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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

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.

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.

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。

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

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.