The effects of intravenous anesthetics on QT interval during anesthetic induction with sevoflurane.

PURPOSE: Sevoflurane is known to prolong the QT interval. This study aimed to determine the effect of the interaction between intravenous anesthetics and sevoflurane on the QT interval. METHODS: The study included 48 patients who underwent lumbar spine surgery. Patients received 3 µg/kg fentanyl and were then randomly allocated to either Group T, in which they received 5 mg/kg thiamylal, or Group P, in which they received 1.5 mg/kg propofol, at 2 min after administration of fentanyl injection for anesthetic induction. Vecuronium (1.5 mg/kg) and sevoflurane (3 % inhaled concentration) were administered immediately after loss of consciousness and tracheal intubation was performed 3 min after vecuronium injection. Heart rate (HR), mean arterial pressure (MAP), bispectral index score (BIS), and the heart rate-corrected QT (QTc) interval on a 12-lead electrocardiogram were recorded immediately before fentanyl administration (T1), 2 min after fentanyl injection (T2), immediately before intubation (T3), and 2 min after intubation (T4). RESULTS: There were no significant differences between the two groups in baseline patient characteristics. BIS and MAP significantly decreased after anesthesia induction in both groups. At T3, MAP in Group T was higher than in Group P, while HR had reduced in both groups. The QTc interval was prolonged after anesthesia induction in Group T, but did not change at any time point in Group P. The QTc interval after anesthesia induction in Group T was longer than in Group P. CONCLUSION: We concluded that an injection of propofol could counteract QTc interval prolongation associated with sevoflurane anesthesia induction.

An observational study of the association between microalbuminuria and increased N-terminal pro-B-type natriuretic peptide in patients with subarachnoid hemorrhage.

BACKGROUND: The urinary albumin/creatinine ratio (ACR) is a significant neurologic prognostic predictor in patients with aneurysmal subarachnoid hemorrhage (SAH). B-type natriuretic peptide (BNP) plays an important role in body fluid regulation in patients with SAH. The present study was performed to determine whether ACR was independent predictor for unfavorable neurological outcome and ACR was associated with increased N-terminal pro-BNP (NT-pro-BNP) after SAH. METHODS: We studied 61 patients undergoing surgery who were admitted within 48 h after aneurysmal SAH onset between July 2008 and June 2010. Hunt and Hess grade and Fisher grade were recorded at admission. The Glasgow Coma Scale (GCS) score was calculated at admission and daily for seven postoperative days. Arterial blood was sampled at admission and for seven postoperative days to determine the PaO2/FIO2 ratio, C-reactive protein level, troponin I level, and NT-pro-BNP level. Urine was sampled at admission and daily for seven postoperative days to determine ACR and vanillylmandelic acid/creatinine ratio (VMACR). Neurological outcomes were assessed at hospital discharge by using the Glasgow Outcome Scale. Receiver operating characteristic curves were constructed for the predictive variables of unfavorable neurological outcomes, and the area under the curve (AUC) was determined. Multivariate logistic regression analyses were performed for the significant predictors of unfavorable neurological outcomes after SAH. Associations with NT-pro-BNP were evaluated by using the Spearman rank correlation test. RESULTS: Of the 61 patients, 24 had unfavorable outcomes. The prevalence rate of microalbuminuria was 85 % (52/61). The highest NT-pro-BNP levels were above the normal range in 57 of 61 patients (93 %). According to the AUC, the Hunt and Hess grade, GCS score, the highest ACR, and highest VMACR were significant predictors of neurological outcome. Multivariate logistic regression analyses showed that the highest ACR and Hunt and Hess grade are independent prognostic predictors of unfavorable neurological outcomes. The highest NT-pro-BNP significantly correlated with the highest troponin I, highest ACR, and VMACR on admission. CONCLUSIONS: The highest ACR is an independent prognostic predictor of unfavorable neurological outcomes after SAH. Moreover, plasma NT-pro-BNP elevation may be associated with the development of microalbuminuria.

[The Interaction of Low-dose Droperidol, Propofol, and Sevoflurane on QTc Prolongation].

BACKGROUND: Droperidol is an effective antiemetic, but its use is limited because of the warning of drug-induced QT prolongation. Some reports showed that low-dose droperidol does not significantly probing QT interval. This study was aimed to determine the effect of low-dose droperidol (1.25 and 2.5 mg) on QTc interval, and the interaction among droperidol, propofol and sevoflurane. METHODS: Patients received either 1.25 mg (group L : n = 25) or 2.5 mg (group H : n = 25) droperidol, and fentanyl (3 µg x kg(-1)) was administered 2.5 min later. One minute after fentanyl administration, anesthesia was induced using propofol (1.5 mg x kg(-1)) and vecuronium. One minute after propofol administration, sevoflurane (3%) was started. Tracheal intubation was performed 3 min after propofol administration, and then sevoflurane was reduced to 1%. RESULTS: Compared to baseline, the QTc interval in group L was unchanged by droperidol. In group H, the QTc interval was significantly prolonged after droperidol injection, but recovered after propofol injection. After tracheal intubation, QTc interval was significantly prolonged in both groups. CONCLUSIONS: Droperidol's effect on QTc prolongation was shown at the dose of 2.5 mg but not 1.25 mg. This prolongation effect was offset by propofol, and was unchanged by sevoflurane.

