective in a rat isolated heart model. We also investigated whether the cardioprotective effect was mediated by nitric oxide (NO).

Methods: Male SD rats were anesthetized by diethyl ether followed by thoracotomy. After isolation, the heart was perfused at a constant pressure of 70 cm H2O, 37°C. Hemodynamic variables, coronary flow (CF), and perfusion temperatures were measured at baseline (control), immediately before 30 min global ischemia, immediately after reperfusion (reperfusion period), 10 min and 180 min after reperfusion. Rats were randomly divided into

a) control,

b) 34°C hypothermia induced by cooling of perfusate during the 30 min global ischemia and consecutive hypothermia period (ischemia group),

c) 34°C hypothermia induced during the reperfusion period (reperfusion group),

d) 34°C hypothermia induced during the reperfusion period with 400 mM L‐NAME (reperfusion/L‐NAME group).

The %LV infarct size was assessed by TTC staining. Results are expressed as mean±SD. Data were compared by two way repeated measured of ANOVA followed by Tukey‐Kramer post hoc test. P< 0.05 was considered as significance.

Results: Hypothermia reduced the %LV infarct size when induced:

1) during global ischemia; from 51.9±19.7% (control) to 11.9±6.3% (ischemia, p< 0.001), or

2) after reperfusion (23.5±10.5%; p=0.002). L‐NAME reversed the reduction of infarct size to 42.5±10.6% (p>0.5).

Temperatures of perfusate reached 34°C within 5 min after the start of cooling in all cases except for the control group.

Conclusions: Hypothermia exhibited a cardioprotective effect even when hypothermia was induced during the reperfusion period in the whole organ model. This suggests that inducing hypothermia of 34°C as quick as possible, even if induction of hypothermia is late by after cardiac arrest, contribute to the cardioprotective effect of mild hypothermia. The cardioprotective effect of mild hypothermia from I/R injury was mediated by NO.

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References:

1) Am J Physiol Heart Circ Physiol 2010

© 2011 European Society of Anaesthesiology

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