[Factors that affect the mortality in patients receiving emergency surgery for ruptured abdominal aortic aneurysms].

This retrospective study was performed to identify the perioperative factors affecting the mortality rate in 28 patients, who had received emergency surgery for ruptured abdominal aortic aneurysms from January, 2005 to June, 2008. Five (17.9%) of these 28 patients died of massive bleeding, sepsis, or multiple organ failure during or within 11 days after surgery. Various factors which might influence the outcomes were compared between the survivors and non-survivors. Preoperative hypotension defined as a systolic blood pressure < or = 80 mmHg associated with hemorrhagic shock was the only significant factor affecting the mortality. There were no significant differences in age, gender, the time from the admittance to the hospital to aortic cross clamping, duration of surgery, and the amount of blood products transfused and intraoperative blood loss, between the two groups. Of great importance is that preoperative hypotension should be corrected before the onset of hemodynamic deterioration.

[Retrospective investigation and analysis of dental injuries during endotracheal intubation].

BACKGROUND: The objective of this study is to clarify the causes of dental injuries (DIs) developed during the direct laryngoscopy for the endotracheal intubation (EI) in our hospital. METHODS: Subjects are 4173 patients who had the EI from April 1, 2006 to March 31, 2007. Mallampati's classification and Miller's classification were used for the evaluation of difficult airway and the dental unsteadiness, respectively. RESULTS: There was no case between 10 and 40 years of age. Twelve cases (0.3%) had the DIs during the observation period. In 8 out of 12 cases (67%), EI was carried out by the residents with less than 3 months of the training period. Three cases (25%) were classified to the II or III grade. The dissociation of the evaluations by a dental anesthesiologist and medical anesthesiologists were found in two cases. Eight cases received temporary treatment by a dental anesthesiologist. CONCLUSIONS: Temporary treatment in the operating room was carried out by a dental anesthesiologist. Careful inquiry is needed for the proper preoperative teeth evaluation, especially in the schoolchild with milk teeth and elderly patients. A precise educational system for the residents is required for the prevention of DIs during the EI.

[Anesthetic management for gastrectomy in two gastric cancer patients after coronary artery bypass grafting using right gastroepiploic artery].

We report two cases for anesthetic management of gastrectomy for gastric cancer which took place after receiving coronary artery bypass grafting (CABG) using the right gastroepiploic artery (RGEA). The first patient was a 75-year-old man after CABG using the RGEA 14 years before. He was diagnosed with gastric cancer and was scheduled for total gastrectomy. Preoperative coronary angiography (CAG) showed complete occlusion of the right coronary artery (RCA), whereas RGEA was patent. Because percutaneous coronary intervention (PCI) was hard to perform on the occluded RCA, proximal gastrectomy was carried out without lymph node dissection. The surgeons judged the surgery enough for radical treatment. Surgery was accomplished without any problems. The second patient was a 76-year-old man after CABG using the RGEA 15 years before. He was diagnosed with advanced gastric cancer and was scheduled for distal gastrectomy. Preoperative CAG showed the RCA partially occluded and the RGEA remaining patent. He received the scheduled surgery after confirmation of the success of PCI, performed preoperatively for reperfusion of the occluded segments. Although the RGEA was incised during the surgery, gastrectomy was accomplished without any problems in the cardiac function.

Role of adrenoceptors in the regulation of dopamine/DARPP-32 signaling in neostriatal neurons.

