束缚应激影响大鼠四氧嘧啶性糖尿病发病的初步研究

将Ｗｉｓｔａｒ雄性大鼠束缚应激，腹腔注射６％四氧嘧啶（１００ｍｇ／ｋｇ），２４ｈ后血糖值为７．３±０．２ｍｏｌ／Ｌ，而未做应激处理的大鼠血糖值为９．９±０．６ｍｍｏｌ／Ｌ；既不应激也不注射四氧嘧啶动物的血糖值为７．０±０．６ｍｍｏｌ／Ｌ，说明束缚应激具有对抗四氧嘧啶致糖尿病的作用。以束缚应激后大鼠腹腔淋巴结提取的抑制因子给大鼠静脉注射，然后再腹腔注射同样剂量的四氧嘧啶。结果显示，注射淋巴结提取物大鼠血糖值为７．３±０．６ｍｍｏｌ／Ｌ，而单纯注射四氧嘧啶大鼠血糖值为９．８±０．８ｍｍｏｌ／Ｌ（Ｐ＜０．０５），说明束缚应激对抗四氧嘧啶致糖尿病作用可能由束缚应激产生的抑制因子所致。     

大鼠致痫后血清和脑组织皮质醇水平的测定及其意义

应用放免技术测定了马桑内酯致痫和对照组大鼠大脑皮层和海马脑组织皮质醇含量及血清皮质醇水平结果显示，血清对照组为２．７７±２．０７ｎｇ／ｍｌ，致痫组为０．９８±０．７５ｎｇ／ｍｌ，两组比较无显著差异（Ｐ＞０．０５）；海马正常对照组为２５．７７±１２．９８ｎｇ／ｇ湿重，致痫组为０．９８±０．４２ｎｇ／ｇ湿重组织，海马致痫组显著降低（Ｐ＜０．０１）；大脑皮层对照组为８．８３±１．９６ｎｇ／ｇ湿重，致痫组为０．３３±０．１１ｎｇ／ｇ湿重组织，大脑皮层致痫组降低极为显著（（Ｐ＜０．００１）。表明致痫后大鼠大脑皮层、海马脑组织皮质醇含量均明显降低，提示皮质醇在癫痫的发病中起重要作用。     

果糖胺测定对判断急性脑血管病血糖增高原因的意义

对３４例血糖增高的急性脑血管病患者行果糖胺测定。其中糖尿病继发脑血管病１３例，果糖胺水平４．７２±１．３６ｍｍｏｌ／Ｌ，与正常对照组（果糖胺１．６７±０．４３ｍｍｏｌ／Ｌ）比较有非常显著性差异（Ｐ＜０．００１）。无糖尿病脑血管病２１例，果糖胺水平２．０３±０．４７ｍｍｏｌ／Ｌ，与正常对照组比较无显著性差异（Ｐ＞０．０５）。糖尿病组与无糖尿病组的果糖胺水平有显著性差异（Ｐ＜０．０１）。提示果糖胺测定可对急性脑血管病血糖增高的原因进行鉴别。     

甘露醇治疗缺血性脑水肿的实验研究

目的重新评价甘露醇治疗脑水肿的效果，并探讨其作用机制，为临床合理用药提供依据。方法用线栓法制成ＳＤ大鼠大脑中动脉缺血性脑水肿模型，分别静注２０％甘露醇１ｇ／ｋｇ×６次、１ｇ／ｋｇ×３次、０．５ｇ／ｋｇ×３次，１０分钟内输完，间隔２ｈ一次。设６次、３次生理盐水对照组，治疗后２ｈ分别测定大脑两半球的脑组织水含量（ＢＷＣ）。结果（１）３次（１ｇ／ｋｇ）组脑水肿区ＢＷＣ与对照组比较明显降低，而６次（１ｇ／ｋｇ）组则无差别，６次组ＢＷＣ明显高于３次组。（２）３次（１ｇ／ｋｇ）及３次（０．５ｇ／ｋｇ）组脑水肿区ＢＷＣ与对照组比较明显降低，但两组间ＢＷＣ无差别。结论半量及全量甘露醇治疗具有相同的脱水效果，但其效果随着使用次数增加而减弱甚至可加重脑水种     

