Total intravenous anesthesia with propofol is associated with a lower rate of postoperative delirium in comparison with sevoflurane anesthesia in elderly patients.

STUDY OBJECTIVE: Postoperative delirium (POD) is a common complication of anesthesia. The incidence of POD in elderly patients ranges from 37% to 53%, and POD increases the morbidity and mortality of elderly patients. However, the effects of anesthetics on POD are not well known. The present study aimed to compare the incidence of POD resulting from propofol and sevoflurane anesthesia. DESIGN: Double-blind prospective study. SETTING: Operating room and postoperative recovery area. PATIENTS: Thirty patients in the sevoflurane anesthesia group and 29 in the propofol anesthesia group. MEASUREMENTS: Statistical analyses were performed using Microsoft Excel 2010 for Windows 7 (Microsoft Corporation, Redmond, Wash). Statistical analysis was performed using Fisher exact test and Student t test. MAIN RESULTS: The incidence of POD in the propofol anesthesia (6.9%) was significantly less than that observed in the sevoflurane anesthesia (26.7%; 038). CONCLUSION: In comparison with sevoflurane anesthesia, propofol anesthesia is associated with a lower incidence of POD in elderly patients.

[Required matters in the study enforcement and the publication].

We must confirm "instructions for authors" in a medical journal before we submit a manuscript to the journal. Human studies must conform to ethical standards, and be approved by the appropriate Institutional Review Board (IRB). Most "instruction for authors" require to obey "WMA Declaration of Helsinki-Ethical Principles for Medical Research Involving Human Subjects", "Uniform requirements for manuscripts submitted to biomedical journals: Writing and editing for biomedical publication" etc. The editors of journal are concerned about appropriate IRB review and informed consent. Lack of appropriate consent or documentation may be grounds for rejection, and we must understand the necessary guidelines before starting a study.

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.

Anesthetic management of peroral endoscopic myotomy for esophageal achalasia: a retrospective case series.

Peroral endoscopic myotomy (POEM) is a newly developed, less invasive treatment for esophageal achalasia that requires general anesthesia under positive pressure ventilation. In this retrospective case series, we describe the anesthetic management of 28 consecutive patients who underwent POEM for esophageal achalasia. Anesthesia was maintained with sevoflurane and remifentanil under positive pressure ventilation through a tracheal tube. Retained contents in the esophagus were evacuated just before anesthesia induction to prevent regurgitation into the trachea. The POEM procedure was performed using an orally inserted flexible fiberscope. Elevation of end-tidal carbon dioxide after initiating esophageal carbon dioxide insufflation was observed in all patients and was treated by minute adjustments to the ventilation volume. Scopolamine butylbromide-induced tachycardia in one patient was treated with landiolol hydrochloride, which is a short-acting beta 1-selective blocker. Minor subcutaneous emphysema around the neck was observed in one patient. POEM was successfully completed, and tracheas were extubated immediately after the procedure in all patients. Our findings suggest that prevention of aspiration pneumonia during anesthesia induction, preparation for carbon dioxide insufflation-related complications, and treatment of scopolamine butylbromide-induced tachycardia play important roles in safe anesthesia management of POEM for esophageal achalasia.

Extent of sympathectomy affects postoperative compensatory sweating and satisfaction in patients with palmar hyperhidrosis.

