Background. Some of the cellular targets affected by volatile anaesthetics (e.g. halothane) which contribute to the negative inotropic effects of these agents are also affected during the progression of diabetic cardiomyopathy. A previous report suggested that halothane inhibited contraction to a lesser extent in papillary muscle from diabetic animals and so the aim of this study was to investigate possible mechanisms underlying this effect. Methods. Contractility and cytosolic calcium ion (Ca2+) transients were measured (fura-2) in ventricular myocytes isolated from control and streptozotocin (STZ)-induced diabetic rats in the absence and presence of halothane 0.6 mmol litre-1 at 1 Hz stimulation. Sarcoplasmic reticulum (SR) Ca2+ content was assessed by rapid application of caffeine. All experiments were carried out at 36-37°C. Results. The amplitude of shortening, the electrically evoked Ca2+ transient, SR Ca2+ content and myofilament Ca2+ sensitivity, though not altered by STZ treatment, were significantly reduced by halothane to a similar extent in control and STZ myocytes. The time course of contraction and Ca2+ transient were prolonged in myocytes from STZ-treated rats compared with controls but this was not altered further by halothane. STZ treatment appeared to reduce Ca2+ efflux from the cell, an effect reversed by halothane. Conclusions. In contrast to a previous report, we could find no evidence of amelioration of the negative inotropic effect of halothane in myocytes from the STZ-induced diabetic rat. Contractility, the cytosolic Ca2+ transient, SR Ca2+ content and myofilament Ca2+ sensitivity were qualitatively similar in control and STZ myocytes and were all depressed to the same extent by halothane.
- Anaesthetics volatile, halothane
- Antibiotics, streptozotocin
- Complications, diabetes
- Heart, ventricular myocytes
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine