[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.

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.

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.

[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.

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.

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.

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.

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.

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.

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.

Effects of neostigmine on bronchoconstriction with continuous electrical stimulation in rats.

PURPOSE: When neostigmine is used to reverse muscle relaxants in patients with asthma without signs of airway inflammation, asthma attack is occasionally encountered. It is likely that abnormally increased electrical impulses traveling from the brain through cholinergic nerves to airway smooth muscles may be one of the pathogeneses of asthma attack. We applied continuous electrical field stimulation (c-EFS) or continuous electrical stimulation (c-ES) of low frequency to the vagal nerve of the rat in vitro and in vivo to determine the role of cholinergic nerve activation in inducing airway constriction. METHODS: Fifty-seven male Wistar rats were used. In an in vitro study we examined whether tetrodotoxin (TTX), an Na(+)-channel blocker, 4-DAMP, a muscarinic M(3) receptor antagonist, or neostigmine could affect c-EFS-induced contraction of the tracheal ring. In an in vivo study, we examined whether c-ES of the vagal nerve could increase maximum airway pressure (P (max)) and whether neostigmine could potentiate c-ES-induced P (max). RESULTS: TTX and 4-DAMP completely inhibited c-EFS-induced contraction whereas neostigmine potentiated c-EFS-induced contraction dose-dependently. P (max) was not increased by neostigmine. P (max) was not increased by 2-Hz c-ES, but was increased by the addition of neostigmine. P (max) was increased by 5-Hz c-ES, and further increased by the addition of neostigmine. CONCLUSION: The contractile response of the tracheal ring to c-EFS is potentiated by neostigmine. P (max) is increased by c-ES of the vagal nerve, and is potentiated by neostigmine. These data suggest that increased activity of the cholinergic nerve could be involved in asthma attack.

S(+)-ketamine suppresses desensitization of γ-aminobutyric acid type B receptor-mediated signaling by inhibition of the interaction of γ-aminobutyric acid type B receptors with G protein-coupled receptor kinase 4 or 5.

BACKGROUND: Intrathecal baclofen therapy is an established treatment for severe spasticity. However, long-term management occasionally results in the development of tolerance. One of the mechanisms of tolerance is desensitization of γ-aminobutyric acid type B receptor (GABABR) because of the complex formation of the GABAB2 subunit (GB2R) and G protein-coupled receptor kinase (GRK) 4 or 5. The current study focused on S(+)-ketamine, which reduces the development of morphine tolerance. This study was designed to investigate whether S(+)-ketamine affects the GABABR desensitization processes by baclofen. METHODS: The G protein-activated inwardly rectifying K channel currents induced by baclofen were recorded using Xenopus oocytes coexpressing G protein-activated inwardly rectifying K channel 1/2, GABAB1a receptor subunit, GB2R, and GRK. Translocation of GRKs 4 and 5 and protein complex formation of GB2R with GRKs were analyzed by confocal microscopy and fluorescence resonance energy transfer analysis in baby hamster kidney cells coexpressing GABAB1a receptor subunit, fluorescent protein-tagged GB2R, and GRKs. The formation of protein complexes of GB2R with GRKs was also determined by coimmunoprecipitation and Western blot analysis. RESULTS: Desensitization of GABABR-mediated signaling was suppressed by S(+)-ketamine in a concentration-dependent manner in the electrophysiologic assay. Confocal microscopy revealed that S(+)-ketamine inhibited translocation of GRKs 4 and 5 to the plasma membranes and protein complex formation of GB2R with the GRKs. Western blot analysis also showed that S(+)-ketamine inhibited the protein complex formation of GB2R with the GRKs. CONCLUSION: S(+)-Ketamine suppressed the desensitization of GABABR-mediated signaling at least in part through inhibition of formation of protein complexes of GB2R with GRK 4 or 5.

[Influence of general anesthetics on the incidence of postoperative delirium in the elderly].

BACKGROUND: Postoperative delirium increases the morbidity and mortality in elderly patients. The present study was carried out to evaluate whether the difference of anesthetics has influence on the incidence of postoperative delirium, retrospectively. METHODS: Among the patients undergoing surgical procedure aged above 75 years, in seventy one patients anesthesia was maintained with sevoflurane (group S), and 38 with propofol (group P). The incidence of delirium postoperatively was obtained retrospectively from their medical chart. The delirium was diagnosed with the confusion assessment method diagnostic algorithm. RESULTS: The incidence of postoperative delirium of group P (15.8%) was significantly lower than that of group S (38.0%, P=0.02). CONCLUSIONS: Propofol anesthesia decreases postoperative delirium in elderly patients compared with sevoflurane anesthesia.

[Relationship between magnesium concentration in cerebrospinal fluid and delayed cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage].

BACKGROUND: The present study was conducted to determine the relationship between magnesium concentration in cerebrospinal fluid (CSF) and delayed cerebral ischemia (DCI) in patients with subarachnoid hemorrhage (SAH). METHODS: We studied 39 consecutive patients undergoing surgery after SAH. A spinal drainage catheter was inserted into the lower lumbar vertebrae before surgery. CSF was then sampled and the magnesium concentration measured. General clinical data, Hunt-Hess (H-H) grade and Fisher grade, aneurysm size and site, intracerebral and intraventricular hemorrhage, and blood glucose levels were all recorded on admission. At the same time, the Glasgow coma scale (GCS) score was calculated. Outcomes were assessed using the Glasgow outcome scale at discharge. DCI was defined as a two-point decrease in the GCS score and/or focal deficit, and was confirmed by cerebral angiography. The recorded values were expressed as the median (interquartile range). RESULTS: Of the 39 patients, 23 (59%) had DCI. The magnesium concentration in the DCI cases was 2.8 (2.7 and 2.9) mg x dl(-1), which was significantly lower than that in the non-DCI cases, i. e., 2.9 (2.8 and 3.0) mg x dl(-1) (P < 0.05). There were no significant differences in the other factors. CONCLUSIONS: The results indicate that preoperative hypomagnesemia within the CSF might play a role in the development of DCI in patients with SAH; however, further studies will be necessary to confirm this observation.