PURPOSE: Endoscopic thoracic sympathectomy (ETS) for the treatment of palmar hyperhidrosis is generally performed at one or two levels ranging between T2 and T4; however, compensatory sweating (CS) is an occasional bothersome side effect. The aim of our study was to evaluate the association between the extent of ETS and the degree of postoperative CS and palmar sweating, as well as patient satisfaction. METHODS: The participants represented a consecutive series of 76 patients who underwent bilateral ETS for palmar hyperhidrosis at level T2 and/or T3. Patients were interviewed by postal questionnaires to assess their self-reported degree of postoperative palmar sweating and CS and their outcome satisfaction. Of the 53 patients who replied to the postal questionnaire, 25 underwent bilateral ETS at one level (group A), and 27 underwent bilateral ETS at two levels (group B). One patient who underwent asymmetrical sympathectomy was excluded. RESULTS: The degree of postoperative palmar sweating was significantly lower in group B than in group A. The severity of CS was significantly higher in group B than in group A. The severity of CS was significantly inversely correlated with the degree of patient satisfaction. However, the degree of postoperative palmar sweating was not correlated with the degree of patient satisfaction. CONCLUSIONS: Compared to ETS at two levels, single-level ETS of T2 or T3 reduces postoperative palmar sweating to a milder degree, and causes CS to a less severe degree. The severity of CS is inversely correlated with the degree of patient satisfaction.

[The factors that require short acting beta-blockers during general anesthesia using remifentanil].

BACKGROUND: Short acting beta-blockers (SBB) have been utilized effectively to prevent adverse cardiac events perioperatively. After recent introduction of remifentanil in Japan, applications of SBB could have been changed because of its intense analgesic and negative chronotrophic effects. Thus, we evaluated the factors that require SBB during general anesthesia using remifentanil. MATERIALS AND METHODS: Total of 1,631 patients who had general anesthesia with remifentanil were enrolled. Groups were divided by the use of SBB. Using logistic multivariable analysis, the factors significantly increasing the chance of using SBB were evaluated including patients' characteristics, surgical procedures, and anesthetic methods. A P value < 0.05 was considered as statistical significance. RESULTS: One hundred thirty one patients received SBB perioperatively, 94 of them received only when awake and 34 of them received during remifentanil anesthesia. Emergency operation and preoperative ECG abnormalities were significant factors requiring SBB during anesthesia using remifentanil (OR; 3.0, 4.9 respectively). CONCLUSIONS: Even with use of remifentanil there are the patients, such as those under emergency operation or with ECG abnormalities who require SBB perioperatively.

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.

Milrinone and levosimendan administered after reperfusion improve myocardial stunning in swine.

OBJECTIVES: We assessed the effect of milrinone application timing after reperfusion against myocardial stunning as compared with levosimendan in swine. Furthermore, we examined the role of p38 mitogen-activated protein kinase (p38 MAPK) in the milrinone-induced cardioprotection. DESIGN: All swine were subjected to 12-minutes ischemia followed by 90-minutes reperfusion to generate stunned myocardium. Milrinone or levosimendan was administered intravenously either for 20 minutes starting just after reperfusion or for 70 minutes starting 20 minutes after reperfusion. In another group, SB203580, a selective p38 MAPK inhibitor, was administered with and without milrinone. Regional myocardial contractility was assessed by percent segment shortening (%SS). RESULTS: Milrinone starting just after reperfusion, but not starting 20 minutes after reperfusion, improved %SS at 30, 60, and 90 minutes after reperfusion compared with that in the control group. SB203580 abolished the beneficial effect of milrinone. On the other hand, levosimendan starting 20 minutes after reperfusion, but not for 20 minutes starting just after reperfusion, improved %SS at 60 and 90 minutes after reperfusion. CONCLUSIONS: Milrinone should be administered just after reperfusion to protect myocardial stunning through p38 MAPK, whereas levosimendan improvement of contractile function could be mainly dependent on its positive inotropic effect.

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.

Overexpression of glutaredoxin protects cardiomyocytes against nitric oxide-induced apoptosis with suppressing the S-nitrosylation of proteins and nuclear translocation of GAPDH.