Studies in animal models of Parkinson's disease have revealed that degeneration of noradrenaline neurons is involved in the motor deficits. Several types of adrenoceptors are highly expressed in neostriatal neurons. However, the selective actions of these receptors on striatal signaling pathways have not been characterized. In this study, we investigated the role of adrenoceptors in the regulation of dopamine/dopamine- and cAMP-regulated phosphoprotein of M(r) 32 kDa (DARPP-32) signaling by analyzing DARPP-32 phosphorylation at Thr34 [protein kinase A (PKA)-site] in mouse neostriatal slices. Activation of beta(1)-adrenoceptors induced a rapid and transient increase in DARPP-32 phosphorylation. Activation of alpha(2)-adrenoceptors also induced a rapid and transient increase in DARPP-32 phosphorylation, which subsequently decreased below basal levels. In addition, activation of alpha(2)-adrenoceptors attenuated, and blockade of alpha(2)-adrenoceptors enhanced dopamine D(1) and adenosine A(2A) receptor/DARPP-32 signaling. Chemical lesioning of noradrenergic neurons mimicked the effects of alpha(2)-adrenoceptor blockade. Under conditions of alpha(2)-adrenoceptor blockade, the dopamine D(2) receptor-induced decrease in DARPP-32 phosphorylation was attenuated. Our data demonstrate that beta(1)- and alpha(2)-adrenoceptors regulate DARPP-32 phosphorylation in neostriatal neurons. G(i) activation by alpha(2)-adrenoceptors antagonizes G(s)/PKA signaling mediated by D(1) and A(2A) receptors in striatonigral and striatopallidal neurons, respectively, and thereby enhances D(2) receptor/G(i) signaling in striatopallidal neurons. alpha(2)-Adrenoceptors may therefore be a therapeutic target for the treatment of Parkinson's disease.

Gradient of bronchial end-tidal CO2 during two-lung ventilation in lateral decubitus position is predictive of oxygenation disorder during subsequent one-lung ventilation.

PURPOSE: Hypoxemia is one of the major problems during one-lung ventilation (OLV). During two-lung ventilation (TLV) using a double-lumen bronchial tube, bronchial endtidal carbon dioxide partial pressure (ETbr(CO2)) can be determined on both sides, independently. The ETbr(CO2) is mainly dependent on the pulmonary perfusion to each lung. If the degree of oxygenation disorder during OLV were to be predictable before starting OLV, this could provide time to prepare for any subsequent hypoxemia. The aim of this study was to investigate whether the difference of ETbr(CO2) (D-ETbr(CO2)) between the dependent and the nondependent lungs during TLV in the lateral decubitus position (LP) could be a predictive factor for the severity of oxygenation disorder under subsequent OLV. METHODS: Eighteen patients undergoing lung surgery were enrolled in this study. Anesthesia was induced with intravenous thiopental and fentanyl, supplemented by the inhalation of sevoflurane. A left-sided double-lumen bronchial tube was placed. The ETbr(CO2) was independently determined on each side during TLV in the supine position (SP) and at 10 min after changing the position from SP to LP. PaO2/inspiratory fraction of oxygen (FIO2) was taken at 15 min after switching from TLV to OLV in LP. RESULTS: The decrease of PaO2/FIO2 at 15 min during OLV in LP correlated with the reduction of the D-ETbr(CO2) predetermined during TLV in LP (r = 0.698; P < 0.01). CONCLUSION: The D-ETbr(CO2) predetermined during TLV in LP could be a predictive factor for the severity of oxygenation disorder after starting OLV in LP.

Thiamylal antagonizes the inhibitory effects of dorsal column stimulation on dorsal horn activities in humans.

In humans, peripheral somatosensory information converges upon dorsal horn neurons in the spinal cord, which can be recorded from the dorsal epidural space as spinal cord potentials (SCPs) following segmental dorsal root stimulation (SS) employing epidural catheter electrodes. Antidromic action potentials and descending inhibition from the dorsolateral funiculus may contribute to SCPs following dorsal column stimulation (DCS). Effects of thiamylal (2.5-7.5 mg/kg, i.v.) on SCPs evoked by independent DCS or SS were compared with those evoked by simultaneous DCS and SS (DCS/SS). DCS- and SS-evoked SCPs recorded from the lumbar enlargement consisted of a sharp negative (N) followed by a slow positive (P) potential. Thiamylal induced dose-dependent increases in amplitude and duration of both N and P potentials evoked by DCS and SS, whether the responses were summed or evoked simultaneously. In awake subjects, N and P potentials produced by simultaneous DCS/SS were significantly smaller than the sum of independent responses. Thiamylal anesthesia antagonized this inhibition; responses to simultaneous DCS/SS were larger than the sum of independent responses. These results suggest that in wakefulness DCS inhibits dorsal horn neuron activity in the lumbar spinal cord, while thiamylal antagonizes DCS-induced inhibition in dose-dependent fashion.