Synthetic atrial natriuretic peptide improves systemic and splanchnic circulation and has a lung-protective effect during endotoxemia in pigs.

BACKGROUND: Pharmacological blockade of the renin-angiotensin system is thought to maintain gut perfusion during circulatory stress and thereby avoid later failure of distant organs. In this controlled experimental study, we investigated the effects of carperitide, a synthetic atrial natriuretic peptide that inhibits the renin-angiotensin system, on the systemic and splanchnic circulation during fluid-resuscitated endotoxemia in pigs. METHODS: Sixteen domestic pigs of both sexes were randomly divided into 2 groups. The pigs were anesthetized and their lungs ventilated before receiving either saline (Group A: n = 8) or carperitide (Group B: n = 8). After a baseline measurement was taken, the pigs from both groups received a continuous infusion (1.7 microg x kg(-1) x h(-1)) of endotoxin for 240 min. Group B received a continuous infusion of carperitide (0.05 microg x kg(-1) x min(-1)) starting 30 min before the endotoxin infusion and lasting until the end of the study, whereas Group A received the same volume of saline. Fluid resuscitation was titrated to maintain pulmonary artery wedge pressure between 10 and 12 mm Hg. Systemic and regional hemodynamics, oxygenation variables, and the arterial-to-intestinal PCO(2) gap were measured at baseline and after endotoxin infusion for 240 min. The primary end points were cardiac index, superior mesenteric artery flow index, and PCO(2) gap at the end of this study (T240). RESULTS: Cardiac index and superior mesenteric artery flow index in Group B were significantly higher than those in Group A at T240 (83 +/- 15 vs 135 +/- 23 mL x kg(-1) x min(-1), P < 0.001; 2.6 +/- 1.4 vs 7.9 +/- 4.8, P = 0.01), respectively. Carperitide administration resulted in a significantly better maintenance of intestinal mucosal perfusion assessed by the PCO(2) gap at T240 (33.0 +/- 14.5 vs 11.6 +/- 10.0 mm Hg, P = 0.004). The PaO(2)/FIO(2) ratio in Group B was significantly greater than that in Group A from T60 to T240. CONCLUSIONS: In this porcine fluid-resuscitated endotoxemia model, a low dose of carperitide administered before endotoxemia maintained systemic and splanchnic circulation, and prevented the deterioration of oxygenation. Atrial natriuretic peptide infusion is a potentially beneficial therapy with respect to systemic and splanchnic circulation as well as the respiratory system during sepsis.

QTc interval and neurological outcomes in aneurysmal subarachnoid hemorrhage.

BACKGROUND: Prolonged heart rate-corrected QT (QTc) interval is frequently observed in subarachnoid hemorrhage (SAH). This study was conducted to determine the relationship between QTc interval and neurological outcome during the acute posthemorrhagic period after aneurysmal SAH. METHODS: We studied 71 patients undergoing surgery who were admitted within 24 h after the onset of aneurysmal SAH. Standard 12-lead electrocardiography was performed on admission (T1) and at 1 and 7 days after operation (T2 and T3). QT intervals were corrected by heart rate according to the Fridericia formula. The Glasgow Coma Scale (GCS) score was calculated over the period T1-T3. Neurological outcome was assessed using the Glasgow Outcome Scale at hospital discharge. RESULTS: Among the 71 patients, 31 had an unfavorable neurological outcome. Although QTc interval prolongation improved in patients with a good outcome, QTc interval prolongation continued in patients with an unfavorable outcome. The areas under the receiver-operator characteristic curves showed that the QTc and GCS score at T3, and the Hunt and Hess grade were significant predictors of an unfavorable neurological outcome. The threshold value, sensitivity, and specificity for the QTc at T3 were 448 ms, 73% [95% confidence interval (CI), 68-78], and 93% (95% CI, 90-96), respectively. CONCLUSION: This study confirms that QTc interval prolongation continues in the SAH patients with an unfavorable outcome but that QTc interval prolongation improves in patients with a good outcome, suggesting that a QTc interval of more than 448 ms at 7 days after operation is a predictor of neurological outcome after SAH.

Anesthetic management of a patient undergoing liver transplantation who had previous coronary artery bypass grafting using an in situ right gastroepiploic artery.

We describe successful anesthetic management during living-donor liver transplantation in a 63-year-old man with previous coronary artery bypass grafting (CABG) that employed an in situ right gastroepiploic artery (RGEA). Anesthesia was maintained with 1.5% isoflurane in air/oxygen and fentanyl. A five-lead electrocardiogram, transesophageal echocardiogram, and pacing pulmonary artery catheter evaluated cardiac function. A pacing wire was inserted through the catheter to prepare for intraoperative severe bradyarrhythmia. Olprinone and nicorandil were continuously infused to prevent decrease in coronary arterial blood flow and the collapse of cardiac function. Avoiding disruption of circulation to coronary arteries through injury or spasm of the RGEA graft and preparing for cardiac insufficiency during liver transplantation of a patient with previous CABG using an in situ RGEA is critical.