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Craniopharyngioma surgery is frequently associated with the occurrence of central diabetes insipidus, and oral rehydration therapy is reliable for postoperative management if the patient’s thirst is normal. A 61-year-old Japanese male patient underwent extended endoscopic transsphenoidal surgery for craniopharyngioma. He was undergoing acute treatment for postoperative central diabetes insipidus and hypopituitarism in the intensive care unit. Two days after the surgery, he started to vomit occasionally, despite receiving oral rehydration therapy for central diabetes insipidus. Despite increasing the dose of parenteral hydrocortisone, the periodic vomiting persisted during fasting periods and progressed to aspiration pneumonia and severe sepsis. Abdominal computed tomography was performed to identify the cause of persistent vomiting and revealed the presence of a pseudo-intestinal obstruction extending from the small to large intestine. When oral rehydration therapy for central diabetes insipidus is accompanied by vomiting symptoms suggestive of hypopituitarism, a holistic evaluation of the gastrointestinal system is advisable.

Objective Several reports have shown the negligible adverse effects of low-dose remifentanil on the autonomic nervous system. We propose that the administration of low-dose remifentanil would be beneficial without adverse respiratory and hemodynamic effects. This study aimed to examine the effects of low-dose remifentanil on postoperative pain relief and heart rate variability (HRV) after surgery. Methods In total, 20 patients, who underwent breast cancer surgery, were analysed for HRV in the post-anaesthesia care unit (PACU). A sedative dose of remifentanil was continuously infused if patients experienced pain while in PACU. The remifentanil infusion dose was determined by achieving analgesia with no adverse effects on hemodynamics and/or respiration. Variables of low-frequency power, high-frequency power and low-frequency power/high-frequency power ratio were measured before and after the administration of remifentanil. Pain score was expressed as the numeric rating scale (NRS) from 0 to 10. Results The mean dosage of remifentanil administered as a continuous infusion was 0.029±0.0042 μg kg-1 min-1. After remifentanil administration, the value of the NRS decreased from 4.2±2.9 to 2.7±2.6. In addition, the value of high-frequency power increased from 35.6±14.3 to 49.4±3.0. Conclusion The continuous infusion of low-dose remifentanil may reduce post-operative pain scores and trigger the relative activation of the parasympathetic nervous system in post-surgical patients. This indicates that continuous infusion of low-dose remifentanil may be a useful option for postoperative pain relief in cases where postoperative pain control proves inadequate even with the application of regional block technique.

Infrahepatic inferior vena cava (IIVC) clamping is beneficial for reducing the amount of bleeding during hepatic surgery, although the associated systemic circulatory deterioration is noticeable. The relationship between changes in the degree of IIVC clamping and postoperative renal function was retrospectively evaluated. A total of 59 patients who underwent elective hepatic surgery with surgical IIVC clamping in the two years were analyzed. In 2016, constant 80% clamping of the IIVC was performed (29 cases), and in 2017, hemodynamically adjusted IIVC clamping was performed (30 cases). Intraoperative parameters, including total blood loss and number of blood transfusions, were examined. The use of each vasoactive agents was analyzed. Renal function in the acute postoperative phase was evaluated using serum creatinine (Cr) and estimated glomerular filtration rate (eGFR) values. Comparison of the two groups showed that bolus doses of both ephedrine and phenylephrine were significantly higher in the 2016 group (P = 0.0221, 0.0017). Continuous doses of dopamine were significantly higher in the 2016 group, while those of noradrenaline were not. Postoperative serum Cr levels relative to baseline (%) were significantly higher in the 2016 group immediately after surgery and on postoperative day (POD) 1 (P = 0.0143, 0.0012). Postoperative eGFR relative to baseline (%) was significantly higher in the 2016 group immediately postoperatively and on PODs 1 and 2 (P = 0.0042, 0.0003, 0.0382). Hemodynamically adjustable IIVC clamping might be superior to uniformly fixed clamping in preserving renal function without compromising the desired effect on hemostasis.

The purpose of this study was to compare the effect of the long-term administration of flurbiprofen and fentanyl in the intensive care unit on natural killer cell cytotoxicity (NKCC), lymphocyte subsets and cytokine levels. In this prospective study, patients scheduled for at least 48 h sedation after neck surgery were randomly assigned to two groups called group N and group F. Group N patients were sedated with propofol and flurbiprofen after surgery (n = 12), while group F patients were sedated with propofol and fentanyl (n = 13). The NKCC, lymphocyte subsets, and plasma levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 were measured before and at the end of surgery, on postoperative day (POD) 1 and POD2. The NKCC was significantly higher on POD1 in group N than in group F (14.5 ± 11.2 versus 6.3 ± 4.1 %, p

This study was conducted to compare recovery times from rocuronium-induced muscle relaxation after reversal with three different doses of sugammadex with succinylcholine during electroconvulsive therapy (ECT).Seventeen patients who were scheduled to undergo ECT were studied. Anesthesia was induced by use of propofol (1.0 mg/kg) followed by either succinylcholine (SCC) (1 mg/kg) or rocuronium (0.6 mg/kg). Assisted mask ventilation was initiated with 100% oxygen. After T1 was assessed as being zero by neuromuscular monitoring, an electroshock stimulus was applied bilaterally. Patients receiving rocuronium were infused with 16, 8, or 4 mg/kg sugammadex immediately after the seizure stopped to reverse the muscle relaxation. Neuromuscular monitoring was continued until recovery of the train-of-four ratio to 0.9 at the tibial nerve in the leg. The times to recovery of T1 to 10 and 90% with both relaxants were compared.The time to recovery of T1 to 90% after 16 mg/kg sugammadex was shorter than that in subjects treated with SCC (p = 0.046), whereas that after 4 mg/kg sugammadex was longer than that in subjects treated with SCC (SCC group: 429 ± 65 s, 16 mg/kg sugammadex group: 387 ± 63 s*, 8 mg/kg sugammadex group: 462 ± 66 s, 4 mg/kg sugammadex group: 563 ± 45 s(*,#); *p0.05 compared with SCC, (#)p0.01 compared with 16 mg/kg sugammadex).This study demonstrates the efficacy of rocuronium-sugammadex as an alternative to SCC for muscle relaxation during ECT, and indicates that 8 mg/kg sugammadex produces equally rapid recovery from rocuronium muscular relaxation compared with spontaneous recovery from 1 mg/kg SCC during ECT.

