Search

We previously showed that preischemic administration of high-dose isoflurane worsened the outcome from severe forebrain ischemia in rats. Conversely, high doses of sevoflurane have been reported to improve the outcome from forebrain ischemia when the insult is moderate. To clarify the dose-dependent effects of sevoflurane on severe forebrain ischemia, we performed an outcome study using an identical protocol to that in our previous study with isoflurane. Fasting male Sprague-Dawley rats underwent surgical preparation for forebrain ischemia under halothane anesthesia. Anesthesia was changed to fentanyl/nitrous oxide to eliminate the halothane, after which 30 minutes of 0.5, 1.0, 1.5, 2.0, or 2.5 minimum alveolar concentration sevoflurane was administered. Ten minutes of ischemia was induced by bilateral carotid occlusion plus systemic hypotension, in which cessation of electroencephalographic activity was confirmed. Sevoflurane was discontinued and anesthesia continued with fentanyl/nitrous oxide for an additional 100 minutes. Outcome evaluation at 5 days postischemia included seizure incidence, mortality rate, neuromotor score, and histologic injuries to the cerebral cortex and hippocampal CA1 and CA3. Different doses of sevoflurane did not statistically affect seizure incidence (10.0% to 18.2%), mortality rate (20.0% to 46.7%), cortical damage (mild to moderate degree), or hippocampal CA1 damage (93.7% to 96.7% neuronal necrosis) or CA3 damage (36.3% to 41.7%). Dose-dependent effects of sevoflurane were not observed for any of the outcome variables assessed in this rat model of severe forebrain ischemia.

Transplantation of bone marrow or adipose-derived mesenchymal stem cells (MSCs) for various neurological disorders has yielded promising results in models of focal cerebral ischemia. Dental pulp stem cells (DPSCs) are a type of MSC. In serum-free culture, they can form neurospheres that contain nestin-positive neuronal progenitor cells. We hypothesized that transplantation of dental pulp-derived neurosphere cells would ameliorate outcomes of global cerebral ischemia, the pathophysiology of which is known to resist conventional treatments. We also hypothesized that transplantation of dental pulp-derived cells would provide some neuroprotection in this pathology due to the presence of DPSCs. Using adult rats, ischemia was induced by two-vessel occlusion of both carotid arteries in combination with systemic hypotension. Allogeneic dental pulp cells from juvenile rats were cultured in advance in serum-free medium to obtain neurospheres. Dental pulp-derived neurosphere cells or dental pulp-derived cells were intravenously administered at 3 h after ischemic insult, with normal saline as a control. Animals were observed for 14 days after ischemia. Neurological outcome was assessed using the water-maze test and neuromotor test. Histological outcome was measured by counting the percentage of dead neurons in the hippocampal CA1 and CA3 regions. Transplantation of both dental pulp-derived neurosphere cells and dental pulp-derived cells significantly improved survival rate and water-maze test results. Neurosphere cell transplantation was related to significantly better neuromotor test and histological outcomes, as indicated by the reduced percentage of dead neurons in CA1. Transplantation of dental pulp-derived neurosphere cells ameliorated outcomes of global cerebral ischemia. It was also demonstrated that dental pulp-derived cell administration provided some neuroprotection.

Studies comparing the recovery profiles of isoflurane- and propofol-based anesthesia for major intracranial surgery have reported contradictory results. The aim of our study was to clarify the emergence status in both regimens by investigating uniformly managed neuroanesthesia cases. The anesthesia database at Yamagata University Hospital covering the period 2002–2005 was retrospectively investigated for adult patients who underwent craniotomy for primary brain tumor excision. General anesthesia was provided by an isoflurane- (ISO group) or propofol-based (PROP group) regimen. Times to extubation and operating room (OR) discharge, perioperative consciousness levels, and perioperative variables were compared. Of the 202 surgeries performed during the study period, 77 and 82 patients were anesthetized with isoflurane and propofol, respectively. Demographic data were comparable between the two groups, although the American Society of Anesthesiology grade was worse in the PROP group. Extubation times [39.5 ± 14.6 min (ISO) vs. 29.5 ± 14.9 min (PROP); P

