TEMPERATURE MODULATES CALCIUM HOMEOSTASIS AND VENTRICULAR ARRHYTHMIASIN MYOCARDIAL PREPARATIONS

Citation
G. Gambassi et al., TEMPERATURE MODULATES CALCIUM HOMEOSTASIS AND VENTRICULAR ARRHYTHMIASIN MYOCARDIAL PREPARATIONS, Cardiovascular Research, 28(3), 1994, pp. 391-399
Citations number
50
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086363
Volume
28
Issue
3
Year of publication
1994
Pages
391 - 399
Database
ISI
SICI code
0008-6363(1994)28:3<391:TMCHAV>2.0.ZU;2-B
Abstract
Objective: The aim was to evaluate the effect of temperature on reoxyg enation induced ventricular arrhythmias in isolated hearts, on delayed after depolarisations and I-ti current in Purkinje fibres, and on sar coplasmic reticular function and Ca2+ handling of single cardiac myocy tes. Methods: Isolated guinea pig hearts were retrogradely perfused at 37 degrees C with a hypoxic medium for 15 min and reoxygenated for 10 min either at 33 degrees C or at 37 degrees C. Intracellular microele ctrodes were used to assess the presence of delayed afterdepolarisatio ns and triggered activity in sheep Purkinje fibres exposed to strophan thidin at different temperatures. I-ti current was evaluated in voltag e clamp experiments. In rat cardiomyocytes, loaded with the fluorescen t Ca2+ dye, indo-1, the sarcoplasmic reticular Ca2+ content was assess ed at 30 degrees C and at 37 degrees C, either by a caffeine spritz pu ffed onto a cell from a patch pipette or by a post-rest contraction. R esults: Hypothermic reoxygenation reduced the incidence of ventricular arrhythmias in isolated hearts (30%, n = 10, at 33 degrees C and 75%, n = 30, at 37 degrees C, p < 0.05). In Purkinje fibres, hypothermia d ecreased the amplitude of delayed afterdepolarisations. Moreover, at 3 2 degrees C, the amplitude of I-ti current was decreased to 59.2(SEM 2 .6)% of the normothermic value [27.5(6.7) nA, n = 4, p < 0.005] and ti me to peak increased to 159.7(10.2)% [value at 37 degrees C = 470(41) ms, n = 4, p < 0.01]. In cardiac cells, sarcoplasmic reticular Ca2+ re lease induced by caffeine spritz or by post-rest contraction was incre ased at 30 degrees C. However, following a pacing period at 1 Hz, hypo thermia prolonged the time to onset of the first spontaneous Ca2+ osci llation [59(14) s at 30 degrees C and 27(9) s at 37 degrees C, n = 5, p < 0.05] and reduced the oscillation frequency [1.1(0.4) min(-1) at 3 0 degrees C and 3.1(0.9) min(-1) at 37 degrees C, n = 5, p < 0.05]. Co nclusions: Mild hypothermia increases sarcoplasmic reticular Ca2+ cont ent but decreases the likelihood of spontaneous Ca release. This may e xplain the reduction of delayed afterdepolarisations and I-ti current amplitude in Purkinje fibres and it could represent a mechanism for th e protection provided by hypothermia against ventricular arrhythmias.