We observed an increase in mean middle cerebral artery blood flow velocity (V mca) after tourniquet deflation during orthopedic surgery under sevoflurane anesthesia in patients with diabetes mellitus or previous stroke. Eight controls, seven insulin-treated diabetic patients, and eight previous stroke patients were studied. Arterial blood pressure, heart rate, V mca, arterial blood gases, and plasma lactate levels were measured every minute for 10 min after tourniquet release in all patients. V mca was measured using a transcranial Doppler probe. V mca in all three groups increased after tourniquet deflation, the increase lasting for 4 or 5 min. However, the degree of increase in V mca in the diabetic patients was smaller than that in the other two groups after tourniquet deflation (at 2 min after tourniquet deflation: control 58.5 ± 3.3, previous stroke 58.4 ± 4.6, diabetes 51.7 ± 2.3; P

Diabetes mellitus is an increasingly common disease that affects people of all ages, resulting in significant morbidity and mortality. Diabetic patients require perioperative care more frequently than their nondiabetic counterparts. The major risk factors for diabetics undergoing surgery are the associated end-organ diseases: cardiovascular disease, autonomic neuropathy, joint collagen tissue, and immune deficiency. Physicians need to pay extra attention to preoperative and preprocedure evaluation and treatment of these diseases to ensure optimal perioperative management.

Diabetes mellitus is an increasingly common disease that affects people of all ages, resulting in significant morbidity and mortality. Diabetic patients require more frequent hospitalization, have greater lengths of stay, and cost more to manage than non-diabetics. The major risk factors for diabetics undergoing surgery are the end-organ diseases associated with diabetes: cardiovascular disease, autonomic neuropathy and immune deficiency. Physicians should pay extra attention to preoperative and preprocedure evaluation and treatment of these diseases to ensure optimal perioperative management. Furthermore, these patients unexpectedly develop hemodynamic instability in response to vasopressor or vasodilator administration during anesthesia, this being of particular importance in patients with concurrent ischemic heart disease in whom it may have a direct effect on mortality. Recent studies have shown that tight glycemic control in diabetic patients undergoing major surgery has been shown to improve perioperative morbidity and mortality.

The purpose of this study was to examine the effects of landiolol on left ventricular (LV) systolic function, using transthoracic echocardiography, during electroconvulsive therapy (ECT). Fourteen patients undergoing ECT were studied. Bilateral ECT was performed after administration of thiopentone (2 mg/kg), succinylcholine (1 mg/kg), and initiation of assisted mask ventilation with 100% oxygen. Patients received a bolus injection of landiolol (0.125 mg/kg) or saline immediately after anesthetic induction and prior to electrical shock. LV systolic function was examined by transthoracic echocardiography prior to anesthetic induction, throughout the ECT procedure, and for 10 min after the seizure. Electrical shock resulted in a significant decrease in fractional area change (FAC) when compared with the awake condition in the control group [FAC when awake: 48 +/- 3%; 1 min after ECT: 38 +/- 4%*; 2 min after ECT: 36 +/- 4%*; 3 min after ECT: 40 +/- 3%*; mean +/- standard deviation, *p < 0.05 compared with awake]. Landiolol infusion stabilized systemic hemodynamics and LV systolic function. The study demonstrated that landiolol is a suitable agent to minimize hemodynamic changes and transthoracic echocardiographic variability after ECT.

We examined the effects of the short-acting beta-1 blocker, landiolol, on hemodynamics during emergence from anesthesia in elderly and middle-aged patients with and without hypertension. Fifty hypertensive and 50 normotensive elderly and middle-aged patients scheduled for orthopedic or gynecological surgery were selected. Immediately after the end of the surgery and termination of administration of all anesthetics, a landiolol infusion was administered at a rate of 0.125 mg/kg/min for 1 min and then decreased to 0.04 mg/kg/min until extubation. Heart rate and blood pressure were recorded every minute from immediately before the administration of landiolol up to discontinuation of landiolol, and every 5 min from the discontinuation of landiolol to 30 min after termination of the infusion. As a control, nine normotensive middle-aged and 10 normotensive elderly patients were also studied. In addition, eight hypertensive middle-aged and eight normotensive elderly patients were also evaluated with administration of a different landiolol infusion dosage. In the non-hypertensive group, with landiolol infusion, heart rate of middle-aged patients remained unchanged, while that of elderly patients decreased during emergence from anesthesia and tracheal extubation. In contrast, in the hypertensive group, the heart rate increased in middle-aged patients and remained unchanged in elderly patients with landiolol infusion during emergence and tracheal extubation. With an increase or decrease in landiolol dosage, heart rate remained unchanged during emergence and tracheal extubation in middle-aged hypertensive and elderly normotensive patients. The present study shows that the chronotropic effect of landiolol is attenuated in middle-aged patients with hypertension during emergence from anesthesia. Anesthesiologists should consider the patient's demographic data, such as age or presence of hypertension, when using landiolol for stabilizing the heart rate during emergence from anesthesia.

Peroxynitrite is a powerful oxidant capable of nitrating phenolic moieties, such as tyrosine or tyrosine residues in proteins and increases after traumatic brain injury (TBI). First, we tested the hypothesis that TBI increases nitrotyrosine (NT) immunoreactivity in the brain by measuring the number of NT-immunoreactive neurons in the cerebral cortex and hippocampus of rats subjected to parasagittal fluid-percussion TBI. Second, we tested the hypothesis that treatment with l-arginine, a substrate for nitric oxide synthase, further increases NT immunoreactivity over TBI alone. Rats were anesthetized with isoflurane and subjected to TBI, sham TBI, or TBI followed by treatment with l-arginine (100 mg/kg). Twelve, 24, or 72 h after TBI, brains were harvested. Coronal sections (10 μm) were incubated overnight with rabbit polyclonal anti-NT antibody, rinsed, and incubated with a biotinylated secondary antibody. The antigen—antibody complex was visualized using a peroxidase-conjugated system with diaminobenzidine as the chromagen. The number of NT-positive cortical and hippocampal neurons increased significantly in both ipsilateral and contralateral hemispheres up to 72 h after TBI compared with the sham-injured group. Remarkably, treatment with l-arginine reduced the number of NT-positive neurons after TBI in both cortex and hippocampus. Our results indicate that l-arginine actually prevents TBI-induced increases in NT immunoreactivity.

Study Objectives To examine the comparative effects of propofol, landiolol, and nicardipine on hemodynamic responses and bispectral index (BIS) changes to endotracheal intubation. Setting Operating room of a university-affiliated general hospital. Patients 27 ASA physical status I and II patients who were scheduled to undergo elective general surgical, urological, or gynecological procedures with general anesthesia. Study Design Prospective, randomized, double-blinded study. Interventions Patients were divided into three groups as follows: Group 1 received propofol, 1 mg/kg; Group 2 received landiolol, 0.1 mg/kg; and Group 3 received nicardipine, 1 mg. After baseline measurements were recorded, anesthesia was induced with propofol, fentanyl, and vecuronium. Patients' lungs were ventilated with 100% oxygen for 120 seconds, at which time one of one of the study drugs was administered. Laryngoscopy and tracheal intubation were performed 4 minutes after anesthetic induction. Measurements Cardiac index (CI) and stroke volume index (SVI) were monitored continuously. Bispectral index was also monitored continuously from 5 minutes after tracheal intubation. Main Results Heart rate values in Group 3 increased 30 seconds after intubation; this increase lasted for 1 minute after intubation. Systolic blood pressure in all three groups decreased after induction of anesthesia and before tracheal intubation, and values returned closer to baseline values 30 seconds after intubation. In the propofol group, CI and SVI decreased after administration of additional propofol, lasting for 30 seconds after intubation. The BIS values rapidly decreased after induction of anesthesia, with no intergroup differences noted in BIS values (propofol group, 39 ± 7; landiolol group, 44 ± 14; nicardipine group, 41 ± 9). However, BIS was significantly lower in the propofol group than in the other two groups from 30 seconds to 5 minutes after intubation. Conclusions Landiolol, 0.1 mg/kg, before intubation provides effective hemodynamic stability in the postintubation period.

The use of volatile anesthetics is reportedly related to altered cerebrovascular carbon dioxide (CO2) reactivity. We examined the comparative effects of sevoflurane versus isoflurane on cerebrovascular CO2 reactivity in patients with previous stroke.Twenty-four patients with previous stroke and 20 patients without previous stroke (serving as controls) were studied. Anesthesia was maintained with either end-tidal 1.0 minimum alveolar concentration (MAC) sevoflurane or 1.0 MAC isoflurane in 33% oxygen and 67% nitrous oxide. A 2.5-MHz pulsed transcranial Doppler (TCD) probe was attached to the patient's head at the right or left temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery (Vmca). After establishing baseline values of Vmca and cardiovascular hemodynamics, we increased end-tidal CO2 by decreasing the ventilatory frequency by 2-5 breaths x min(-1).We found that values for absolute and relative CO2 reactivity in the sevoflurane groups were lower than those in the isoflurane groups (absolute CO2 reactivity in the sevoflurane groups: control, 3.3 +/- 0.4*; previous stroke, 3.4 +/- 0.4*; absolute CO2 reactivity in the isoflurane groups: control, 4.2 +/- 0.3; previous stroke, 4.5 +/- 0.4, cm x s(-1) x mmHg(-1); *P0.05 compared with isoflurane group). There were no significant differences in the values for absolute and relative CO2 reactivity between the controls and the previous-stroke patients within each of the sevoflurane and isoflurane groups.Our findings suggest that, in patients with previous stroke, cerebrovascular CO2 reactivity under sevoflurane anesthesia was lower than that under isoflurane anesthesia.