Prostaglandin E(1) (PGE(1)) has been shown to provide short-term neuroprotection against various types of brain ischemia in a dose-dependent manner in mice. However, these findings were obtained from experiments performed without any control over physiological parameters. We performed an outcome study where physiological parameters were controlled in an attempt to confirm the dose-dependant neuroprotective effects of PGE(1).A rat model of severe forebrain ischemia was used. Two doses of PGE(1) were administered during the pre-ischemic period, a low dose (LowPG group) and a high dose (HighPG group). Normotension was maintained in the LowPG group, while hypotension was induced in the HighPG group. In separate groups, normal saline (Control) or sodium nitroprusside (SNP) were infused to compare outcomes under similar blood pressure conditions. Histological outcomes in the hippocampal CA1 and entorhinal cortex were evaluated 5 days post-ischemia.HighPG resulted in hyperglycemia. The percentage of dead neurons in the hippocampal CA1 and entorhinal cortex were similar in the Control, SNP, and HighPG groups, the percentage being significantly attenuated in the LowPG group (CA1: Control = 92.8 +/- 2.4%, LowPG = 85.0 +/- 8.5%, HighPG = 95.3 +/- 2.4%, and SNP = 96.4 +/- 0.7%, P0.01; entorhinal cortex: Control = 73.8 +/- 4.0%, LowPG = 53.2 +/- 12.3%, HighPG = 72.1 +/- 12.6%, and SNP = 76.5 +/- 4.1%, P0.01).Pre-ischemic administration of low-dose PGE(1) in rats provided neuroprotection against severe forebrain ischemia. A dose dependency was not observed with PGE(1) dose and outcome.

Background Dexmedetomidine (Dex) provides sedation and analgesia by acting on central alpha-2 receptors and is suitable for use after extubation because it has little respiratory depression. Considering the sympathoinhibitory and anxiolytic action of Dex, there is the possibility that Dex might reduce the incidence of atrial fibrillation (AF), which is recognized as a common complication after cardiovascular surgery. We investigated whether the postoperative incidence of AF decreased in patients who received Dex only during the nighttime in the intensive care unit (ICU). Methods We retrospectively reviewed ICU charts to determine the incidence of AF and associated factors during the 2-day period after tracheal extubation in patients who underwent cardiovascular surgery from November 2009 to November 2010. The patients were divided into a Dex group (n = 16) and a non-Dex group (n = 29). Results There were no differences in AF risk factors except for diabetes between the two groups. The average rate of Dex administration was 0.3 ± 0.2 μg/kg/h. There were also no differences between the groups in heart rate during the daytime, central venous pressure, body temperature, white blood cell count, serum level of C-reactive protein, catecholamine use, beta-blocker use, and amount of fentanyl. AF developed in one patient in the Dex group (6.3 %) and ten patients in the non-Dex group (34.5 %) during the observation period, and the difference was significant (p = 0.035). None of the risk factors for AF was significantly associated with AF in univariate analysis; however, multivariate logistic regression analysis using age, Dex use, and beta-blocker use, extracted because their p values in univariate analysis were not exceeding 0.15, showed that Dex use was the only factor associated with the development of AF (p = 0.045, odds ratio 9.75 [1.05–90.8]). Conclusions The results suggest that adequate sedation with Dex during the nighttime can reduce the incidence of AF in cardiovascular surgery patients after extubation.

Isoflurane improves outcome against cerebral ischemia in the rat. However, the optimal neuroprotective concentration has not been defined. We examined the effects of different isoflurane concentrations on outcome from severe forebrain ischemia in the rat. Fasted rats were subjected to 0.5, 1.0, 1.5, 2.0, or 2.5 minimum alveolar concentration (MAC) isoflurane during 10 min bilateral carotid occlusion plus systemic hypotension. Each isoflurane concentration was administered only before ischemia. Arterial blood pressure was not pharmacologically manipulated. After ischemia, the anesthetic regimen was changed to fentanyl/nitrous oxide and maintained for 2 h. Pericranial temperature was maintained normothermic during the experiment. Neuromotor score, % dead hippocampal CA1 neurons, and cortical injury were measured 5 days postischemia. Preischemic arterial blood pressure decreased as MAC was increased. Animals administered1.0 MAC frequently exhibited postischemic seizures resulting in increased mortality. There was no difference among MAC conditions for % dead CA1 neurons (93 approximately 95%). In the cortex, neuronal necrosis was less severe with 0.5 MAC and 1.0 MAC isoflurane relative to1.0 MAC values. The neuromotor score in the 1.0 MAC isoflurane group was superior to the 2.5 MAC group. Dose-dependent effects of preischemic administration of isoflurane on histologic and behavioral outcome after severe forebrain ischemia were observed. Isoflurane MAC values1.5 provided superior overall outcome relative to larger isoflurane concentrations.