免疫抑制剂硫唑嘌呤对慢性脑血管痉挛的防治作用

目的观察免疫抑制药物对慢性脑血管痉挛的预防作用。方法采用本单位以往建立的犬“二次蛛网膜下腔出血”模型，观察硫唑嘌呤对慢性脑血管痉挛的预防作用。结果在蛛网膜下腔出血第７天，硫唑嘌呤组的基底动脉口径为（８７.１±２５．９）％，管壁ＭＤＡ含量为０．０３±０．０１ｎｍｏｌ／ｍｇ；而安慰剂组的血管口径为（５２．７±１７．１）％，ＭＤＡ含量为０．１０７±０．０５ｎｍｏｌ／ｍｇ。组织学检查发现硫唑嘌呤组的血管壁结构破坏明显较安慰剂组轻。结论蛛网膜下腔出血后慢性脑血管痉挛主要是免疫系统参与的炎症反应的结果，抗炎抗免疫疗法能有效预防慢性脑血管痉挛。     

胰蛋白酶抑制剂对实验性缺血性脑水肿的作用

目的观察各种胰蛋白酶抑制剂对大鼠缺血性脑水肿的作用。方法大鼠脑缺血模型采用线栓法，脑含水量测定采用称重法，常规病理学检查。结果５５ｍｇ／ｋｇ和１６５ｍｇ／ｋｇ胰蛋白酶抑制剂（ＳＢＴＩ）对ＬＭＣＡＯ３ｈ大鼠脑含水量无显著影响（Ｐ均＞０．０５）；６６０００ＫＩＵ／ｋｇ特血乐、５００００Ｕ／ｋｇ尿胰蛋白酶抑制剂（ＵＴＩ）可显著降低脑水肿大鼠脑含水量（Ｐ均＜０．０５），并可减轻缺血区神经元变性及间质水肿程度。结论６６０００ＫＩＵ／ｋｇ特血乐、５００００Ｕ／ｋｇＵＴＩ具有减轻实验性缺血性脑水肿的作用。     

黄芪的抗神经细胞缺氧损伤作用

目的观察黄芪抗神经细胞缺氧损伤的作用。方法用氰化钠造成体外培养新生大鼠大脑皮层神经细胞缺氧模型，比较黄芪组和对照组的细胞形态、存活细胞数（四唑盐微量自动比色检测Ａ值）、乳酸脱氢酶（ＬＤＨ）值和钾离子（Ｋ＋）流出的变化。结果缺氧４８小时后，对照组Ａ值由缺氧前的０３２５±００３１降至０１４５±００１１，ＬＤＨ和Ｋ＋漏出量分别由６５８０±２９０Ｕ／Ｌ、５２３±０１１ｍｍｏｌ／Ｌ增至１４８８０±８４０Ｕ／Ｌ、７３１±０１８ｍｍｏｌ／Ｌ。而此时黄芪组Ａ值为０１７８±００１１、ＬＤＨ漏出量为１２７２５±７８４Ｕ／Ｌ，Ｋ＋含量为６９３±０１５ｍｍｏｌ／Ｌ。与对照组相比，黄芪组受损程度明显减轻。结论黄芪具有一定的抗神经细胞缺氧损伤作用     

脑缺血再灌注后脑组织c-fos基因表达与丹参的影响

采用线栓法制成大鼠大脑中动脉缺血再灌注模型，用地高辛精标记ｃ－ｆｏｓ探针进行原位杂交。结果示缺血再灌注鼠栓塞侧皮层及海马ｃ－ｆｏｓ基因表达显著增多，图像分析灰阶值为１１８．６±５．１，对侧为１５９．６±３．１（Ｐ＜０．００１）。丹参组栓塞侧皮层及海马ｃ－ｆｏｓ基因表达亦增多，灰阶为１３５．００±２．０５，对侧为１６７．００±２．００（Ｐ＜０．００１）。丹参组与缺血再灌注组比较，栓塞侧丹参组ｃ－ｆｏｓ基因表达显著低于缺血再灌组（Ｐ＜０．０５），而两组栓塞对侧比较无显著差异。本实验表明，脑缺血再灌注后脑组织ｃ－ｆｏｓ基因表达显著增多，丹参能部分抑制缺血后ｃ－ｆｏｓ基因的表达，这可能是其治疗缺血性脑血管病的机理之一。     