Purpose: On the basis of previous findings that the anandamide antagonist AM281, an endogenous cannabinoid receptor antagonist, could restore the hemodynamic and cerebral blood flow changes and improve the mortality rate in non-diabetic rats during sepsis, this study was conducted to examine whether AM281 could restore the hemodynamic variables and improve the mortality rate in streptozotocin-induced diabetic rats during sepsis. Methods: The study was designed to include three sets of experiments, each set of experiment being conducted in both diabetic and non-diabetic animals: (1) measurement of changes in systemic hemodynamics and carotid artery blood flow, (2) measurement of biochemical variables and (3) assessment of mortality rate. Systemic hemodynamics, carotid artery blood flow changes and biochemical variables were assessed at pre-treatment and 1, 2 and 3 h after the treatment was performed. Results: In both non-diabetic and diabetic rats, administration of lipopolysaccharide (LPS) induced a reduction in hemodynamic variables, these reductions being greater in diabetic than in non-diabetic rats. In diabetic rats, administration of AM281 could only partially prevent these hemodynamic changes, these changes being insufficient to elevate these variables to control values. Significant differences were observed in mortality rates at 6 and 12 h between non-diabetic and diabetic groups with the same treatment. At 12 h, only non-diabetic AM281 group rats were still alive (mortality rate 50%). Conclusion: Administration of AM281 only partially prevented the hemodynamic, biochemical and carotid artery blood flow changes associated with LPS-induced septicemia in diabetic rats, as compared with non-diabetic rats in whom these changes were prevented to a greater extent.

Although the factors influencing seizure duration during electroconvulsive therapy (ECT) remain unknown, most anesthetic and hypotonic agents have some impact on seizure duration, ictal and postictal electrophysiological variables and the clinical efficacy of ECT. When a longer seizure duration is needed, etomidate, methohexital or a combination of small doses of a short-acting opiate with propofol are used.

The purpose of this study was to examine whether selective iNOS inhibition can restore the hemodynamic changes and reduce the nitrotyrosine levels in the cerebral cortex of rats with streptozotocin-induced diabetes during endotoxin-induced shock. The study was designed to include three sets of experiments: (1) measurement of changes in systemic hemodynamics, (2) measurement of biochemical variables, including iNOS activity and nitrotyrosine formation in the brain, and (3) assessment of mortality rate. Rats were randomly divided into four groups: group 1, control; group 2, LPS: Escherichia coli endotoxin, 10.0 mg/kg (i.v.) bolus; group 3 (i.v.) LPS and L-N6-(1-iminoethyl)-lysine (L-NIL), 4mg/kg (i.p.); and group 4, LPS and NG-nitro-L-arginine methyl ester (L-NAME), 5 mg/kg (i.p.). In nondiabetic rats, administration of L-NIL prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels induced by LPS. Administration of L-NAME partially prevented these LPS-induced changes. On the other hand, in diabetic rats, administration of L-NIL only partially prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels associated with LPS. Administration of L-NAME, however, had no effects on these LPS-induced changes in diabetic rats. There was a significant difference in nitrotyrosine levels between nondiabetic and diabetic rats in groups 2, 3, and 4 at 2 and 3 h after the treatment (at 3 h; nondiabetic--control, 4.6 +/- 0.4; LPS (i.v.), 8.9 +/- 1.0, LPS (i.v.) + L-NIL, 4.7 +/- 0.5; LPS (i.v.) + L-NAME, 7.1 +/- 0.9; diabetic--control, 5.5 +/- 0.4; LPS (i.v.), 13.6 +/- 1.2; LPS (i.v.) + L-NIL, 9.0 +/- 0.9; LPS (i.v.) + L-NAME, 13.0 +/- 1.0; densitometric units). Insulin therapy resulted in a decrease in iNOS activity (at 3 h: 1.0 +/- 0.5 fmol mg min), nitrotyrosine formation (at 3 h; 5.0 +/- 0.5, densitometric units), and mortality rates (30% at 6 h, 50% at 12 h) in the LPS (i.v.) + L-NIL group of diabetic rats. Selective iNOS inhibition in diabetic rats could not improve hemodynamic instability, chemical changes, iNOS activity, and nitrotyrosine formation during septic shock compared with the improvements observed in nondiabetic rats. Tight glucose control along with administration of L-NIL can result in more effective restoration of the biochemical changes of septicemia in diabetic rats. Thus, hyperglycemia may be one of the mechanisms related to the aggravation of endotoxin-induced shock.

The purpose of this study was to retrospectively examine whether sevoflurane anesthesia had any ameliorative effects on postoperative cognitive dysfunction in patients undergoing coronary artery bypass graft (CABG) surgery.One hundred and nine patients underwent elective CABG surgery at our institution from May 1999 to May 2001. From May 1999 to August 2000, the main anesthetic regime used included a propofol infusion with no volatile anesthetic being administered during the surgery. From September 2000 to May 2001, the main anesthetic regime used was 1.5%-2.0% sevoflurane from the postinduction period until the end of the surgery. All patients underwent a battery of neurological and neuropsychological tests 1 day before and 6 months after the operation.The use of sevoflurane did not have any significant effects on the postoperative levels of cognitive dysfunction. In contrast, multiple logistic analysis showed that age [odds ratio (OR), 1.3; P = 0.047], diabetes mellitus (OR, 2.5; P = 0.03), and atherosclerosis of the ascending aorta (OR, 1.4; P = 0.047) appeared to be predictive factors of postoperative cognitive dysfunction.This retrospective study showed no relationship between postoperative cognitive dysfunction and the use of sevoflurane.

We report here the anesthetic management of a patient with schizophrenia and pseudocholinesterase deficiency. Electroconvulsive therapy was performed using succinylcholine and rocuronium as the neuromuscular blocking agents in the first seven and latter six treatments, respectively. The recovery time from muscle relaxation after succinylcholine administration was remarkably longer than that after rocuronium-sugammadex administration. Rocuronium and sugammadex appear to be useful in situations in which succinylcholine is contraindicated.