Several studies have reported that height is inversely associated with risk of cardiovascular disease but positively associated with cancer risk. On the other hand, evidence has been accumulating that anemia reflects poor health and increased vulnerability to poor outcomes in older persons. Moreover, alcohol consumption has also been reported to be associated with mortality. However, no studies have reported on a possible association between height and risk of anemia in relation to drinking status.We conducted a cross-sectional study of 1287 men aged 40-89 years undergoing general health check-ups.Independent from classic cardiovascular risk factors, we found a significant inverse association between height and anemia for non-drinkers and a J-shaped association for drinkers. The multivariable odds ratio (ORs) of an increment of 1 SD (standard deviation) in height (6.68 cm) for anemia for non-drinkers was 0.59 (0.45-0.77). For drinkers, with the second quartile of height (Q2) as the reference group, the multivariable OR of anemia was 2.68(0.90-7.96) (p = 0.075) for the lowest height quartile (Q1), 2.73(0.92-8.08) for the third quartile (Q3) and 4.82(1.65-14.10) for the highest quartile (Q4) (p = 0.004).Height was found to be associated with anemia for rural Japanese men and drinking status is likely to affect those associations.

Manipulations of plasma catecholamine concentrations influence outcome from ischemic brain insults. It has been suggested that these effects are mediated by influences on brain catecholamine concentrations. This study examined whether major changes in brain norepinephrine concentrations can alter outcome from severe forebrain ischemia. Sprague-Dawley rats were administered 50 mg/kg i. p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were left untreated (control). One week later, these rats were subjected to either 7 or 8 min of normothermic forebrain ischemia (bilateral carotid occlusion and MABP=30 mmHg) and allowed to recover for 4 days. Histologic damage was then evaluated. In other control and DSP-4-treated animals, hippocampal microdialysate norepinephrine concentrations were measured before, during and after 8 min of forebrain ischemia. Norepinephrine concentrations were also determined in brain homogenates from non-ischemic DSP-treated and control rats. A 95% depletion of norepinephrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control. During ischemia, microdialysate norepinephrine concentrations increased in control but not in DSP-4-treated rats (P=0.002). For plasma, intra-ischemic epinephrine concentrations increased 8-10-fold and returned to baseline values post-ischemia with no differences between groups. Plasma norepinephrine values remained unchanged in both groups. Histologic damage resulting from either 7 or 8 min of ischemia in hippocampal structures, caudoputamen, and neocortex was similar between DSP-4-treated and control groups. This study could not identify any effect of major changes in brain norepinephrine concentrations on ischemic brain damage. These data indicate that peripheral catecholamine effects on near-complete forebrain ischemic outcome are unlikely to be mediated by effects on central catecholamine concentrations.

UNLABELLED We postulated that adrenergic responses to global cerebral ischemia are anesthetic-dependent and similar in both brain and arterial blood. Rats were anesthetized with isoflurane (1.4%), ketamine (1 mg x kg(-1) x min(-1)), or fentanyl (25 microg x kg(-1) x h(-1))/70% N2O. The carotid arteries were occluded for either 20 min with mean arterial pressure (MAP) 50 mm Hg (incomplete ischemia) or 10 min with MAP 30 mm Hg (near-complete ischemia). Norepinephrine was measured in hippocampal microdialysate. Norepinephrine and epinephrine were measured in arterial plasma. In both hippocampus and plasma, basal norepinephrine was similar among anesthetics. During incomplete ischemia, hippocampal norepinephrine was twofold greater with fentanyl/N2O than with isoflurane (P = 0.037), but plasma norepinephrine and epinephrine were similar and unchanged among all three anesthetics. During near-complete ischemia, hippocampal norepinephrine was threefold greater with ketamine than fentanyl/N2O (P = 0.005), whereas plasma norepinephrine and epinephrine were markedly greater with fentanyl/N2O than with ketamine (P < 0.0005) or isoflurane (P = 0.05). There was no correlation between norepinephrine concentrations in hippocampus and plasma for either incomplete or near-complete ischemia. This study demonstrates that adrenergic responses to global ischemia are anesthetic-dependent, particularly during more severe insults. The absence of a correlation between plasma and brain catecholamine concentrations indicates that adrenergic responses to ischemia are independent in brain and blood. IMPLICATIONS It has been proposed that anesthetics modulate cerebral ischemic outcome by influencing peripheral adrenergic responses to ischemia. This experiment demonstrates that anesthetics differentially modulate adrenergic responses to ischemia but that effects in plasma and brain are independent. This suggests that events detected in the peripheral circulation do not implicate direct mechanisms of action of catecholamines at the neuronal/glial level.