Cuff occlusion on the left upper arm increases flow of the left internal mammary artery and bypass flow to the left anterior descending artery.

PURPOSE: Changes in vascular resistance in the left forearm may affect the flow of left internal mammary artery (LIMA)- to left anterior descending artery (LADA) bypass, because the LIMA is a major branch of the subclavian artery. We studied the effects of occlusion of the left upper arm on blood flow of LIMA-to-LADA bypass in patients undergoing coronary artery bypass grafting (CABG). METHODS: In ten patients, the blood volume shed from LIMA with the distal end open (LIMA free flow) was stored for 1 min before and during cuff inflation in CABG surgery. LIMA-LADA bypass flow was measured with ultrasonic flow-metry before and after cuff inflation on the left upper arm in an other ten patients. Mean arterial blood pressure (MAP), heart rate (HR), and electrocardiograms (ECGs) were monitored throughout the studies. RESULTS: LIMA free flow (ml x min(-1)) increased from 50.3 +/- 7.1 to 60.9 +/- 8.4 (P < 0.01) at the end of 1-min cuff inflation. LIMA-LADA bypass flow (ml x min(-1)) increased from 31.4 +/- 3.7 to 39.7 +/- 4.0 (P section sign 0.05) at 1 min after cuff inflation. MAP, HR, and ST segments on ECGs did not show any significant changes related to measurement times. CONCLUSION: LIMA-LADA bypass flow increased after cuff inflation on the left upper arm and returned to the baseline values after cuff deflation. Anesthesiologists should be aware of this relationship between local vascular resistance and bypass flow for the evaluation of LIMA-LADA anastomosis.

Effects of nasal application of an epinephrine and lidocaine mixture on the hemodynamics and nasal mucosa in oral and maxillofacial surgery.

PURPOSE: Our purpose was to investigate the influences of nasal pretreatment with a mixed solution of epinephrine and lidocaine (E-L pretreatment) on the systemic hemodynamics and the mucosa of the inferior nasal concha, which is carried out for expansion of the nasal cavity and the prevention of mucosal injury before nasotracheal intubation. PATIENTS AND METHODS: Subjects included 29 adult patients undergoing oral and maxillofacial surgery. This study consisted of 2 parts. In part 1 (n = 18), the effects of E-L pretreatment on the systemic hemodynamics were studied before (pre-Anesth group, n = 10) and after (post-Anesth group, n = 8) induction of anesthesia. Changes of the mucosal volume and the blood flow of the inferior nasal concha also were observed by optic bronchoscopy and noncontact type laser-Doppler flowmetry, respectively. In part 2 (n = 11), changes in the serum concentrations of epinephrine and lidocaine after the E-L pretreatment were determined by high performance liquid chromatography and enzyme immunoassay, respectively. RESULTS: The heart rate increased at 2 and 3 min after E-L pretreatment in pre-Anesth group (P < .05), but not in post-Anesth group. The cross section of the nasal cavity decreased from 66% to 42% (n = 8, P < .05). The mucosal blood flow decreased from 60 to 22 AU (n = 8, P < .01). The serum epinephrine concentration increased from 24 to 185 pg/mL. CONCLUSIONS: The E-L pretreatment provided characteristic evidence for useful expansion of the nasal cavity and for reduction of the nasal mucosal blood flow with less systemic hemodynamic effects, although further investigation is needed for the determination of the proper epinephrine concentration in E-L pretreatment.