The purpose of this study was to examine the comparative effects of AM281, a cannabinoid antagonist, and norepinephrine (NE) on systemic hemodynamics, and renal and mesenteric artery blood flow in an endotoxin shock model.The study was designed to include two sets of experiments: (1) measurements of changes in systemic hemodynamics and organ artery blood flows (n = 20), and (2) measurements of biochemical variables (n = 20). For each set of experiments, male 7-week-old Wistar rats were randomly divided into four groups: group 1, controls (n = 5); group 2, receiving lipopolysaccharide (LPS: Escherichia coli endotoxin, 10.0 mg.kg(-1) intravenous bolus) (n = 5); group 3, receiving intravenous LPS and NE (continuous infusion at 0.2 microg.kg.min(-1)) (n = 5); group 4, receiving LPS and AM281 (0.1 mg.kg.min(-1)) (n = 5). Systemic hemodynamics, regional artery blood flow changes, and biochemical variables were assessed before treatment and 1 and 3 h after treatment.Infusion of NE or AM281 prevented endotoxin-induced decreases in systemic arterial pressure, aortic blood flow, carotid artery blood flow, and renal artery blood flow. Both AM281 and NE inhibited endotoxin-induced increases in cytokine production, with significant differences observed among the three groups at 1 and 3 h after treatment. Endotoxin-induced decreases in mesenteric arterial blood flow were restored by AM281 but not by NE. AM281 improved arterial oxygenation and reduced lactate overproduction and body temperature elevation induced by endotoxin.Although NE and AM281 both prevented endotoxin-induced deterioration of systemic hemodynamics, AM281 yielded better preservation of mesenteric blood flow and attenuation of cytokine production than NE.

平成17年の4週間に群馬大学医学部附属病院で行われた全身麻酔予定手術222例における麻酔関連薬物破棄量を検討した. 麻酔方法は, 患者の年齢等を考慮しながらプロポフォール1～2mg/kg, ベクロニウム0.1mg/kgで導入し, 亜酸化窒素4l/分-酸素2l/分-セボフルランでの麻酔維持を基本とした. 麻酔導入時の血行動態の変動に対しての各種薬物使用は各担当麻酔科医の判断とした. 心臓・血管外科手術の麻酔方法は, ミダゾラム0.1mg/kg, フェンタニル10μg/kg, ベクロニウム0.1mg/kgで導入し, プロポフォール4～6mg/kg, セボフルラン0.5～1.0%とフェンタニルの間欠投与で維持し, フェンタニルの使用量は最高20μg/kgまでとした．222例の注射器の平均使用本数は8.8±8.5本, 全破棄した薬物の金額は142±343円, 一部破棄した薬物の金額は954±876円であった. プロポフォールは222例中169例で破棄があり, 平均残量は88±48mg, ベクロニウムは222例中162例で破棄があり, 平均残量は4.5±2.8mg, エフェドリンは222例中156例で破棄があり, 平均残量は34±7mgであった. プロポフォール, ベクロニウム, エフェドリンは7割以上の症例で破棄されていた. 麻酔科医は使用しなかった麻酔関連薬物量およびその金額を正確に把握し, それらの量や金額を減らすことに注意することも肝要であると思われる.

Study Objective The goal of this study was to characterize the hemodynamic response to propofol vs propofol with fentanyl when used for sedation after esophagectomy or cardiac surgery. Design Prospective, randomized, controlled study. Setting University Hospital, Intensive Care Unit. Patients Thirty patients undergoing elective cardiac surgery and 26 patients undergoing esophagectomy were examined. Intervention Patients were randomized to receive propofol (0.5 mg/kg bolus over 10 minutes, followed by continuous infusion at 1 mg/kg per hour) with or without fentanyl (2.0 μ g/kg per hour) to achieve sedation overnight while in the intensive care unit. Randomization was performed in a double-blind manner. Measurement Mean arterial pressure (MAP) was monitored throughout the treatment period, and sedation level was measured. Sedation level was targeted to achieve a Ramsay score of 4. Main Results The number of patients experiencing a greater than 20% drop in baseline MAP was higher in cardiac patients receiving propofol alone (11 of 15 patients, 73%) than in cardiac patients receiving propofol with fentanyl (4 of 15 patients, 27%). Furthermore, the time of optimal sedation was lower in the cardiac patients who received propofol than in cardiac patients who received propofol with fentanyl group (propofol alone, 79%; propofol with fentanyl, 88%). In contrast, there was no difference in the number of esophagectomy patients experiencing a greater than 20% drop in baseline MAP or in the mean time of optimal sedation when comparing the 2 treatment regimens. Conclusions Propofol has a differential effect on hemodynamics and sedation when comparing patients after cardiac surgery and esophagectomy.

We sought to examine what factors, including cerebrovascular carbon dioxide (CO(2)) reactivity, are related to a decrease in internal jugular venous oxygen saturation (SjvO(2)) during normothermic cardiopulmonary bypass (CPB) in patients with diabetes mellitus.Twenty-three diabetic patients scheduled to undergo elective coronary artery bypass grafting were studied. As a control, 27 age-matched control patients without diabetes mellitus were also examined. After the induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor SjvO(2). Arterial and jugular venous blood gases were measured during CPB. The cerebrovascular CO(2) reactivity was measured after the induction of anesthesia and before the start of surgery using a 2.5-MHz pulsed transcranial Doppler probe.The SjvO(2) values in the diabetic group were lower than those in the control group at the initiation of CPB and at 20, 40, and 60 min after the start of CPB. The values for pre- and post-CO(2) reactivity in the control group did not significantly differ (pre-CPB: 4.8% +/- 2.3% mmHg(-1); post-CPB: 5.9% +/- 4.4% mmHg(-1)). In contrast, the values for CO(2) reactivity were lower post CPB than pre-CPB in the diabetic group (Pre-CPB: 6.3% +/- 2.9% mmHg(-1); post-CPB: 4.7% +/- 2.6% mmHg(-1); P0.05). In the diabetic group, glycosylated hemoglobin A1c (HbA1c) is considered to be a factor related to a decrease in SjvO(2) during CPB.Cerebrovascular CO(2) reactivity in diabetic patients decreased after the cessation of CPB but not in the control patients. In addition, HbA1c is also thought to be a factor related to a decrease in SjvO(2) in diabetic patients.