To evaluate the influences of CO(2) insufflation on changes in blood gas analysis and end tidal CO(2) tension (PetCO(2)) during posterior retroperitoneoscopic adrenalectomy in the prone position.Arterial blood gas analysis and measurements of PetCO(2) were carried out during CO(2) insufflation in 16 patients who underwent posterior retroperitoneoscopic adrenalectomy in the prone position (PRA group). The results were compared to 10 patients who underwent open posterior adrenalectomy (OPA group). Ventilation was artificially controlled during the study period in all cases.Arterial pH, PaCO(2), PetCO(2) and PaO(2) were not significantly different between the PRA and OPA groups. However, the PaCO(2)-PetCO(2) gradient in the PRA group was significantly higher than that in the OPA group (p0.01).Transperitoneal absorption of CO(2) occurs in patients undergoing retroperitoneoscopy in the prone position. The alveolo-arterial CO(2) gradient may be the only parameter which indicates the absorption of CO(2) during PRA.

Background and Purpose —Neuronal injury results from an insufficient supply of oxygen to the brain. This experiment examined whether a pharmacologically induced rightward shift of the partial pressure of oxygen at which 50% of hemoglobin is saturated (P50) would improve outcome from either incomplete and/or near-complete forebrain ischemia–induced hypoxia in the rat. Methods —For incomplete ischemia (attenuated electroencephalogram), fasted rats (n=17 to 19 per group) were given a synthetic allosteric modifier of hemoglobin affinity for oxygen (RSR13; 150 mg/kg IV) before or immediately after 20 minutes of bilateral carotid occlusion combined with a decrease in mean arterial pressure to 40 mm Hg. For near-complete ischemia (isoelectric electroencephalogram), rats (n=15 per group) were given RSR13 (150 mg/kg) at onset of reperfusion after 10 minutes of bilateral carotid occlusion combined with a decrease in mean arterial pressure to 30 mm Hg. In both experiments, control rats were given vehicle (0.9% NaCl IV) only. Outcome (defined as percent dead hippocampal CA1 neurons) was determined at 5 days after ischemia. Results —RSR13 (150 mg/kg) produced a 68% rightward shift of P50 (34±3 to 57±8 mm Hg). RSR13 reduced CA1 damage resulting from incomplete ischemia by 28% ( P =0.02), but only when administered at the onset of reperfusion. RSR13 had no effect on outcome from near-complete ischemia. Conclusions —A postischemic pharmacologically induced increase in P50 may improve outcome from incomplete global cerebral ischemia. More severe (near-complete) ischemia negates this benefit.