There is increasing evidence demonstrating that glutaredoxin 1 (GRX1), a cytosolic enzyme responsible for the catalysis of protein deglutathionylation, plays distinct roles in inflammation and apoptosis by inducing changes in the cellular redox system. In this study, we investigated whether and how the overexpression of GRX1 protects cardiomyocytes against nitric oxide (NO)-induced apoptosis. Cardiomyocytes (H9c2 cells) were transfected with the expression vector for mouse GRX1 cDNA, and mock-transfected cells were used as a control. Compared with the mock-transfected cells, the GRX1-transfected cells were more resistant to NO-induced apoptosis. Stimulation with NO significantly increased the nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a pro-apoptotic protein, in the mock-transfected cells, but did not change GAPDH localization in the GRX1-transfected cells. Furthermore, we found that NO stimulation clearly induced the oxidative modification of GAPDH in the mock-transfected cells, whereas less modification of GAPDH was observed in the GRX1-transfected cells. These data suggest that the overexpression of GRX1 could protect cardiomyocytes against NO-induced apoptosis, likely through the inhibition of the oxidative modification and the nuclear translocation of GAPDH.

Direct protective effects of dexmedetomidine against myocardial ischemia-reperfusion injury in anesthetized pigs.

Systemic administration of α2-adrenergic agonists has been shown to protect ischemic myocardium, but the direct effects on ischemia-reperfused myocardium have not yet been clarified. This study was carried out to determine the effects of intracoronary dexmedetomidine (DEX) on the myocardial ischemia-reperfusion injury in anesthetized pigs. In open-chest pigs, the left anterior descending coronary artery was perfused through an extracorporeal circuit from the carotid artery. They received intracoronary infusion of DEX at a rate of 1 ng · mL(-1) (group LD, n = 9), 10 ng · mL(-1) (group MD, n = 9), or 100 ng · mL(-1) (group HD, n = 9) of coronary blood flow or vehicle (group C, n = 12) for 30 min before ischemia. Myocardial stunning was produced by 12-min ischemia of the perfused area of left anterior descending coronary artery and 90-min reperfusion. The effect on reperfusion-induced arrhythmias was evaluated using the incidence of ventricular tachycardia or fibrillation after reperfusion. Regional myocardial contractility was evaluated with segment shortening (%SS). Dexmedetomidine significantly reduced the incidence of reperfusion-induced ventricular arrhythmias. Dexmedetomidine significantly improved the recovery of percentage segment shortening at 90 min after reperfusion (32.6% ± 3.1% in group C, 58.2% ± 2.1% in group LD, 61.1% ± 1.8% in group MD, and 72.0% ± 2.0% in group HD). Dexmedetomidine suppressed the increase in plasma norepinephrine concentration after reperfusion. The results indicate that DEX would exert the protective effect against ischemia-reperfusion injury by the direct action on the myocardium, which is not mediated through the central nervous system.

The presence of transverse cervical and dorsal scapular arteries at three ultrasound probe positions commonly used in supraclavicular brachial plexus blockade.

BACKGROUND: Ultrasound-guided supraclavicular brachial plexus block carries a risk for puncture of vascular structures. In this study, we determined the frequency with which the transverse cervical artery (TCA) and the dorsal scapular artery (DSA) are detected by ultrasound evaluation at 3 probe positions during supraclavicular block. METHODS: Ultrasound examinations of the supraclavicular region were performed in 53 healthy adult volunteers. Ultrasound images of the supraclavicular region were acquired at 3 probe positions: position A (the brachial plexus and the subclavian artery both lying on the first rib); position B (the brachial plexus on the first rib; the artery on the pleura); and position C (the brachial plexus between the anterior and middle scalene muscles). The primary outcome variables were the frequencies with which TCA and DSA were detected by 2-dimensional and color Doppler imaging at 3 specified probe positions. RESULTS: One hundred six supraclavicular regions were examined in 53 subjects. The subclavian artery was detected in all subjects. TCA was more often detected than DSA, 94 (88.7%, 95% confidence interval [CI] 80.7%-93.8%) and 36 (34%, 95% CI 25.3%-43.9%) of 106 scans, respectively (McNemar P value <0.001). TCA was detected in 2 (1.9%, 95% CI 0.3%-7.3%), 31 (29.2%, 95% CI 20.9%-38.9%), and 61 (57.5%, 95% CI 47.5%-66.9%) of scans at probe positions A, B, and C, respectively, whereas DSA was detected in 3 (2.8%, 95% CI 0.7%-8.6%), 23 (21.7%, 95% CI 14.5%-30.9%), and 10 (9.4%, 95% CI 4.8%-17.0%) of scans at probe positions A, B, and C, respectively. Thus, the TCA and DSA were less likely to be present with probe position A (all P < 0.001). CONCLUSION: TCA was more often detected than DSA in the vicinity of the brachial plexus in the supraclavicular region. Both TCA and DSA were least likely to be present in probe position A. Color Doppler, particularly for probe position A, may help to reduce the risk for inadvertent vascular puncture during ultrasound-guided supraclavicular block.