Objectives The mechanisms of postoperative cognitive dysfunction in patients with diabetes after coronary artery bypass grafting are not fully understood. We sought to determine which type 2 diabetes–related factors contributed to postoperative cognitive dysfunction at 7 days and 6 months after coronary artery bypass grafting. Methods One hundred eighty patients with type 2 diabetes who were scheduled for elective coronary artery bypass grafting were studied. As a control group, 100 patients without diabetes mellitus matched for age, sex, and educational level were examined. Hemodynamic parameters (arterial and jugular venous blood gas values) were measured during cardiopulmonary bypass. All patients underwent a battery of neurologic and neuropsychologic tests the day before surgery, 7 days after surgery, and 6 months after surgery. Results Age (odds ratio 1.5, 95% confidence interval 1.3-1.8, P = .03), presence of hypertension (odds ratio 1.8, 95% confidence interval 1.3-2.0, P = .01), jugular venous oxygen saturation less than 50% time (odds ratio 1.5, 95% confidence interval 1.1-2.0, P = .045), presence of ascending aorta atherosclerosis (odds ratio 1.5, 95% confidence interval 1.1-2.6, P = .01), diabetic retinopathy (odds ratio 2.0, 95% confidence interval 1.3-3.0, P = .01), and insulin therapy (odds ratio 2.0, 95% confidence interval 1.3-3.0, P = .05), were associated with cognitive impairment at 7 days. Insulin therapy (odds ratio 2.0, 95% confidence interval 1.3-3.8, P = .01), diabetic retinopathy (odds ratio 1.3, 95% confidence interval 1.2-2.9, P 1c (odds ratio 1.9, 95% confidence interval 1.3-3.1, P = .047) were associated with cognitive impairment at 6 postoperative months. Conclusions Insulin therapy, diabetic retinopathy, and hemoglobin A 1c were factors in cognitive impairment at 7 days and 6 months after coronary artery bypass grafting in patients with type 2 diabetes.

In this study, we examined whether cerebrovascular carbon dioxide (CO(2)) reactivity was related to the response of jugular venous oxygen saturation (SjvO(2)) to phenylephrine infusion in diabetic patients during cardiopulmonary bypass. Forty diabetic patients scheduled for coronary artery bypass graft surgery were studied, and 40 age-matched nondiabetic cardiopulmonary bypass patients served as controls. Cerebrovascular CO(2) reactivity was measured continuously using transcranial Doppler. Mean arterial blood pressure (MAP) was increased by repeated phenylephrine infusion until reaching 100% of baseline values. There was a significant difference in absolute CO(2) reactivity between the diabetic and control groups (controls, 2.8 +/- 0.7 cm. s(-1). mm Hg(-1); diabetics, 2.2 +/- 1.1 cm. s(-1). mm Hg(-1); P = 0.02). Among the diabetics, absolute CO(2) reactivity in insulin-dependent patients was less than that in noninsulin-dependent patients (diet therapy group, 3.2 +/- 0.7; glibenclamide group, 2.6 +/- 0.7; insulin-dependent group, 1.0 +/- 0.7; P < 0.01). There was a correlation between absolute CO(2) reactivity and the mean slope of SjvO(2) versus MAP for increasing MAP (r = 0.54; P < 0.0001). In conclusion, we found that the interrelationship between SjvO(2) responsiveness to phenylephrine infusion and cerebrovascular CO(2) reactivity, as well as impaired cerebrovascular autoregulation, were associated with previous hyperglycemia.

In this study, we evaluated the time course of changes in inducible nitric oxide synthase (iNOS) in the brain by using the rat model of sepsis induced by cecal ligation and puncture (CLP) and examined whether selective iNOS inhibition can prevent the hemodynamic and neurological changes induced by sepsis. Male Wistar rats were randomly divided into four groups: control, sham, CLP, and CLP + the selective iNOS inhibitor L-N6-(1-iminoethyl)-lysine (L-NIL). Septic shock was induced in the rats by CLP under pentobarbital anesthesia, and then we measured hemodynamic variables, neurological indicators, blood gases, plasma levels of nitrate/nitrite (an indicator of the biosynthesis of NO), and brain iNOS activity and nitrotyrosine levels after 1, 6, 12, and 24 h. Plasma nitrite was increased at 12 and 24 h in the CLP group. The activity of iNOS in the brain was increased at 12 and 24 h after CLP (at 12 h: control, 0.3 +/- 0.05; sham, 0.3 +/- 0.1; CLP, 1.3 +/- 0.08*; CLP + L-NIL, 0.33 +/- 0.1 fmol x mg(-1) x min(-1); at 24 h: control, 0.27 +/- 0.08; sham, 0.31 +/- 0.1; CLP, 1.0 +/- 0.3*; CLP + L-NIL, 0.34 +/- 0.1 fmol x mg(-1) x min(-1); mean +/- SD; *P0.05). Brain nitrotyrosine was increased at 24 h after CLP (at 24 h: control, 6.7 +/- 0.4; sham, 6.7 +/- 0.5; CLP, 11.2 +/- 2.8*; CLP + L-NIL, 7.52 +/- 0.5 densitometric units; means +/- SD; *P0.01). In contrast, in both the CLP and CLP + L-NIL groups, the consciousness reflex was significantly decreased at 24 h after CLP. Selective iNOS inhibition restored the hemodynamic changes induced by sepsis but could not improve neurological dysfunction.