Both dizocilpine (MK-801) and isoflurane antagonize glutamatergic neurotransmission. In this study, we examined the relative neuroprotective effects of these drugs administered in equianesthetic doses before the onset of focal cerebral ischemia. Rats were anesthetized with 1.0%-1.5% isoflurane and surgically prepared for filament occlusion of the middle cerebral artery (MCAO). After preparation, one group (n = 22) remained anesthetized with 0.7% isoflurane. Another group (n = 18) was given dizocilpine (1 mg/kg intraperitoneally), and isoflurane was discontinued. The third group (n = 18) was allowed to awaken immediately after the onset of ischemia. MCAO persisted for 75 min. Epidural temperature was controlled at 37.5[degree sign]C during ischemia and the first 22 h of recovery. A 7-day recovery interval was allowed. Total infarction volumes (mean +/- SD) were less for the dizocilpine group (100 +/- 65 mm3) versus the awake group (182 +/- 36 mm3; P = 0.001). Infarction volumes did not differ significantly between the isoflurane group (142 +/- 81 mm3) and either the dizocilpine (P = 0.11) or the awake group (P = 0.15). Isoflurane was examined at doses used clinically but smaller than those found to reduce N-methyl-D-aspartate (NMDA)-mediated injury in vitro. This study supports the hypothesis that NMDA receptor activation is injurious during focal ischemia and that amelioration of focal ischemic brain damage by NMDA receptor antagonists persists under normothermic conditions. Implications: Rats underwent focal cerebral ischemia with rigid maintenance of brain normothermia. The glutamate receptor antagonist dizocilpine was effective in reducing cerebral infarction size during persistent conditions of brain normothermia. In contrast, isoflurane administered at equianesthetic doses did not reduce infarction size. This study supports the hypothesis that N-methyl-D-aspartate receptor activation is injurious during focal ischemia and that amelioration of focal ischemic brain damage by N-methyl-D-aspartate receptor antagonists persists under normothermic conditions. (Anesth Analg 1998;87:72-8)

64歳女性の膵頭十二指腸切除術(診断;膵頭部嚢胞腺癌)の麻酔管理を,持続硬膜外麻酔および笑気-酸素-イソフルランで行なった。手術操作に伴い血圧が上昇し,その管理は困難であった。カテコラミン産生腫瘍が疑われ,病理診断でパラガングリオーマと診断された。このような症例はまれではあるが,万一遭遇した場合には術中管理に難渋する。したがって,確定診断のついていない後腹膜腫瘍の麻酔管理に際しては,迅速な循環管理が行なえるよう十分な準備が必要であると思われた。

症例は26歳,女性.18歳の時にもやもや病と診断され,左浅側頭動脈-中大脳動脈吻合術を受け,その後,時々構音障害や眩暈,右手麻痺発作を起こしていたが,特に治療は受けていない.今回妊娠37週で,分娩管理を目的に入院となった.陣痛,経膣分娩による過換気,血圧変動による脳梗塞•脳出血を避けるため,帝王切開術のための麻酔として全身麻酔を選択した.麻酔はミダゾラムとフェンタニールおよび亜酸化窒素-酸素-セボフルランで導入•維持した.また術後鎮痛に硬膜外ブロックを用いた.母子ともに順調に経過した.もやもや病合併患者の分娩は,帝王切開術が望ましく,またその管理には産科,小児科,脳外科,麻酔科の協力が必要であると考えられた.

The medial prefrontal cortex (mPFC) has been proposed to be essential for extinction of fear memory, but its neural mechanism has been poorly understood. The present study examined whether synaptic transmission in the hippocampal-mPFC pathway is related to extinction of context-dependent fear memory in freely moving rats using electrophysiological approaches combined with behavioral analysis. Population spike amplitude in the mPFC was decreased during the first extinction trial by exposure to contextual fear conditioning. This synaptic inhibition was reversed by repeated extinction trials, accompanied by decreases in fear-related freezing behavior. These results suggest that alteration of synaptic transmission in the hippocampal-mPFC pathway is associated with the extinction processes of context-dependent fear memory. Further experiments were performed to elucidate whether early postnatal stress alters the synaptic response in the mPFC during extinction trials using a juvenile stress model, based on our previous findings that early postnatal stress affects the behavioral response to emotional stress. Adult rats that previously were exposed to five footshocks (FS) (shock intensity, 0.5 mA; intershock interval, 28 seconds; shock duration, 2 seconds) at postnatal day 21 to 25 (week 3; 3W-FS) exhibited impaired reversal of both inhibitory synaptic transmission and freezing behavior induced by repeated extinction trials. The neuronal and behavioral deficits observed in the 3W-FS group were prevented by pretreatment with the serotonin(1A) receptor agonist tandospirone (1 mg/kg, i.p.). These results indicate the possiblity that aversive stress exposure during the third postnatal week impaired extinction processes of context-dependent fear memory. The deficits in extinction observed in the 3W-FS group might be attributable to dysfunction of hippocampal-mPFC neural circuits involving 5-HT(1A) receptor mechanisms.