尼莫地平对急慢性脑血管痉挛的不同作用

目的：通过观察尼莫地平对蛛网膜下腔出血后急性和慢性脑血管痉挛的不同作用，为临床合理使用尼莫地平提供依据。方法：在家犬上复制蛛网膜下腔出血模型，分别观察在急性期和慢性期尼莫地平的解痉作用。并观察连续给尼莫地平对慢性脑血管痉挛有无预防作用。结果：在急性痉挛时，静脉注射尼莫地平０．１ｍｇ／ｋｇ后３０分钟，基底动脉口径由５９％±１３．６％扩大到９６．２％±１２．１％（Ｐ＜０．０１）；然而在慢性期，同样注射尼莫地平后，动脉口径扩张不明显（Ｐ＞０．０５）。在出血早期常规连续给尼莫地平（４０ｍｇ，口服，６小时１次，连续７天）无明显预防效果。结论：尼莫地平对急性期痉挛有明显扩张效果，而对慢性期痉挛无效。且常规剂量尼莫地平对慢性脑血管痉挛无明显预防作用。     

U74006F对缺血前高血糖大鼠局部脑缺血再灌注损伤保护作用的研究

目的 探讨Ｕ７４００６Ｆ对缺血前高血糖大鼠局部脑缺血再灌注损伤保护作用。方法 线栓法建立脑缺血再灌注模型。大鼠缺血前３０分钏注射５０％葡萄糖，使之处于高血糖状态，再灌注前静注Ｕ７４００６Ｆ（６ｍｇ／ｋｇ）。另设枸橼酸盐组与对照组。然后比较３组大鼠梗死面积、神经功能缺损症状和脑组织病理改变。结果 Ｕ７４００６Ｆ组梗死面积较枸橼酸盐组平均缩小６４％（Ｐ〈０．０１），神经功能评分显著降低（Ｐ〈０．０５），病理改变明显减轻，对照组损伤程度也显著轻于枸橼酸盐组（Ｐ〈０．０５）。结论 高血糖可加重脑缺血再灌注操作。Ｕ７４００６Ｆ对高血糖状态下大鼠缺血再灌注损伤有明显保护作用。     

The effects of hyperglycemia on ischemic cell change and reactive neuronal change in neonatal rat brain following transient forebrain ischemia

To examine the effects of hyperglycemia on a transient ischemia in the neonatal brain, neuropathological and biochemical evaluations were performed. In 10-day-old rats, brain ischemia was induced by permanent occlusion of the right external and internal carotid and subclavian arteries and the clamping of the left external and internal carotid arteries for 2h. The peritoneal injection of a 50% glucose solution (0.10 ml/15 g weight) 5 min before the induction of brain ischemia increased the plasma glucose concentration to 20-25 mmol/l during ischemia. It preserved brain tissue glucose levels at 1h of ischemia in the glucose-treated group, while tissue glucose was exhausted in the saline-injected group. Tissue lactate concentrations increased slightly at the end of the ischemic insult (6.7 mmol/kg) in the saline-injected group and remarkably (18.7 mmol/kg) in the glucose-treated group. Two distinct forms of ischemic neuronal change were found in this study: ischemic cell change and reactive neuronal change. A quantitative neuropathological assessment indicated that hyperglycemia significantly reduced the volume of ischemic cell change in the neocortex from 85% to 33%, but not that of reactive neuronal change (from 5.5% to 2.4%). These results indicated that hyperglycemia attenuated ischemic cell change, but not reactive neuronal change, in the neonatal rat brain and suggested that it reduced ischemic cell change probably because of reserved brain glucose.     