[Cesarean section for case with preoperatively-suspected placenta accrete followed by hysterectomy due to uncontrollable massive bleeding].

A 42-yr-old pregnant woman highly suspicious of the placenta accreta was scheduled for cesarean section (c-section) under general anesthesia. She had received emergency c-section for the placenta previa at 36 years of age and three episodes of intrauterine curettage for spontaneous abortion. While the possibility of placenta accreta was pointed out and the risks accompanying with it were explained at the 7th week of pregnancy, she insisted on having a baby. C-section was intended at around the 30th week of pregnancy and 1,200 ml of autologus blood was stored for the predictable massive bleeding. Bilateral embolization of the internal iliac artery was also planned. The baby was delivered uneventfully. However, the adherence of the placenta was so tight that the placenta could not be separated from the uterine wall. The arterial embolization immediately after the delivery did not work as effectively as to control massive bleeding. It took about 1 hour to control the massive bleeding of up to 9000 ml by difficult hysterectomy. Since we had prepared for such a situation, we could well catch up with the massive bleeding. The mother and baby were discharged well from the hospital 29th day after the c-section.

[Combination of spinal and inhalation anesthesia for nephrectomy in a cirrhotic patient].

We report a 75-year-old man with the liver cirrhosis of Child-Pugh B who underwent nephrectomy. Preoperative serum examination revealed increases in GOT, GPT, LDH and total bilirubin, decreases in cholinesterase and albumin, and prolongation of prothrombin time. We selected spinal anesthesia using bupivacaine and fentanyl rather than epidural anesthesia in combination with isoflurane inhalation anesthesia to supplement intra-operative anesthesia and post-operative pain relief. We explained the risks of blood coagulopathy and the predictable venous dilatation in the epidural space to the patient and relatives on obtaining informed consent. The surgery was completed uneventfully in 2.5 hours. Post-operative pain control was satisfactory and hepatic dysfunction did not deteriorate in the postoperative period.

Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation.

Stroke is a devastating complication in cardiovascular surgery, and neuronal damage is worsened by intracranial pressure elevation caused by cerebral venous circulatory disturbances (CVCD). However, we have previously reported that CVCD before cerebral ischemia decreases the infarct area. In the present study, focal cerebral ischemia was induced in spontaneously hypertensive rats by filament insertion through the carotid artery. Rats were divided into the following four groups: sham-operated, mild or severe venous congestion (VC), and DPCPX. The DPCPX group received the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) prior to mild VC. Behavior, infarct volume, edema and S-100 protein were evaluated among the four groups. The infarct volume rates in mild VC and severe VC groups were significantly less than that in sham-operated and DPCPX groups. However, the mortality of the severe VC group worsened in a time-dependent manner. We observed a significant decrease in edema in the mild VC group compared to the DPCPX group. Behavioral scores also indicated that the mild VC group had fewer neurological deficits than the other three groups, including the DPCPX group. We were able to induce rapid cerebral protection via adenosine A1 receptor activation by administering an appropriate degree of VC prior to cerebral ischemia produced by middle cerebral artery occlusion. Our work suggests possible mechanisms by which such effective VC may lead to cerebral protection and adenosine A1 receptor activation.

Effects of systemic deep hypothermia and subarachnoid block on the longitudinally conducting evoked spinal cord potentials in man.

