Objective To investigate the effect of sevoflurane on the monophasic action potentials (MAPs) in isolated rat hearts after ischemia-reperfusion. Methods Twenty-four healthy SD male rats, weighing 280–320 g, were randomly divided into three groups after successful preparation of a Langendorff isolated heart perfusion model with a stabilization period perfusion of 15 min with Krebs–Henseleit (K–H) fluid (n = 8): the control group (group A, continuously perfused with K–H fluid for 105 min), the ischemia-reperfusion group (group B, continuously perfused with K–H fluid for 15 min, and then exposed to 60 min of global ischemia induced by Thomas solution followed by 30 min of reperfusion), and the sevoflurane group (group C, K–H fluid contained 1.0 MAC sevoflurane, and other procedures were same as in group B). Heart rate (HR) and MAPs including time course (MAPD50 or MAPD90) of the epicardium (Epi) and endocardium (Endo) were recorded at the time of balance perfusion for 15 min (T0), continuous perfusion for 15 min (T1), reperfusion for 15 min/continuous perfusion for 105 min (T2), and reperfusion for 30 min/continuous perfusion for 120 min (T3), and the transmural dispersion of repolarization (TDR) was calculated. The incidence of arrhythmia, time for restoration of spontaneous heart beat, and duration of arrhythmia were recorded during the period of reperfusion. Results HR in group B and group C was lower at T2 and T3 than that in group A, while that in group B was significantly lower than that in group A at T2 and T3, and HR in group C was higher than that in group B at T2 and T3 (P < 0.05). There was no difference of TDR in each group at T0 and T1 (P > 0.05), while TDR in group B was increased at T2 and T3 compared with that in group C and group A (P < 0.05). TDR in group C was decreased compared with that in group B at T2 and T3 (P < 0.05), while there was no such difference between group C and group A (P > 0.05). The time for restoration of spontaneous heart beat and duration of arrhythmia in group C were shorter than those in group B (P < 0.05), while cardiac arrhythmia scores in group B were higher than those in group C (P < 0.05). There was no difference of MAPD50 in each group (P > 0.05). The MAPD90 in group B was much longer than that in other groups at T2 and T3 (P < 0.05), while there was no such difference between group C and group A (P > 0.05). The prolonged MAPD90 at T2 and T3 in group B strikingly differed from that at T0 and T1 (P < 0.05). Nevertheless, there was no such difference in other groups at different time points (P > 0.05). Conclusion Sevoflurane alleviates reperfusion arrhythmia induced by myocardial ischemia-reperfusion through the shortening of MPAD90 in isolated rat hearts.
The objectives were to observe the effects of different concentrations of desflurane on QT, QTc, Tp-e, Tp-e/QT, and the index of cardiac electrophysiological balance (iCEB). Sixty patients were randomly divided into group D1, group D2, and group D3 by using a random number table, 20 in each group. After entering the operating room, patients received 10 mL/kg hydroxyethyl starch, 0.1 mg/kg midazolam, 0.1 mg/kg vecuronium, 3 μg/kg fentanyl, and 0.3 mg/kg etomidate intravenously and then accepted intubation and mechanical ventilation. The desflurane evaporator was opened. The concentrations of desflurane in the D1, D2, and D3 groups were maintained at 0.6, 1.3, and 2.0 minimum alveolar concentration (MAC), respectively. Twelve-lead ECGs were recorded at time before induction (T1) and at 20 min after desflurane reached the required concentration (T2). HR and MAP were recorded measure and the QT interval, QTc interval, Tp-e interval, Tp-e/QT ratio, and iCEB were calculated. Compared with before inhalation (T1), the QTc interval was prolonged in the D1, D2, and D3 groups after inhalation of different concentrations of desflurane for 20 min (T2) (P < 0.05) and the Tp-e/QT ratio decreased in the D1 and D2 groups at T2 (P < 0.05). Compared with the D1 and D2 groups, the Tp-e/QT ratio of the D3 group increased at T2 (P < 0.05). There was no significant difference in Tp-e interval and iCEB at any time (P > 0.05). The study suggested that inhalation of desflurane at a normal concentration cannot cause arrhythmogenic characteristics and affect the cardiac electrophysiological stability.
The aim of this study is to investigate the changes in QT, QTc, and Tp-e intervals and Tp-e/QT ratio on surface electrocardiogram (ECG) signals during anaesthesia induction using propofol or sevoflurane after preoperative cefuroxime infusion. Some 120 cases of gynaecological patients are randomly divided into propofol (P) and sevoflurane (S) groups (n=60). After cefuroxime (1.5 g) was infused in the two groups of patients, propofol target controlled infusion (TCI) was conducted in the P group for 5 min to realise a plasma concentration of 4 μg/ml while patients in the S group inhaled anaesthesia by infusing 1.3 MAC sevoflurane for 6 min. The 12-lead ECGs were separately collected before infusing cefuroxime (T1), after infusing cefuroxime (T2), and after infusing propofol or sevoflurane (T3) to measure QT and Tp-e intervals, calculate QTc and Tp-e/QT, and record MAP and HR. Finally, we demonstrated that QT, QTc, and Tp-e intervals and Tp-e/QT ratio had no change (P > 0.05) after cefuroxime infusion in the two groups of patients compared with that before infusing antibiotics. Moreover, after conducting preoperative cefuroxime infusion, using propofol and sevoflurane had no influence on Tp-e interval, but sevoflurane can significantly prolong QT and QTc intervals (P < 0.05).
Objective: To compare the value of ECG markers such as QT interval, Tp-e interval and index of cardiac electrophysiological balance (iCEB) in evaluating the effect of sevoflurane on cardiac electrophysiology. Methods: Sixty patients undergoing elective gynecological surgery were randomly divided into group S1, group S2 and group S3, 20 cases in each group. Patients were received 10ml/kg of hydroxyethyl starch, 0.1mg/kg of midazolam, 0.1 mg/kg of vecuronium, 3μg/kg of fentanyl and 0.3mg/kg of etomidate intravenously. Mechanical ventilation was performed after endotracheal intubation. Sevoflurane concentration was maintained at 0.6 MAC, 1.3 MAC and 2.0 MAC in group S1, group S2 and group S3 respectively. The QT interval, QRS interval and Tp-e interval were measured before anesthesia induction (T1), 5 minutes after tracheal intubation (T2), and 20 minutes after rising to the set concentration of sevoflurane (T3). The QTc interval, Tp-e/QT ratio and iCEB were measured and calculated. MAP and HR were recorded at the same time. Results Compared with T1-2, MAP and HR decreased at T3 in S1-3 group (P < 0.05); Compared with T1, iCEB increased at T2-3 in S1-3 groups, QTc interval prolonged at T3 in S1-3 groups (P < 0.05). Compared with T2, iCEB increased at T3 in S1-3 groups. Compared with S1 group , the Tp-e Shortened, iCEB increased in S2-3 groups . Compared with S2 group, iCEB decreased in S3 group at T3. Conclusion: iCEB is more sensitive and objective, and can better predict the risk of arrhythmia. iCEB can be used as the preferred index to evaluate the electrophysiological effects by anesthetics in clinic.
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