For the management of general anesthesia in the patients with severe motor and intellectual disabilities, airway and respiratory disorders are severe and may cause fatal events. We retrospectively examined these risk factors.We assessed adverse airway and respiratory events associated with anesthesia from perioperative and anesthetic records of these patients retrospectively.Forty-one cases (31 were for fundoplication, and 10 were for gastrostomy or jejunostomy) were involved. On anesthetic introduction, in 9 cases tracheal intubation was difficult (failed in 1 case). These and other 4 cases had developed pharyngeal and laryngeal edema. Manual ventilation by facemask was successful in all cases. During the postoperative period, pneumonia (5 cases), pleural effusion (1 case), and apnea (2 cases) occurred unexpectedly.Patients with severe motor and intellectual disabilities belong to the group with high risk for general anesthesia.

Laparoscopic microwave coagulation therapy (LMCT) is indicated for the patients with hepatocellular carcinoma, especially when hepatic function is compromised. We retrospectively investigated the effects of perioperative administration of prostaglandin El on post-operative hepatic function in patients receiving LMCT.Patients receiving LMCT for the treatment of hepatocellular carcinoma associated with compensated cirrhosis were included. Prostaglandin El administration was commenced after the induction of general anesthesia, with infusion rate at 0.01-0.02 microg x kg(-1) min(-1). Post-operative changes of serum albumin, serum total bilirubin, ALT, AST, lactate dehydrogenase, serum cholinesterase, platelet count, and percent prothrombin time were serially measured in patients with and without prostaglandin E1 administration.Perioperative prostaglandin El administration inhibited post-operative serum bilirubin increase and preserved prothrombin time compared to non-treated group.It was suggested that prostaglandin El possessed hepatoprotective property in compensated cirrhosis patients with hepatocelluar carcinoma receiving LMCT.

A patient developed tension pneumothorax immediately after extubation. The patient was a 53-year-old man, who underwent total gastrectomy under general anesthesia combined with epidural anesthesia. The posterior mediastinum drainage tube was placed near the site of esophago-jejunum anastomosis. Surgeons reported that they might have injured left diaphragmatic pleura during the procedure. Postoperative chest X-ray showed no abnormal findings in the both lung fields. Patient's trachea was extubated when he emerged from anesthesia. However, Spo2 rapidly dropped from 100 to 88. Re-intubation was performed, and positive pressure ventilation was resumed. The Spo2 returned quickly to 100 without hemodynamic change. Auscultation revealed reduced respiratory sound from the left lung. Diagnosis of tension pneumothorax was made from emergency chest X-ray. Patient's respiration improved when chest tube was inserted, but a large amount of air was continuously drained. Air leakage decreased significantly when the mediastinum drainage tube was tentatively occluded. The possible mechanism of the positive pressure in the thoracic cavity was assumed that air was introduced with spontaneous inspiration from the drainage tube, and damaged pleura played as a check valve.

previously. A routine chest roentgenogram taken during an annual check-up showed a suspicious shadow. The patient was referred to another hospital for a complete medical evaluation. Left lung cancer was diagnosed. His electrocardiogram (ECG) showed a negative T wave in leads V5 and V6, indicating a pattern of old septal and inferior myocardial infarction with mild left ventricular (LV) hypertrophy. Furthermore, epicardial echocardiography (EE) revealed interventricular septal hypertrophy (ISH) and LV outflow hypertrophy, without deterioration of LV wall motion but with mild mitral regurgitation (MR). His cardiac index (CI), ejection fraction (EF), and EE-derived LV-Ao PG were 3.85 l·min 1·m 2, 86%, and 72 mmHg, respectively. Finally, HOCM accompanied with MR were diagnosed. The patient was scheduled for right upper lobectomy in the same hospital without any specific medical treatment for HOCM prior to surgery. The patient was premedicated with intramuscular atropine (0.5 mg) and hydroxyzine (50mg) prior to the induction of anesthesia. On arrival at the operating theater, his heart rate was 78 beats·min 1, and his systolic and diastolic blood pressure showed 132/86mmHg. After the placement of an epidural catheter via the thoracic segment T8/9, anesthesia was induced with bolus intravenous (iv) fentanyl (0.8μg·kg 1) and propofol (1mg·kg 1), as well as with continuous infusion of propofol (10mg·kg 1·h 1), followed by vecuronium (0.03 mg·kg 1). Hypotension (60 mmHg) and profound bradycardia (35 beats·min 1) were observed after anesthesia was induced. Hypotension was controlled rapidly both by volume replacement and intermittent administration of bolus iv methoxamine (1mg), whereas bradycardia persisted at less than 40 beats·min 1. The anesthetists discontinued the induction of anesthesia and cancelled the operation. Ten minutes later, the heart rate of the patient gradually recovered to a level of 50 beats·min 1. Oral atenolol (50mg·day 1) and disopyramide (300 mg·day 1) were started immediately