The present study reports the effects of systemic deep hypothermia (SDH) and subarachnoid block (SAB) on the longitudinally conducting evoked spinal cord potential (conducting ESCP) in man. Before induction of anesthesia, a pair of bipolar catheter electrodes was introduced to the epidural space: one at the level of the cervical enlargement and the other at the lumbosacral enlargement. The conducting ESCP was produced by electrical stimulation through the upper electrode and recorded through the lower electrode, and vice versa. SDH Study: Subjects were 6 patients who underwent replacement surgery of an aortic aneurysm with deep hypothermia anesthesia. The peak latency of the ESCP was gradually prolonged and the duration was widened with cooling via extracorporeal circulation. The amplitude of ESCP showed a biphasic change over the course of cooling with a turning point of around 30 degrees C in esophageal temperature. The ESCP was well observed until blood temperatures as low as near 10 degrees C. The result shows that ESCP is available as an intra-operative monitoring parameter of the spinal function even under SDH. SAB Study: Subjects were 7 patients, 6 of whom had SAB and the remaining 1 intravenous application of a local anesthetic. The conducting ESCP was markedly depressed or disappeared completely even after SAB with clinical doses of various local anesthetics, while it was hardly affected by the intravenous application. The result implies that SAB causes, at least partially, the conduction block within the spinal cord.

[Labor management using epidural anesthesia in a gravida patient with high spinal injury].

Since autonomic hyperreflexia (AH) is a serious complication during labor in a gravida with spinal cord injury, anesthetic measures should be taken for the suppression of AH even in a sensory-loss condition. Several reports have described various methods for the suppression of AH, in which epidural anesthesia has been advocated as a useful means for the prevention or amelioration of AH. However, it is difficult to evaluate the efficacy of epidural anesthesia due to the lack of sensory and motor functions. We report a primipara who had spinal cord injury below the T 3 level at the age of 17 due to a traffic accident and underwent successful vaginal delivery twice under epidural anesthesia at the ages of 30 and 32. For the first delivery, we placed two epidural catheters. We controlled the rate and the content of epidural infusion through the two different injection sites so as to meet delivery process. For the second delivery we did epidural anesthesia in the same way. Tubal-ligation was also performed under epidural anesthesia after the second delivery. No major obstetric complication including AH occurred in either of delivery. The woman with high spinal injury could have two healthy children without major complications during labor by the cooperation of gynecologists and anesthesiologists.

[Intra-operative monitoring of EEG].

The fundamentals and clinical applications of intra-operative EEG monitoring are described. EEG monitored on line at bedside is useful for the evaluation of the depth of anesthesia and sedation, and also for the early detection of cerebral ischemia and seizure. However, EEG monitoring is not easy in the operating room, where a number of electrical machines and medical personnel are working. The authors have introduced a basal lead for the recording of brain-stem electrical activity and a fiberoptic EEG instrument for the exclusion of electrical noises. Recently, EEG instruments with computer-processing function, which are small in size and easy to manage, have been developed one after another. Computer-processed EEG is sequentially expressed as a digitalized value. Today, computer-processed EEG is more popular than raw EEG as an intra-operative monitoring of cerebral function, while raw EEG is superior to computer-processed EEG in the detection of seizure waves. The authors recommend multi-modality monitoring including non-invasive measurements of oxygen saturation and blood flow for the safe maintenance of cerebral

The neuropeptide neuromedin U promotes IL-6 production from macrophages and endotoxin shock.

Neuromedin U (NMU) is a neuropeptide involved in appetite, circadian rhythm, and pronociception. However, the NMU receptor NMU-R1 has been shown to be expressed in immune cells and NMU promotes mast cell-dependent inflammation. In this study, we demonstrated that NMU plays an important role in IL-6 production in macrophages. NMU-deficient mice were resistant against cecal ligation puncture- as well as LPS-induced septic shock. IL-6 but not TNF-alpha levels were markedly reduced in LPS-treated NMU-deficient mice compared with wild type mice. Both NMU and NMU-R1 were expressed in wild type peritoneal macrophages, and treatment with LPS resulted in up-regulation of NMU but down-regulation of NMU-R1 expression, however, no down-regulation of NMU-R1 was observed in NMU-deficient macrophages where LPS-induced IL-6 production was severely reduced. These data suggest that LPS-induced IL-6 expression is partly dependent on autocrine/paracrine activation of the NMU-NMU-R1 signals in macrophages.