Milrinone-induced postconditioning reduces hepatic ischemia-reperfusion injury in rats: the roles of phosphatidylinositol 3-kinase and nitric oxide.

BACKGROUND: Ischemic postconditioning (PostC) protects the liver against ischemia-reperfusion (IR) injury. Milrinone, a phosphodiesterase 3 inhibitor, has been reported to exhibit preconditioning properties against hepatic IR injury; however, its PostC properties remain unknown. This study investigated whether milrinone has PostC properties against hepatic IR injury and the roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS). MATERIALS AND METHODS: Male Wistar rats were separated into six groups: (1) group S: animals that underwent sham operation without ischemia, (2) group C: ischemia followed by reperfusion with no other intervention, (3) group M: milrinone administered immediately after reperfusion, (4) group MW: wortmannin, a PI3K inhibitor, injected before milrinone administration, (5) group MN: l-NAME, a NOS inhibitor, injected before milrinone administration, and (6) group MD, milrinone administered 30 min after reperfusion. Except for group S, all groups underwent 1 h of warm ischemia of median and left lateral lobes, followed by 5 h of reperfusion. Biochemical liver function analysis and histologic examination were performed. RESULTS: Serum aspartate aminotransferase, alanine aminotransferase, and lactic dehydrogenase levels, histologic damage scores, and apoptotic rate in group M were significantly lower than those in group C. The inhibition of PI3K or NOS prevented this protective effect. Milrinone administered 30 min after reperfusion did not show obvious protective effects. CONCLUSIONS: Milrinone-induced PostC protects against hepatic IR injury when it is administered immediately after reperfusion, and PI3K and NOS may play an important role in this protective effect.

The interaction of antiemetic dose of droperidol with propofol on QT interval during anesthetic induction.

PURPOSE: We investigated the effect of low-dose droperidol on heart rate-corrected QT (QTc) interval and interaction with propofol. METHODS: Seventy-two patients undergoing upper limb surgery were included in this study. Patients were randomly allocated to one of three groups: group S (n = 24), which received 1 ml saline; group D1 (n = 24), which received 1.25 mg droperidol; or group D2 (n = 24), which received 2.5 mg droperidol. One minute later, fentanyl (3 µg/kg) was administered. Two minutes after fentanyl administration, anesthesia was induced using propofol (1.5 mg/kg) and vecronium. Tracheal intubation was performed 3 min after the administration of propofol. Heart rate, mean arterial pressure, bispectral index, and QTc interval were recorded at the following time points: immediately before the droperidol injection (baseline); 3 min after the saline or droperidol injection; 3 min after the propofol injection; and 2 min after tracheal intubation. RESULTS: Compared to baseline, the QTc interval in group S and group D1 was significantly shorter after propofol injection, but recovered after tracheal intubation. In group D2, the QTc interval was significantly prolonged after droperidol injection, but recovered after propofol injection, and was significantly prolonged after tracheal intubation. CONCLUSIONS: We found that saline or 1.25 mg droperidol did not prolong QTc interval, whereas 2.5 mg droperidol prolonged the QTc interval significantly, and that propofol injection counteracted the prolongation of the QTc interval induced by 2.5 mg droperidol.

Differential effects of propofol and sevoflurane on QT interval during anesthetic induction.

There have been conflicting reports on whether propofol prolongs, shortens, or does not change QT interval. The aim of this study was to determine the effect of target-controlled infusion (TCI) of propofol on heart rate-corrected QT (QTc) interval during anesthetic induction. We examined 50 patients undergoing lumbar spine surgery. Patients received 3 µg/kg of fentanyl and were randomly allocated to one of the following 2 groups. Group S patients received 5 mg/kg of thiamylal followed by sevoflurane, 5 % at the inhaled concentration. Group P patients received propofol using TCI system at 5 µg/mL for 2 min followed by 3 µg/mL. Tracheal intubation was performed after vecuronium administration. Heart rate (HR), mean arterial pressure (MAP), bispectral index score (BIS), and QTc interval in 12-lead electrocardiogram were recorded at the following time points: just before fentanyl administration (T1), 2 min after fentanyl injection (T2), 1 min after thiamylal injection or 2 min after the start of TCI (T3), just before intubation (T4), and 2 min after intubation (T5). BIS and MAP significantly decreased after anesthetic induction in both groups. HR decreased after anesthetic induction and recovered after tracheal intubation in group P, whereas it did changed in group S throughout the study period. QTc interval was shortened at T3 and T4 in group P, but prolonged at T3, T4, and T5 in group S, as compared with T1. Propofol TCI shortens QTc interval, whereas sevoflurane prolongs QTc interval during anesthetic induction.