Deteriorated neurological outcome is not rare after major surgeries. With aging of the surgical population in Japan, an increasing frequency of perioperative cerebral ischemia is expected. To avoid neurological deterioration after surgery and general anesthesia, especially in high-risk patients, it is important to provide appropriate CNS-oriented anesthesia management. Controlling factors such as cerebral perfusion pressure, arterial blood gases, blood glucose concentration and body temperature may influence brain metabolism and neurological outcome. Inhalational anesthetics may also play an important role in perioperative neurological management, because numerous studies have demonstrated some degree of neuroprotective effect with halothane, sevoflurane, desflurane and isoflurane. Among these inhalational anesthetics, isoflurane has been most extensively studied regarding neuroprotection against cerebral ischemic insult. Although no clinical outcome trials have been performed, both in vivo and in vitro studies have consistently shown that the isoflurane provides neuroprotection. However, it is also suggested that factors such as sympathetic reactivity, brain temperature, anesthetic dosage, timing of anesthetic administration, and co-administration of nitrous oxide might affect the neuroprotective effect of isoflurane.

We report a case of palsy of the brachial plexus and facial nerve manifested after surgery for lung cancer in a 77-year-old female who also had a retroodontoid pseudotumor. Lobectomy was conducted with the patient in a left lateral position. For the purpose of cervical stabilization, the orthopedic surgeon recommended the use of a cervical collar. During the operation, both of her arms were abducted at nearly 80 degrees. On the second postoperative day, the patient complained of sensory disturbances in the lateral area of her left brachium and forearm, which are innervated by the 5th and 6th cervical spinal nerves from the brachial plexus. She also complained that she could not abduct and flex her left shoulder, and could not flex her left elbow at all. Simultaneously, facial nerve palsy was observed in her left lower lip. During the operation, her shoulders were forcibly rotated internally and were extremely abducted, resulting in a narrowed distance between the lower jaw and the shoulder and stretching of the brachial plexus. Under this situation, the cervical collar was pressing strongly upon her neck and lower jaw, which might have produced the brachial plexus complication and facial nerve palsy.

This study examined the importance of brain norepinephrine concentration on outcome from a focal ischemic insult. Fasted temperature-controlled male Wistar rats pretreated with DSP-4, (N-(chloroethyl)-N-ethyl-2-bromobenzylamine), to selectively deplete brain norepinephrine, were subjected to reversible filament occlusion of the middle cerebral artery for 75 min in the awake state. After 3 days recovery, total infarct volume in DSP-4 treated rats (185 +/- 107 mm3) was reduced vs. untreated control animals (242 +/- 71 mm3, P = 0.04). Subcortical infarct volume was also smaller in the DSP-4 group (93 +/- 44 vs. 121 +/- 28 mm3, P = 0.02). Cortical infarct volume was not statistically different between groups. Neurologic function correlated with infarct-size. These findings suggest that brain norepinephrine affects stroke development either by direct neuronal toxicity and/or through influences on the penumbral circulation. Dampening of the central stress response induced by the onset of stroke may thus be advantageous.