Lactate reverses insulin-induced hypoglycemic stupor in suckling-weanling mice: biochemical correlates in blood, liver, and brain

The recovery of weanling mice from insulin-induced hypoglycemic stupor-coma after injection of sodium -L(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the beta-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in alpha-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO-3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and alpha-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates).(ABSTRACT TRUNCATED AT 250 WORDS)     

Laminar distribution of GABA (gamma-aminobutyric acid) in the dorsal lateral geniculate nucleus, Area 17 and Area 18 of the visual cortex, and the superior colliculus of the cat

The laminar distribution of gamma-aminobutyric acid (GABA) was studied in certain structures of the visual system of the adult cat. A microassay method to measure GABA (10(-12) mol) was established using enzymatic cycling of NADP-NADPH. In the dorsal lateral geniculate nucleus, GABA concentration was highest in lamina A (average concentration 23 mmol/kg dry weight) and lowest in lamina C. In the visual cortex (Areas 17 and 18), the concentration of GABA was 10-12 mmol/kg dry weight in layers I-IV and 5-8 mmol/kg dry weight in layers V and VI. No significant difference was found in the GABA distribution in Areas 17 and 18. In the superior colliculus, the highest level of GABA was found in the upper part of the superficial gray layer (40 mmol/kg dry weight), whereas the deep layers contained GABA at a concentration of 23-28 mmol/kg dry weight. The results of the GABA distribution measurements revealed an orderly, layer-specific disposition of the neurotransmitter in the cat visual system. GABA may play an important role in the function of the visual system.     

Quantitation of high energy phosphate compounds and metabolic significance in the developing dog brain.

The phosphate metabolites, PCr, ATP, ADP and inorganic phosphate (Pi), were quantitated in the brain of the newborn, neonatal, juvenile and adult dog to investigate the potential control mechanisms responsible for increased ATP demands during development. The concentrations of PCr and Pi were measured in vivo by MRS using the enzymatic-measured ATP as the internal standard. Phosphocreatine values increased during development from 2.08 mmol/kg wet weight in the 0-2 day newborn to 5.11 mmol/kg wet weight in the adult brain and paralleled the increases in the total creatine pool (PCr + Cr) from 4.12 to 10.05 mmol/kg wet weight. Brain ATP concentrations increased approximately 40% during postnatal development; however, when expressed as intracellular concentration, no increase in ATP was apparent due to the age-dependent decrease in extracellular space. The Pi concentration, estimated by MRS, increased significantly during postnatal development with a range of 1.78 to 2.52 mmol/kg wet wt, then decreased to 1.97 mmol/kg wet weight at adulthood. In those developmental stages where total Pi was measured enzymatically on freeze-clamped tissue, the NMR visible Pi comprised about 48 to 93% of the total, with the highest percentage being visible in the newborn brain. The intracellular pH decreased from 7.21 in the newborn to 7.10 in the adult. With development, the free ADP concentration, calculated from the components of the creatine kinase equilibrium, ranged from 27 to 34 microM. These values are close to the apparent in vitro Km of ADP for oxidative phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of indomethacin on edema following single and repetitive cerebral ischemia in the gerbil

BACKGROUND AND PURPOSE: Repetitive periods of cerebral ischemia result in more severe injury than a single period of ischemia of similar total duration. We investigated the possibility of prostaglandin mediation of this increased injury by attempting to modify brain edema formation with indomethacin pretreatment. METHODS: Under halothane/N2O anesthesia, groups of gerbils underwent bilateral carotid occlusion to induce forebrain ischemia. Group I underwent a single 15-minute period of carotid occlusion. Group II underwent three 5-minute periods of occlusion at hourly intervals. Groups III and IV were similar to groups I and II, respectively, but received 0.2 mg/kg indomethacin before carotid occlusion. Cortical and cerebellar water and sodium contents were determined in control animals (n = 6) at time zero and in experimental animals 24, 48, and 72 hours after ischemia (n = 6-10 gerbils/group at each time point). RESULTS: Cortical water and sodium contents in group II peaked 48 hours after insult (82.15 +/- 0.31% and 420 +/- 14 meq/kg dry wt, respectively) and were significantly higher than control and group I values at both 24 and 48 hours. Cortical water did not change from control in group I animals. Indomethacin pretreatment significantly attenuated increases in water and sodium content seen at 48 hours in gerbils undergoing repetitive ischemia (peak 80.02 +/- 0.45% and 300 +/- 39 meq/kg dry wt), but did not affect mortality. CONCLUSIONS: Indomethacin lessens edema after repetitive cerebral ischemia, suggesting that elevations of cyclooxygenase products are responsible, at least in part, for severe brain edema following repetitive ischemia.     

