Abstract
The effects of propofol and thiopentone on myocardial contractility and global ischaemia were evaluated using an isolated non-working perfused rat heart preparation. Contractility was assessed using a tension transducer linked to the cardiac apex, and the contractility was expressed as a ratio of the deflection size before and after infusion of the drug. Ischaemia-induced leakage of myocardial proteins and ions (potassium and magnesium) was assessed by comparing the concentrations in the effluent perfusate immediately before and after 60 min of isothermic ischaemia, in the presence of propofol, thiopentone or plain Krebs’ buffer solution (control). Mean contractility ratios of 1.15 and 1.3 were obtained with control and propofol groups respectively (NS), but were reduced to 0.5 in the thiopentone group (P < 0.001). The magnitude of the postischaemic leakage of proteins and potassium was similar in each group; however, the post-ischaemic leakage of magnesium was greater in the thiopentone group than in the propofol or control groups. These data suggest that, compared with thiopentone, propofol is not a potent negative inotrope, and that it may cause less disturbance of myocardial magnesium homeostasis during myocardial ischaemia.
Résumé
Les effets du propofol el du thiopentone sur la contractilité myocardique et l’ischémie globale furent évalués utilisant une préparation isolée de cœur de rat perfusé au repos. La contractilité fut évaluée utilisant un transducteur de pression lié à l’apex et la contractilité fut exprimée par le ratio de la déflection avant et après perfusion des médicaments. La fuite des protéines myocardiques et des ions (potassium et magnésium) induite par ischémie fut évaluée en comparant des concentrations à la sortie dans le liquide de perfusion immédiatement avant et après 60 minutes d’ischémie isothermique en présence de propofol, thiopentone ou une solution de Krebs (contrôle). Des ratios de contractilité moyenne de 1.15 et 1.3 furent obtenus dans les groupes controle et propofol respectivement (NS), mais furent diminués à 0.5 dans le groupe thiopentone (P < 0.001). L’étendue de la fuite post-ischémique des protéines et du potassium était similaire dans chaque groupe, cependant elle etait plus grande pour le magnésium dans le groupe thiopentone comparativement aux groupes controle et propofol. Ces données suggèrent que comparativement au thiopentone, le propofol ne possède pas un effet inotrope négatif puissant et qu’il peut causer moins de perturbation de l’homéostasie du magnésium myocardique lors de l’ischémie myocardique.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Patrick MR, Blair IJ, Feneck RO, Sebel PS. A comparison of the haemodynamic effects of propofol and thiopentone in patients with coronary artery disease. Postgrad Med J 1985; 62 (Suppl): 23–7.
Clayes MA, Gepts E, Camu F. Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth 1988; 60: 3–9.
Coates DP, Monk CR, Prys-Roberts C, Turtle M. Haemodynamic effects of infusion of the emulsion formulation of propofol during nitrous oxide anaesthesia in humans. Ancsth Analg 1987; 66: 64–70.
Pinaud M, LePage JY, Juge C, Helias J, Cozian A, Souron R. Joint isotope and haemodynamic studies of the effects of propofol on left ventricular function in the patient suffering from coronary heart disease. Ann Fr Anesth Reanim 1987; 6: 243–6.
Kling D, Bachmann B, Moosdorf R, Hempelmann G. The haemodynamic effects of propofol with midazolam: a study in patients undergoing coronary surgery. Der Ancsthesist 1987; 36: 640–5.
Van Aken H, Brussel T. Propofol causes cardiovascular depression 11 (Letter). Anesthesiology 1990; 72: 394–5.
Sebel PS, Lowden JD. Propofol: a new intravenous anesthetic. Anesthesiology 1989; 71: 260–77.
Sebel PS, Lowden JD. (Letter). Anesthesiology 1990; 72: 396.
Monk CR, Coates DP, Prys-Roberts C, Turtle MJ, Spelina K. Hacmodynamic effects of a prolonged infusion of propofol as a supplement to nitrous oxide anaesthesia. Br J Anacsth 1987; 54: 954–60.
Garvey E, Counihan TB, Ryan MP. Investigation of cardioprotection by (3-adrenoreceptor antagonists in clinical and experimental myocardial infarction. Br J Pharmacol 1983; 80: 698–9.
Nayler WG. Bcta-blockers in experimental myocardial infarction. Acta Med Scand 1981; 651 (Suppl): 139–45.
Iseri LT, French JH. Magnesium: nature’s physiological calcium channel blocker. Am Heart J 1984; 108: 188–93.
Sheehan JP, Seelig MS. Interactions of magnesium and potassium in the pathogencsis of cardiovascular diseases. Magnesium 1984; 3: 301–14.
Ryan MP. Diuretics and potassium/magnesium depletion. Directions for treatment. Am J Med 1987, 82: 38–47.
Bersohn MM, Shine KI, Sterman WD. Effects of increased magnesium on recovery from ischaemia in rat and rabbit hearts. Am J Physiol 1982; 242: H89-H93.
Hearst DJ, Stewart DA, Braimbridge MV. Myocardial protection during ischemic cardiac arrest. J Thorac Cardiovasc Surg 1978; 75: 877–85.
Goodchild CS, Serrao JM. Cardiovascular effects of propofol in the anaesthetized dog. Br J Anacsth 1989; 63: 87–92.
Becker KE. Plasma levels of thiopental necessary for anesthesia. Anesthesiology 1978; 49: 192–6.
Spelina KR, Coates DP, Monk CR, Prys-Roberts C, Norley I, Turtle MJ. Dose requirements of propofol by infusion during nitrous oxide anaesthesia in man. Br J Anacsth 1984; 58: 1080–4.
Servin F, Desmonts JM, Haberer JP, Cockshott ID, Plummer GF, Farinotti R. Pharmacokinetics and protein binding of propofol in patients with cirrhosis. Anesthesiology 1988; 69: 887–91.
Rusy BF, Komai H. Anesthetic depression of myocardial contractility: a review of possible mechanisms. Anesthesiology 1987; 67: 87–92.
Hirche HJ, Franz L, Bos R, Bissig RL, Schamm M. Myocardial extracellular hydrogen ion and potassium increase and noradrenaline release as a possible cause of arrhythmias following acute coronary occlusion in pigs. J Mol Cell Cardiol 1980; 12: 579–93.
Watts JA, Koch CD, LaNone KF. Effects of calcium on energy metabolism: calcium and heart function after ischaemia. Am J Physiol 1980; 238: H909-H916.
Borchgrevink PC, Bergan AS, Bakoy OE, Jynge P. Magnesium and repcrfusion of ischemic rat heart as assessed by P-31N.M.R. Am J Physiol 1989; 225: H1-H8.
Matsuda H. Open-state substructure of inwardly rectifying potassium channels revealed by magnesium block in guinea pig heart cells. J Physiol 1988; 397: 237–58.
Kerrick WGL, Donaldson SDB. Effects of magnesium on submaximal calcium activated tension in skinned fibres of frog skeletal muscle. Biochim Biophys Acta 1972; 4: 367–74.
Turlapaty PD, Altura BD. Magnesium deficiency produces spasm of the coronary arteries: relationships to etiology of sudden death in ischemic heart disease. Science 1980; 208: 198–200.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Kavanagh, B.P., Ryan, M.P. & Cunningham, A.J. Myocardial contractility and ischaemia in the isolated perfused rat heart with propofol and thiopentone. Can J Anaesth 38, 634–639 (1991). https://doi.org/10.1007/BF03008201
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF03008201