High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: role of mitochondrial KATP channels.

BACKGROUND: The current study was carried out to determine whether fasudil hydrochloride (fasudil), a Rho-kinase inhibitor, has myocardial postconditioning (PostC) activity under hyperglycemia as well as normoglycemia, and if so, whether the effects could be mediated by mitochondrial ATP-sensitive potassium (m-KATP) channels. METHODS: Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. After opening the chest, all rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received low-dose (0.15 mg/kg) or high-dose (0.5 mg/kg) fasudil or diazoxide, an m-KATP channel opener, at 10 mg/kg, just before reperfusion under normoglycemic or hyperglycemic conditions. In another group, rats received 5-hydroxydecanoic acid (5HD), an m-KATP channel blocker, at 10 mg/kg, before high-dose fasudil. Myocardial infarct size was expressed as a percentage of area at risk (AAR). RESULTS: Under normoglycemia, low-dose and high-dose fasudil and diazoxide reduced myocardial infarct size (23 ± 8%, 21 ± 9% and 21 ± 10% of AAR, respectively) compared with that in the control (42 ± 7%). Under hyperglycemia, low-dose fasudil (40 ± 11%) and diazoxide (44 ± 14%) could not exert this beneficial effect, but high-dose fasudil reduced myocardial infarct size in the same manner as under normoglycemia (21 ± 13%). 5HD prevented fasudil-induced reduction of myocardial infarct size (42 ± 13%). CONCLUSION: Fasudil induces PostC against myocardial infarction via activation of m-KATP channels in the rat. Although hyperglycemia attenuates the PostC, high-dose fasudil can restore cardioprotection.

A new technique for post-pyloric feeding tube placement by palpation in lean critically ill patients.

Various techniques have been described for blind bedside placement of a post-pyloric feeding tube. However, there is no universal method and the technique depends on the local institutional resources and expertise. The purpose of this study was to evaluate a simple new technique for the bedside placement of a post-pyloric feeding tube in an intensive care unit using palpation to confirm tube position. We studied 47 consecutive ventilated patients (mean body mass index 22.4 ± 4.2 kg/m(2)) requiring enteral tube feeding for nutritional support. We monitored the maximum intensity point of injected air 'bubbling' by palpation and estimated tube position. We monitored the movement of the maximum intensity point from the left upper quadrant to the right upper quadrant. If the maximum intensity point on the right upper quadrant diminished or weakened, we considered the tube had proceeded beyond the pylorus. By palpation, we could feel the bubbling of the injected air in all patients, but four patients were excluded because of failure to complete the protocol. The overall success rate including the four excluded cases was 85.1% (40/47) on the first attempt and 91.5% (43/47) when we included the second attempt. The median time for 40 successful tube placements on the first attempt was 10 (7 to 23) minutes. Our new palpation technique can successfully detect the position of a feeding tube in the stomach and help guide the tube to the correct location in the post-pyloric portion of the stomach in lean critically ill patients.

Inhalation of hydrogen gas protects against myocardial stunning and infarction in swine.