不同药物麻醉后大鼠全脑缺血脑温的变化

目的 了解不同常用麻醉药物后麻醉大鼠全脑缺血脑温的变化。方法 选用乌拉坦（1g/kg)、戊巴比妥钠（40mg/kg)、水合氯醛（400mg/kg)、巴比妥钠（300mg/kg)和苯巴比妥钠（200mg/kg)腹腔麻醉大鼠后全脑缺血测量脑组织温度的动态变化。结果 这些药物麻醉大鼠后行四动脉阻断全脑缺血，脑温进一步下降；但不同药物的作用各异。结论 本实验的结果说明了在脑缺血同一个实验过程中尽量避免使用不同各类的麻醉药物引起的脑温波动，进而影响实验结果的准确性。     

Outcome and frequency of sodium disturbances in neurocritically ill patients

Sodium disturbances are frequent and serious complications in neurocritically ill patients. Hyponatremia is more common than hypernatremia, which is, however, prognostically worse. The aim of this study was to analyse outcome and frequency of sodium disturbances in relation to measured serum osmolality in neurologic-neurosurgical critically ill patients. A 5-year retrospective collection of patients (pts) and laboratory data were made from the Laboratory Information System database in the Clinical Biochemistry Department. The criteria for patients’ inclusion was acute brain disease and serum sodium (SNa⁺) <135 mmol/l (hyponatremia) or SNa⁺ >150 mmol/l (hypernatremia). Hypoosmolality was defined as measured serum osmolality (SOsm) <275 mmol/kg, hyperosmolality as SOsm >295 mmol/kg. We performed analysis of differences between hyponatremia and hypernatremia and subanalysis of differences between hypoosmolal hyponatremia and hypernatremia. From 1,440 pts with acute brain diseases there were 251 (17 %) pts with hyponatremia (mean SNa⁺ 131.78 ± 2.89 mmol/l, SOsm 279.46 ± 11.84 mmol/kg) and 75 (5 %) pts with hypernatremia (mean SNa⁺ 154.38 ± 3.76 mmol/l, SOsm 326.07 ± 15.93 mmol/kg). Hypoosmolal hyponatremia occurred in 50 (20 % of hyponatremic patients) pts (mean SNa⁺ 129.62 ± 4.15 mmol/l; mean SOsm 267.35 ± 6.28 mmol/kg). Multiple logistic regression analysis showed that hypernatremia is a significant predictor of mortality during neurologic-neurosurgical intensive care unit (NNICU) stay (OR 5.3, p = 0.002) but not a predictor of bad outcome upon discharge from NNICU, defined as Glasgow Coma Scale 1–3. These results showed that hypernatremia occurred less frequently than all hyponatremias, but more often than hypoosmolal hyponatremia. Hypernatremia was shown to be a significant predictor of NNICU mortality compared to hyponatremia.     

A randomised, controlled pilot study to investigate the potential benefit of intervention with insulin in hyperglycaemic acute ischaemic stroke patients