Background and Purpose— The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. Methods— Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient’s head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO 2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO 2 increased and remained stable for 5 to 10 minutes. Results— Significant differences were observed in absolute and relative CO 2 reactivity between the diabetes and control groups (absolute CO 2 reactivity: control, 2.8±0.7; diabetes mellitus, 2.1±1.3; P 2 reactivity: control, 6.3±1.4; diabetes mellitus, 4.5±2.7; P U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute ( P =0.002) and relative ( P =0.002) CO 2 reactivity, glycosylated hemoglobin ( P =0.0034), and fasting blood sugar ( P =0.01) (Scheffé’s test, Mann-Whitney U test). There was an inverse correlation between absolute CO 2 reactivity and glycosylated hemoglobin ( r =0.69, P Conclusions— Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.

Adrenomedullin is a potent vasodilatory peptide. Plasma adrenomedullin (AM) concentrations increase during and after cardiopulmonary bypass (CPB). However, the cause of this increase and its site of production have not been identified. We investigated the role of the hepatosplanchnic and cerebral circulations in the increase of plasma AM and investigated whether tissue hypoxygenation is a cause of the AM increase seen during CPB. We measured plasma total AM (AM-T) and the biologically active form of AM, mature AM (AM-m), in seven patients undergoing CPB. Both plasma AM-T and AM-m concentrations increased significantly 60 min after weaning from CPB. At this time point, arterial AM-T and AM-m concentrations were 18-fold and 10-fold larger, respectively, than baseline values measured after the induction of anesthesia. The plasma AM-m concentration and the ratio of AM-m/AM-T in blood from the hepatic vein were significantly larger than those from the radial artery or jugular bulb. The AM-m/AM-T ratio decreased during CPB, suggesting that production of the intermediate form of AM, AM-glycine, is more than that of AM-m. The oxygen tension of the hepatic venous blood (PhvO2) was significantly less during CPB. Plasma AM-m concentrations sampled from the hepatic vein showed a significant negative correlation with PhvO2 at 10 min (r = 0.824; P < 0.02) and 60 min (r = 0.828; P < 0.02) after the onset of CPB. These data suggest that the hepatosplanchnic circulation is an important source of AM-m during CPB. Furthermore, hypoxygenation of the hepatosplanchnic region may be an important cause of this AM-m increase.

Study objective To examine whether increasing mean arterial pressure (MAP) with the administration of phenylephrine would improve internal jugular venous oxygen saturation (SjvO2) during normothermic cardiopulmonary bypass (CPB) in patients with preexisting stroke. Design Prospective, controlled study. Setting Cardiovascular center and university hospital. Patients 17 patients with preexisting stroke who were scheduled for elective coronary artery bypass graft (CABG) surgery, and a control group of 17 age-matched patients without preexisting stroke. Interventions After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor SjvO 2 . After measuring the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values immediately before the start of the study protocol, MAP was increased by the repeated administration of a 10 μg bolus of phenylephrine, until it reached 200% of baseline values. Measurements Partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values before and after the treatment were recorded. Main results There was no significant difference between the groups in SjvO 2 values at baseline (Mann-Whitney U test: p = 0.22). SjvO 2 values in both groups were increased after the administration of phenylephrine (SjvO 2 values in the control group: 60 ± 5%, SjvO 2 values in the stroke group: 57 ± 5%). There was no significant difference between the stroke and control groups in SjvO 2 values after the administration of phenylephrine (Mann-Whitney U test: p = 0.08). Conclusions Increasing MAP improves SjvO 2 in patients with or without preexisting stroke during normothermic CPB.

BACKGROUND There have been many studies regarding the etiology of postoperative cognitive dysfunction after coronary artery bypass graft (CABG) surgery. Although its etiology remains unresolved, one possible factor related to postoperative cognitive dysfunction is a reduced internal jugular venous oxygen hemoglobin saturation (SjvO2) during the rewarming period. The purpose of this study was to examine the effect of rewarming rates on SjvO2 during rewarming. METHODS One-hundred patients scheduled for elective CABG surgery were randomly divided into two groups; control group (0.48 +/- 0.09 degrees C, n = 50), slow rewarming group (0.24 +/- 0.09 degrees C, n = 50). After the induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor SjvO2 continuously. Hemodynamic parameters, arterial and jugular venous blood gases were measured at nine time-points. RESULTS Cerebral desaturation (defined as a SjvO2 value below 50%) during rewarming was more frequent in the control group than in the slow group. Cerebral desaturation time (duration when SjvO2 was less than 50%) and the ratio of the cerebral desaturation time to the total CPB time in the control group differed significantly from those in the slow group (control group: 17 +/- 11 min, 12 +/- 4%, slow group: 10 +/- 8 min, 7 +/- 4%, respectively, P < 0.05). There was no significant difference in mini-mental state examination on the day before the operation nor at 1 month after the surgery among four values (the day before the operation: control group; 48 +/- 8, slow group; 48 +/- 7, at one month after the surgery: control group; 46 +/- 7, slow group; 45 +/- 9). CONCLUSIONS A slow rewarming rate could reduce the chance of a decrease in SjvO2 during rewarming.