OBJECTIVES: The present study was carried out to determine whether inhalation of hydrogen (H(2)) gas protects myocardium against ischemia-reperfusion (I/R) injury in swine. DESIGN: In anesthetized open-chest swine, myocardial stunning was produced by 12-minute occlusion of left anterior descending coronary artery (LAD) followed by 90-minute reperfusion in the first study. Group A inhaled 100% oxygen, and group B inhaled 2% H(2) plus 98% oxygen during ischemia and reperfusion. In the second study, myocardial infarction was produced by 40-minute occlusion of LAD followed by 120-minute reperfusion. Group C inhaled 100% oxygen during ischemia and reperfusion. Group D inhaled 2% H(2) plus 98% oxygen. Group E inhaled 4% H(2) plus 96% oxygen. RESULTS: The change of segment shortening (%SS) from baseline at 90 minutes after reperfusion in group B was 74 ± 13 (mean ± SD) %, which was significantly higher than that in group A (48 ± 15%). Myocardial infarct size in group E (32 ± 10%), but not in group D (40 ± 9%) was smaller than that in group C (46 ± 6%). CONCLUSIONS: Inhalation of 2% H(2) gas improves myocardial stunning, and inhalation of 4% but not 2% H(2) gas reduces myocardial infarct size in swine.

Hyperglycemia raises the threshold of levosimendan- but not milrinone-induced postconditioning in rat hearts.

BACKGROUND: The authors examined whether milrinone and levosimendan could exert cardiac postconditioning effects in rats under normoglycemia and hyperglycemia, and whether the effects could be mediated by mitochondrial permeability transition pore (mPTP). METHODS: Wistar rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received milrinone or levosimendan just before reperfusion under normoglycemic or hyperglycemic conditions with or without atractyloside, an mPTP opener. RESULTS: Under normoglycemia, both 30 µg/kg milrinone (29 ± 12%) and 10 µg/kg levosimendan (33 ± 13%) reduced infarct size compared with that in the control (58 ± 7%). Under hyperglycemia, milrinone (34 ± 13%) reduced infarct size at the same dose as under normoglycemia. In contrast, neither 10 nor 30 µg/kg levosimendan protected hyperglycemic hearts, and only 100 µg/kg levosimendan (32 ± 9%) reduced infarct size compared with that in the hyperglycemic control (58 ± 13%). All of these cardioprotective effects under normoglycemia and hyperglycemia are abolished by atractyloside. CONCLUSION: Milrinone and levosimendan exert postconditioning effects via inhibition of mPTP opening. Hyperglycemia raises the threshold of levosimendan-induced postconditioning, while milrinone-induced postconditioning is not influenced by hyperglycemia.

Comparison between propofol and dexmedetomidine in postoperative sedation after extensive cervical spine surgery.

PURPOSE: Patients undergoing extensive cervical spine surgery (ECSS) occasionally require emergency reintubation due to postoperative airway complications. To avoid it, an endotracheal tube is retained in patients maintained under sedation overnight. This study was conducted to determine whether dexmedetomidine would be superior in sedative effects to propofol for postoperative sedation after ECSS. METHODS: We studied 32 consecutive patients undergoing ECSS who required prophylactic intubation postoperatively under sedation overnight. The patients were randomly divided into two groups. Group D (n = 16) received dexmedetomidine 0.1 µg/kg/min for 10 min as a loading dose, followed by a continuous infusion at 0.4 µg/kg/h. Group P (n = 16) received propofol 0.1 mg/kg/min for 10 min as a loading dose, followed by a continuous infusion at 1 mg/kg/h. All patients received analgesia with buprenorphine. Ramsay sedation scale, extremity movement, and pain intensity were recorded every 2 h. Dexmedetomidine and propofol dosages were adjusted to maintain a desired sedation level. Nursing staff adjusted dopamine to maintain systolic blood pressure >100 mmHg and administered atropine when the heart rate was <50 bpm. RESULTS: The proportions of adequate sedation level, movement, and pain status were similar between groups. In group D, heart rates were lower, frequency of atropine use was greater, and dopamine dose was higher than in group P. CONCLUSION: Both sedatives are efficacious after ECSS; however, dexmedetomidine decreased heart rate and required higher dose of dopamine.