BACKGROUND: Hyperglycaemia on presentation with acute ischaemic stroke (AIS) is associated with poor outcome, but intervention is unproven. We investigated the safety and tolerability of one method of glycaemic control. METHODS: Patients within 24 h of AIS and plasma glucose 8-20 mmol/l were randomised to receive either rigorous glycaemic control (RC) or standard management (SM) for 48 h. RC comprised i.v. insulin at a variable rate adjusted for target glucose concentration of 5-8 mmol/l, and intravenous crystalloid. The SM group received intravenous crystalloid alone in an open-label design. RESULTS: Thirteen patients were randomised to RC and 12 to SM (age 75 +/- 6.2 years; 40% male; 20% lacunar stroke; time to treatment 8 +/- 6.1 h; plasma glucose 10.6 +/- 0.9 mmol/l; known diabetes 52%; NIHSS 8, range 2-28). The glucose concentration-time curve was reduced in the RC group (AUC 324 +/- 15 versus 385 +/- 28 h.mmol/l, p = 0.04). By 48 h, plasma glucose in both groups was 6.8 +/- 1.1 and 7.5 +/- 1.3 mmol/l respectively, but mean hourly insulin requirements in the RC group had dropped from 3.25 +/- 0.32 units to 1.25 +/- 0.5 units (p < 0.01). One transient episode of hypoglycaemic symptoms occurred in the RC group. CONCLUSION: Glycaemic control with sliding scale insulin for 48 h is feasible and well-tolerated after AIS. Treatment after 48 h may be unnecessary.     

Tolerability of oral loading of divalproex sodium in child psychiatry inpatients

OBJECTIVE: To determine a well-tolerated oral load of divalproex sodium that quickly and reliably achieves therapeutic drug levels in child psychiatry inpatients. METHODS: A retrospective chart review revealed that during a 6-month period, divalproex sodium therapy was initiated in 16 male inpatients (ages 5-14 years). The patients were divided into two groups based on the initial dosing regimen. The first group received approximately 15 mg/kg/day based on actual weight, and the second group received approximately 15 mg/kg/day based on an adjusted ideal body weight (IBW). Weight was adjusted in these patients according to the following formula: IBW + 40% (Observed Weight - IBW). A trough blood level was obtained on day 5 of therapy. RESULTS: Initial drug levels ranged from 46-146 ug/mL (mean = 90.6), of which 13 of 16 (81.3%) were considered within therapeutic range (50-120 ug/mL). Eight of 16 patients (50%) had reported side effects, including sedation and gastrointestinal upset. The majority of these side effects occurred in patients with drug levels > or = 90 ug/mL and were noted to improve with 1-2 days of therapy +/- dosage adjustment. Overweight patients (> or = 15% above IBW) who received the unadjusted 15 mg/kg oral load had significantly higher drug levels than their normal weight counterparts and overweight children who received weight-adjusted dosing (p < 0.003). CONCLUSION: A 15 mg/kg/day oral load of divalproex sodium resulted in therapeutic drug levels on day 5 of treatment and is well tolerated in normal weight children. Overweight children are significantly more likely to experience supratherapeutic drug levels on this regimen, which may affect tolerability. Overweight children appear to benefit from weight-adjusted oral loading.     

Lactate attenuates neuron specific enolase elevation in newborn rats.

This study was undertaken to investigate the protective role of lactate on the hypoxic brain in newborn rats. A total of 107 7-day-old Wistar rats were divided into three groups. The lactate accumulation group was given 5% oxygen and 95% nitrogen for 30 minutes. The lactate elimination group was given 5% oxygen, a concentration of 7.5% carbon dioxide, and 87.5% nitrogen for 30 minutes. The control rats were placed in room air. Lactate levels in the brain tissue were higher in the lactate accumulation group than in those of the control group (control: 1.78 +/- 0.91, lactate accumulation: 11.42 +/- 1.64 mmol/kg) and significantly decreased in the lactate elimination group (4.10 +/- 1.73 mmol/kg). Blood pH remained at the same levels in the two groups. Neuron specific enolase in the cerebrospinal fluid, which is the initial neurocyte damage marker, was significantly elevated in the lactate elimination group (control: 18.3 +/- 7.5, lactate accumulation: 18.8 +/- 7.9, lactate elimination: 63.1 +/- 61.3 ng/mL). Brain adenosine 5'-triphosphate levels were significantly decreased in the lactate elimination group. Histologic findings of the brain at 72 hours after the load revealed no abnormal changes in any of the groups examined. The authors conclude that lactate accumulation plays a protective role on the hypoxic brain in newborn rats.