Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia

Changes in brain temperature are known to modulate the marked neuronal damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utilizing a dialysis electrode combined with ferrocene bovine serum albumin (BSA), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of postischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, although the intra-ischemic [Glu](e) elevation did not differ from that during intra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than directly modulating intra-ischemic [Glu](e) dynamics.     

Prostaglandin synthesis inhibitor affects humoral conditions and oxygen metabolism during normothermic cardiopulmonary bypass

We have reported that infusion of prostaglandin synthesis inhibitor (PGSI) reduced the severity of hypotension during normothermic cardiopulmonary bypass (CPB). In the present study, we investigated the effects of PGSI on humoral conditions and whole body oxygen metabolism during normothermic CPB conducted for 60 min in 8 adult goats. The PGSI group (n = 4) was administered 100 to 150 mg of flurbiprofen, a potent PGSI, before and during CPB, and the control group (n = 4) was administered noradrenaline (NA) to restore hypotension. The prostaglandin E2 (PGE2) and NA concentrations in the PGSI group were significantly lower than those of the control group (PGE2 8.8 +/- 1.0 versus 30.3 +/- 11.5 pg/ml, NA 431 +/- 197 versus 3847 +/- 2,153 pg/ml). The adrenaline concentration was not significantly different between the groups. The oxygen consumption and the oxygen extraction rate were not significantly different between the groups, but the blood lactate level in the PGSI group was lower than that of the control group (34.3 +/- 7.6 versus 43.7 +/- 3.8 mg/dl). In conclusion, PGSI improves humoral disorder and thus prevents inadequate tissue oxygen delivery.     

Intravascular Temperature Control System to Maintain Normothermia in Organ Donors

Introduction  Temperature regulation in humans is controlled by the hypothalamus. After death by neurological criteria, the hypothalamus ceases to function and poikilothermia ensues. Preservation of normothermia in those patients destined to become organ donors is an important part of maintaining the normal physiology of the organs and organ systems. Typical means of achieving normothermia include increasing the temperature of the ambient air, infrared warming lights, instillation of warmed intravenous fluids, and warm air or water blankets. Methods  In this prospective case series of five organ donors, we used an intravascular temperature modulation catheter (Alsius, Irvine, CA) to maintain normothermia in organ donors declared dead by neurological criteria. Data on accuracy of temperature maintenance at 37°C and nursing ease of use were collected. Results  This intravascular temperature modulation catheter provided an accurate method of temperature regulation in brain death donor and easier to use from a nursing workload perspective. Conclusions  Intravascular warming is a viable method for the maintenance of normothermia in organ donors. The experience here provides some insight into the ability of these devices to warm patients in other clinical situations. Originally presented at the Neurocritical Care Society, 2nd Annual Meeting, San Diego, CA, 2004.     

Anesthetic management of a patient with mitochondrial myopathy,encephalopathy, lactic acidosis,and stroke-like episodes (MELAS) during laparotomy

A 53-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) underwent a gastrectomy. We administered bicarbonated Ringer's solution, which has a physiological concentration of bicarbonate. The level of serum lactate did not increase significantly, and metabolic acidosis did not occur throughout surgery or for 3 h after surgery. Aggressive warming was needed to maintain normothermia, presumably because the mitochondrial respiratory chain, which is responsible for thermogenesis, is impaired in MELAS patients. It is important to maintain normothermia in MELAS patients in order to avoid further mitochondrial metabolic depression.     

Re-evaluation of ischemia-induced neuronal damage in hippocampal regions in the normothermic gerbil

Summary It has not been discussed whether transient forebrain ischemia of 5-min duration, which is a model frequently used to evaluate pharmacological protection against ischemic injury, is an optimal model in the CA1 field of this animal whose brain temperature is maintained at normothermic levels. The temperature of the brain during an ischemic insult strongly affects the extent of the resulting neuronal injury. If the brain temperature is not regulated, it usually falls in the gerbil by 2°–4°C during 5-min ischemia. However, the brain temperature during ischemic insult was not regulated in many previous studies. In the present study, the effects of transient (1 to 5 min) forebrain ischemia on the development of neuronal degeneration in hippocampal regions of the gerbil whose brain temperature was maintained at 37°C were examined. In the CA1 field of the hippocampus, transient ischemia of 3- and 4-min duration caused almost the same maximal damage (88%–91% neuronal loss) as observed in the gerbils subjected to 5-min ischemia. Transient ischemia of 2-and 2.5-min duration provoked substantial neuronal damage in 25% and 55% of experimental gerbils, respectively. These results indicate that 5-min bilateral forebrain ischemia is more than is necessary to examine ischemiainduced neuronal degeneration in hippocampal CA1 field of the gerbil whose brain temperature is maintained at normothermic levels. In the normothermic gerbil brain, an ischemic period of 3-min already induces extensive neuronal death in the CA1 and, thus, constitutes a sensitive model to evaluate faint protective effects of drugs against ischemic injury in the normothermic gerbil.Supported by Grant-in-Aid for Encouragement of Young Scientist (03857019) from the Ministry of Education, Science and Culture of Japan and the Sasakawa Health Science Foundation to A.M., and Grants-in-Aid for General Scientific Research (01400004 and 03557007) from the Ministry of Education, Science and Culture of Japan, Japan Foundation for Aging and Health and Mitsui Life Social Welfare Foundation to K.K.     

亚低温治疗对重型颅脑损伤患者血中神经元特异性烯醇化酶的影响及其临床意义

目的观察亚低温治疗后重型颅脑损伤患者血中神经元特异性烯醇化酶(NSE)的动态变化,为评价亚低温的脑保护作用提供量化指标。方法45例重型颅脑损伤患者被随机分为亚低温治疗组(22例)和常温治疗组(23例),脑温分别控制在(34．2±0．2)℃和(36．9±0．3)℃。动态监测患者治疗前及治疗后24、48、72、96 h血中NSE变化,并于3个月后对患者预后进行评估。结果亚低温治疗组患者血中NSE浓度在治疗后24、48、72 h显著降低．3个月后预后显著改善。结论亚低温治疗可以减轻神经元损伤,显著抑制NSE释放,增强神经元对脑外伤的耐受性,对重型颅脑损伤患者具有保护作用。