The neuropeptide neuromedin U activates eosinophils and is involved in allergen-induced eosinophilia.

Neuromedin U (NMU) is a neuropeptide expressed not only in the central nervous system but also in various organs, including the gastrointestinal tract and lungs. NMU interacts with two G protein-coupled receptors, NMU-R1 and NMU-R2. Although NMU-R2 is expressed in a specific region of the brain, NMU-R1 is expressed in various peripheral tissues, including immune and hematopoietic cells. Our recent study demonstrated an important role of NMU in mast cell-mediated inflammation. In this study, we showed that airway eosinophilia was reduced in NMU-deficient mice in an allergen-induced asthma model. There were no differences in the antigen-induced Th2 responses between wild-type and NMU knockout mice. NMU-R1 was highly expressed in the eosinophil cell line, and NMU directly induced Ca(2+) mobilization and extracellular/signal-regulated kinase phosphorylation. NMU also induced cell adhesion to components of the extracellular matrix (fibronectin and collagen type I), and chemotaxis in vitro. Furthermore, NMU-R1 was also expressed in human peripheral blood eosinophils, and NMU induced cell adhesion in a dose-dependent manner. These data indicate that NMU promotes eosinophil infiltration into inflammatory sites by directly activating eosinophils. Our study suggests that NMU receptor antagonists could be novel targets for pharmacological inhibition of allergic inflammatory diseases, including asthma.

[Anesthetic management for a patient with multiple sclerosis].

A 49-year-old woman with multiple sclerosis (MS) received emergency laparotomy for panperitonitis. She had been suffering from MS for 13 years, and her main clinical symptoms were disorders in sight, walking and touch sensation below T 7. We used propofol and fentanyl for induction and maintained anesthesia with nitrous oxide, sevoflurane and additional fentanyl. Intubation was carried out without muscle relaxant. Train of four ratio was monitored during surgery. Thus the use of muscle relaxant was suppressed to the minimum requirement. Circulatory function was stable and no cardiovascular agent was used throughout the surgery. Awakening from anesthesia was smooth and exacerbation of the neurological abnormalities was not observed after surgery. She was transferred uneventfully to a recuperative hospital on the 13th postoperative day.

The neuropeptide neuromedin U promotes inflammation by direct activation of mast cells.

Neuromedin U (NMU) is a neuropeptide that is expressed in the gastrointestinal tract and central nervous system. NMU interacts with two G protein-coupled receptors, NMU-R1 and NMU-R2. Whereas NMU-R2 localizes predominantly to nerve cells, NMU-R1 is expressed in peripheral tissues including lymphocytes and monocytes, suggesting a role of NMU in immunoregulation. However, the functions of NMU in peripheral tissues have not been clarified. In this study, using NMU-deficient mice, we first demonstrated that NMU plays an important role in mast cell-mediated inflammation. Complete Freund's adjuvant-induced mast cell degranulation as well as edema and neutrophil infiltration, which occurred weakly in mast cell-deficient WBB6F(1)-W/W(v) mice, did not occur in NMU-deficient mice. Moreover, intraplantar injection of NMU into paws induced early inflammatory responses such as mast cell degranulation, vasodilation, and plasma extravasation in WT mice but not in WBB6F(1)-W/W(v) mice. NMU-R1 was highly expressed in primary mast cells, and NMU induced Ca(2+) mobilization and degranulation in peritoneal mast cells. These data indicate that NMU promotes mast cell-mediated inflammation; therefore, NMU receptor antagonists could be a novel target for pharmacological inhibition of mast cell-mediated inflammatory diseases.

Neuroprotective effect of epidural electrical stimulation against ischemic spinal cord injury in rats: electrical preconditioning.

BACKGROUND: Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. METHODS: Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. RESULTS: Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. CONCLUSIONS: Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.