Canadian Journal of Anesthesia

, 48:784 | Cite as

Thiopentone does not block ischemic preconditioning in the isolated rat heart

  • J. Müllenheim
  • A. Molojavyi
  • B. Preckel
  • V. Thämer
  • W. Schlack
Cardiothoracic Anesthesia, Respiration and Airway



Ischemic preconditioning protects the heart against subsequent prolonged ischemia by opening of adenosine triphosphate-sensitive potassium (KATP) channels. Thiopentone blocks KATP channels in isolated cells. Therefore, we investigated the effects of thiopentone on ischemic preconditioning.


Isolated rat hearts (n = 56) were subjected to 30 min of global no-flow ischemia, followed by 60 min of reperfusion. Thirteen hearts underwent the protocol without intervention (control, CON) and in 11 hearts (preconditioning, PC), ischemic preconditioning was elicited by two five-minute periods of ischemia. In three additional groups, hearts received 1 (Thio 1,n = 11), 10(Thio 10,n = 11) or 100 μg·mL−1 (Thio 100,n = 10) thiopentone for five minutes before preconditioning. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial performance and cellular injury, respectively.


Recovery of LV developed pressure was improved by ischemic preconditioning (after 60 min of reperfusion, mean ± SD: PC, 40 ± 19% of baseline) compared with the control group (5 ± 6%,P < 0.0l) and this improvement of myocardial function was not altered by administration of thiopentone (Thio 1, 37 ± 15%; Thio 10, 36 ± 16%; Thio 100, 38 ± 16%,P=0.87–0.99 vs PC). Total CK release over 60 min of reperfusion was reduced by preconditioning (PC, 202 ± 82 U·g−1 dry weight) compared with controls (CON, 383 ± 147 U·g−1,P < 0.0l) and this reduction was not affected by thiopentone (Thio 1, 213 ± 69 U·g−1; Thio 10, 211 ± 98U·g−1; Thio 100, 258 ± 128 U·g−1,P=0.62–1.0vs PC).


These results indicate that thiopentone does not block the cardioprotective effects of ischemic preconditioning in an isolated rat heart preparation.

Le thiopental n’entrave pas le préconditionnement ischémique dans le cœur de rat isolé



Le préconditionnement ischémique protège le cœur contre l’ischémie ultérieure prolongée en ouvrant les canaux potassiques sensibles à l’adénosine triphosphate (KATP). Or, le thiopental bloque les canaux KATP dans des cellules isolées. Nous avons donc recherché les effets du thiopental sur le préconditionnement ischémique.


Des cœurs de rats isolés (n = 56) ont été soumis à 30 min d’ischémie globale à débit nul, puis de 60 min, à une reperfusion. Treize cœurs ont subi le protocole sans intervention (témoin, TEM) et dans onze cœurs (groupe de préconditionnement, PC) le préconditionnement ischémique a été amorcé par deux périodes de cinq minutes d’ischémie. Dans trois groupes additionnels, les cœurs ont reçu 1 (Thio 1, n = 11), 10 (Thio 10, n = 11) ou 100 μg·mL−1 (Thio 100, n = 10) de thiopental pendant cinq minutes avant le préconditionnement. La pression du ventricule gauche (VG) développée et la libération de créatine kinase (CK) ont été mesurées en qualité de variables de la performance myocardique et de la lésion cellulaire, respectivement.


La récupération de la pression du VG développée a été améliorée par le préconditionnement ischémique (après 60 min de reperfusion, la moyenne ± l’écart type : PC, 40 ± 19 % de la mesure de base) comparée au groupe témoin (5 ± 6 %, P < 0,01). Cette amélioration de la fonction myocardique n’a pas été modifiée par l’administration de thiopental (Thio 1, 37 ± 15 %; Thio 10, 36 ± 16 %; Thio 100, 38 ± 16%, P = 0,87 - 0,99 vs PC). La libération totale de CK après 60 min de reperfusion a été réduite par le préconditionnement (PC, 202 ± 82 U·g−1 de poids anhydre) comparé au témoin (TEM, 383 ± 147 U·g−1, P < 0,01) et cette réduction n’a pas été affectée par le thiopental (Thio 1, 213 ± 69 U·g−1; Thio 10, 211 ± 98 U·g−1; Thio 100, 258 ± 128 U·g−1, P = 0,62– 1,0 vs PC).


Ces résultats indiquent que le thiopental ne bloque pas les effets cardioprotecteurs du préconditionnement ischémique dans une préparation de cœur de rat isolé.


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Copyright information

© Canadian Anesthesiologists 2001

Authors and Affiliations

  • J. Müllenheim
    • 1
  • A. Molojavyi
    • 2
  • B. Preckel
    • 1
  • V. Thämer
    • 2
  • W. Schlack
    • 1
  1. 1.Klinik für Anaesthesiologie Heinrich-Heine-UniversitätDüsseldorfGermany
  2. 2.Department of Physiology, Institut IHeinrich-Heine-UniversitätDüsseldorfGermany

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