Background Isoflurane-anesthetized rats have better outcome from global cerebral ischemia than rats anesthetized with fentanyl and nitrous oxide. The authors wanted to determine whether circulating catecholamine concentrations depend on the anesthetic agent and whether sympathetic ganglionic blockade affects anesthetic-mediated differences in outcome from near-complete forebrain ischemia. Methods For two different experiments, normothermic Sprague-Dawley rats that had fasted were assigned to one of four groups and subjected to 10 min of 30 mm Hg mean arterial pressure and bilateral carotid occlusion. Rats were anesthetized with 1.4% isoflurane or fentanyl (25 microg x kg(-1) x h(-1)) and 70% nitrous oxide, with or without preischemic trimethaphan (2.5 mg given intravenously). In experiment 1, arterial plasma catecholamine concentrations were measured before, at 2 and 8 min during, and after ischemia (n = 5-8). In experiment 2, animals (n = 15) underwent histologic analysis 5 days after ischemia. Results In experiment 1, intraischemic increases in plasma norepinephrine and epinephrine levels were 28 and 12 times greater in the fentanyl-nitrous oxide group than in the isoflurane group (P Conclusions Isoflurane attenuated the peripheral sympathetic response to ischemia and improved histologic outcome compared with fentanyl and nitrous oxide. This outcome benefit was reversed by sympathetic ganglionic blockade. The beneficial effects of isoflurane may result from a neuroprotective influence of an intermediate sympathetic response that is abolished by trimethaphan.

The administration of aprotinin has been associated with a reduction in cardiac surgery-related stroke. Intrinsic neuroprotective properties of this drug have not been evaluated in laboratory outcome models of cerebral ischemia. The purpose of this study was to determine whether aprotinin exhibits neuroprotective effects against either global or focal cerebral ischemia in the rat. Fasted rats were administered aprotinin (30,000 or 60,000 KIU/kg) or vehicle (0.9% NaCl) IV before global ischemia (10 min bilateral carotid occlusion with mean arterial pressure 30 mm Hg) or focal ischemia (75 min of transient middle cerebral artery occlusion [MCAO]). Five days after global ischemia, the percentage of dead hippocampal CA1 neurons (mean +/- SD) was similar among the groups (small-dose aprotinin: 49 +/- 31, n = 15; large-dose aprotinin: 55 +/- 31, n = 13; vehicle: 47 +/- 31, n = 16; P = 0.74). After 7 days' recovery from MCAO, no difference among the groups was observed for either neurologic score (P = 0.99) or cerebral infarct volume (small-dose aprotinin: 136 +/- 80 mm (3), n = 23; large-dose aprotinin: 132 +/- 101 mm3, n = 11; vehicle: 121 +/- 81 mm3, n = 21; P = 0.87). Implications: Aprotinin offers no neuroprotection against either global or focal cerebral ischemia in the rat when administered as a single preischemic bolus. (Anesth Analg 1999;88:1-7)

Background It has been postulated that anesthetic agents that reduce cerebral metabolic rate will protect the brain against ischemia when electroencephalographic (EEG) activity is persistent, but will provide no protection when ischemia is severe enough to cause EEG isoelectricity. No outcome studies have addressed this issue. The authors studied anesthetic agents to determine if they provide differential effects on outcome from global cerebral ischemic insults that cause either an attenuated or isoelectric EEG. Methods Fasted rats were subjected to either (1) incomplete ischemia (attenuated EEG; 20 min of mean arterial pressure [MAP] = 50 mmHg and bilateral carotid occlusion) or (2) near-complete ischemia (isoelectric EEG; 10 min of MAP = 30 mmHg and bilateral carotid occlusion) while anesthetized with 1.4% isoflurane, 1 mg x kg(-1) x min(-1) ketamine, or 25 microg x kg(-1) x h(-1) 70% nitrous oxide and fentanyl. The brain was maintained at normothermia during ischemia and for 22 h after ischemia. Five days later, hippocampal CA1 and cortical injury were measured. Results There was no difference among anesthetic agents during incomplete ischemia for mean +/- SD percentage dead CA1 neurons (fentanyl, 38%+/-20%; isoflurane, 31%+/-10%; ketamine, 40%+/-19%; P = 0.38). During near-complete ischemia, there was a difference among anesthetic agents (fentanyl, 88%+/-9%; isoflurane, 37%+/-20%; ketamine, 70%+/-28%; P = 0.00008). Isoflurane was protective compared with fentanyl (P = 0.00007) and ketamine (P = 0.0061). There was no difference between fentanyl and ketamine (P = 0.143). Similar observations were made in the cortex. Neurologic function correlated with histologic damage. Conclusions Outcome from near-complete but not incomplete cerebral ischemia depended on the anesthetic agent administered during the ischemic insult.