The purpose of this study was to compare the effect of propofol versus thiopentone on haemodynamics during electroconvulsive therapy (ECT), as estimated by echocardiography. Twenty-eight ASA 1 or 2 patients scheduled for ECT were randomly divided into two groups, to receive propofol 1 mg/kg (propofol group, n=14) or thiopentone 2 mg/kg (thiopentone group, n=14). Bilateral ECT was performed after the administration of propofol or thiopentone, succinylcholine and following assisted mask ventilation with 100% oxygen. Cardiac function was examined by transthoracic echocardiography, prior to induction of anaesthesia and throughout ECT until ten minutes after the seizure. In the propofol group, increased end-systolic area (ESA) and decreased fractional area change (FAC) were observed at one minute after the electrical shock compared with the awake condition. In the thiopentone group, increased ESA and decreased FAC were observed from one to three minutes after the electrical shock compared with the awake condition. There was no statistically significant change in after load in the propofol group during the study. In contrast, increased after load was observed from one to three minutes after the electrical shock in the thiopentone group (awake condition, 26±7 mmHg/cm 2 [mean±SD]; one minute after ECT, 42±7*; two minutes after ECT, 44±6*; three minutes after ECT; 40±5*, respectively)(*P We concluded that a lesser haemodynamic change occurs after propofol anaesthesia (1 mg/kg) compared with thiopentone anaesthesia (2 mg/kg) during ECT.

Carotid endarterectomy (CEA) is a preventative procedure performed in the presence of well-defined indications. Although the impact of the type of anesthetic method on outcomes has been extensively studied, it remains unresolved whether regional or general anesthesia is superior in CEA. The use of a carotid shunt is based on neurological monitoring during clamping. Although various techniques have been used to monitor cerebral perfusion under general anesthesia and detect cerebral ischemia during carotid artery cross-clamping, none are completely reliable. Drastic hemodynamic changes may be observed during both the intraoperative and postoperative periods. It is essential to maintain adequate systemic and cerebral hemodynamics during the perioperative period.

Background. One of the key mechanisms leading to β-adrenergic receptor-specific desensitization is the phosphorylation of agonist-occupied receptors by the specific β-adrenergic receptor kinase (GRK2). The present study examines whether GRK2 is altered during septic shock in rats. Materials and methods. Male Wistar rats (7 weeks) weighing between 250 and 300 g were anesthetized with pentobarbital (10 mg/kg ip). Escherichia coli endotoxin (10 mg/kg in 0.3 mL of saline) or saline (0.3 ml) was injected intravenously via the dorsal vein. Hemodynamic parameters and humoral mediators were measured at 2 h after the administration of endotoxin. The hearts were immediately excised to examine β-adrenergic receptor density and GRK2 level. We also studied the inotropic response to isoproterenol at the same time in other animals. Results. Myocardial β-adrenergic receptor density in the membrane fraction was decreased after an intravenous administration of 10 mg/kg LPS (LPS group: baseline value; 82 ± 11 fmol/mg protein; 120 min after LPS; 58 ± 11 fmol/mg protein, P < 0.05). GRK2 levels in the membrane and cytosolic fraction of the control group did not change. In the LPS group, GRK2 levels in the membrane fraction were increased at 60 and 120 min after the treatment (60 min; control, 4.5 ± 0.4; pithed control, 4.4 ± 0.6; LPS group, 6.2 ± 0.3; pithed LPS group, 5.5 ± 0.4; 120 min: control, 4.4 ± 0.3; pithed control, 4.9 ± 0.7; LPS group, 7.1 ± 0.3; pithed LPS group, 5.9 ± 0.4; densitometric unit, respectively: P < 0.05). Conclusions. GRK2 levels in the membrane fraction are increased during septic shock in rats. GRK2 might play a role in the impairment of the β-adrenergic receptor signal transduction system.

Hepatic sinusoidal endothelial cells (SECs) are more vulnerable to hypoxia or hypothermia than hepatocytes. To test the hypothesis that hepatic venous desaturation during cardiopulmonary bypass (CPB) leads to impairment of SEC function, we studied the plasma kinetics of endogenous hyaluronate (HA), a sensitive indicator of SEC function, and hepatosplanchnic oxygenation during and after CPB. Twenty-five consecutive patients scheduled for elective coronary artery bypass graft surgery, who underwent normothermic (35 degrees C; n = 15) or mild hypothermic (32 degrees C; n = 10) CPB participated in this study. A hepatic venous catheter was inserted into each patient to monitor hepatosplanchnic oxygenation and serum levels of HA concentration. Hepatic venous oxygen saturation decreased essentially to a similar degree during normothermic and mild hypothermic CPB. Hepatosplanchnic oxygen consumption and extraction increased during normothermic (P0.05), but not mild hypothermic, CPB. Both arterial and hepatic venous HA concentrations showed threefold increases during and after CPB in both groups. A positive correlation was found between hepatosplanchnic oxygen consumption and arterial HA concentrations during CPB, suggesting a role of changes in hepatosplanchnic oxygen metabolism in the mechanisms of increases in serum HA concentrations. The failure of the liver to increase HA extraction to a great degree suggests that a functional impairment of the SEC may contribute to the observed increase of serum HA.Hepatic sinusoidal endothelial cells (SECs) are pivotal in the regulation of sinusoidal blood flow. This study showed that SEC function might be impaired during and after cardiopulmonary bypass, irrespective of the temperature management.