应用胰岛素对颅脑外伤后高血糖预后探讨

目的:探讨及早应用胰岛素对颅脑外伤后高血糖患者治疗转归的影响。方法:对83例颅脑外伤后血糖升高者于入院时及伤后第1、2、3、5、7、10、14(如血糖仍未恢复正常者酌情延长时间)日晨空腹抽血检测血糖。且在使用胰岛素期间对末梢血糖进行动态的监测直至清晨空腹静脉血糖连续2次正常,同时制定饮食护理措施及对患者或家属进行相应的健康教育。结果:血糖升高者中72.12％(59例)的患者血糖在1-3d内恢复正常,且预后与血糖正常者无差别。组中仅7例患者血糖持续升高,均因伤情重而死亡,占本组重症(GCS≤8分)患者(25例)的29.41％,明显低于文献报道组。结论:对颅脑外伤后高糖血患者尽早应用胰岛素,能改善患者预后,降低死亡率。     

危重新生儿应激性高血糖及其预后分析

目的探讨危重新生儿预后与应激性高血糖之间的关系。方法对85例危重新生儿入院后即采静脉血用葡萄糖氧化酶法测血糖,血糖>7mmol/L诊断为高血糖,此后应用微量血糖仪进行动态监测。结果入院时高血糖者56例,占65.9%,治愈组与死亡组的血糖值分别为7.38±2.70、17.8±8.50mmol/L(P<0.01);无脏器功能衰竭、单器官及多器功能衰竭患儿的血糖分别为6.02±2.82、10.8±3.85、14.1±4.80mmol/L(P<0.01)。高血糖与器官功能衰竭关系密切,血糖越高,病情越严重,预后越差。结论危重新生儿血糖水平可作为预后判断的一项依据。     

颅脑损伤与胰岛素抵抗的相关性研究

目的分析颅脑损伤的严重性、血糖与胰岛素水平三者之间的关系。方法92例颅脑损伤患者按入院时GCS评分分为轻度、中度及重度颅脑损伤三组，分别于伤后24h、48h、72h测定空腹血糖、血清胰岛素值，并计算稳态模式中的胰岛素抵抗指数（HOMA—IR）。患者出院时按GOS标准评估预后。采用SPSS11．5统计软件对数据进行处理，分析GCS、空腹血糖、胰岛素水平的关系。结果出院时按GOS标准．良好72例，差12例，死亡8例．死亡率8．7％。92例颅脑损伤患者伤后连续3d空腹血糖及胰岛素水平在轻度、中度、重度颅脑损伤三组患者中有显著差异（P〈0．01或P〈0．05）。颅脑损伤程度越重．血糖和HOMA—IR越高。结论空腹血糖值和HOMA—IR值可作为评估颅脑损伤严重程度的参考指标。     

Alcohol consumption and impaired glycoregulation results in a population of 6665 salaried employees

Alcohol consumption and glycosuria were found to be associated (p < 0.001) in a population of 6571 salaried employees who underwent a systematic examination. The prevalence of glycosuria was found to range from 1.3% among 2609 non-drinkers to 5% among 816 heavy drinkers (six glasses or more of alcoholic beverage daily). This association was still significant after adjustement for age, sex and body mass index. Similarly, a positive association was observed between fasting glycemia and alcoholic intake in a subgroup of 998 subjects when such a result was available (p < 0.05).     

Focal ischemia of the rat brain,with special reference to the influence of plasma glucose concentration

Summary Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery in hypoglycemic, normoglycemic, as well as in acute and chronic diabetic rats. The brain damage was studied after 4 days. The volume of infarction was decreased in hypoglycemia (29±19 mm³ (mean±SD) versus 58±35 mm³,P<0.0046), unaltered in acute diabetes (61±45 mm³), and increased in chronic diabetes (91±22 mm³,P<0.0463). The cortex adjacent to the infarct showed selective neuronal injury affecting the cortical layers 2 and 3. The damage was enhanced by hypoglycemia and prevented in most of the diabetic animals. The findings indicate that different mechanisms cause infarction and selective neuronal injury outside infarcts, but that both are influenced by the plasma glucose concentration.     

Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.     

高血糖导致肾脏高灌注的机制研究

探讨了高血糖对整体大鼠和离体灌注鼠肾（ＩＰＲＫ）血流动力学的影响及其机制。结果显示：高血糖在整体大鼠和ＩＰＲＫ均可引起肾血浆流量（ＲＰＦ）、肾小球滤过率（ＧＦＲ）的增加；在ＩＲＰＫ阻断管－球反馈后，高血糖不再能诱发上述改变；结构和葡萄糖相似的Ｄ－α－甲基－葡萄糖苷在ＩＰＲＫ可引起与相同渗透浓度的葡萄糖相似的ＲＰＦ，ＧＦＲ增加；血红蛋白不改变高血糖对肾血流动力学的影响。提示：高血糖可支接引起肾脏高灌注、高滤过，其机制主要是对管一球反馈的抑制，此抑制效应可能与葡萄糖的结构相关。内皮由来性舒张因子（ＥＤＲＦ）在高血糖导致的ＩＰＲＫ高灌注中不起主要作用。     

Diabetic and nondiabetic hyperglycemia in the ICU

Hyperglycemia is a common feature in critically ill patients, whether they are diabetic or not, and it is associated with unfavorable outcome. The more severe the underlying disease, the more important the hyperglycemia appears to be although, we still cannot define whether hyperglycemia is just a marker of the severity of the acute illness or rather an active contributor to poor outcome. The review of the literature on this subject published from 2001 up today conveys a massive amount of information the interpretation of which is equivocal, due to the heterogeneity of patients (nondiabetic vs. diabetic, medical intensive care unit (ICU) pts vs. surgical ICU pts) and of interventions (dose and modality of insulin infusion).The association between high glucose level and mortality is strong in critically ill patients without a previous history of diabetes. Admission hyperglycemia seems to be an independent risk factor of in-hospital mortality in patients both with and without diabetes in cardiac, cardiothoracic and neurosurgical ICUs. No data are still available on general surgical ICU patients.Tight control of blood glucose levels has been demonstrated to improve outcome in both diabetic and nondiabetic critically ill patients. In surgical ICUs, tight glucose control improves mortality and reduces morbidity only among patients admitted in ICU for more than 5 days, while outcome is not improved in patients who stay in ICU for less than 3 days.However, it is not yet understood if such favorable effect is secondary to glucose control itself or if insulin plays a part, by means of its nonglucose, anabolic effects. More randomized controlled trials are needed, addressing specific issues—such as the optimal target glucose concentration and the most effective insulin regimen—especially in the general surgical patient.     

Immunological blockade of endogenous thyrotropin-releasing hormone impairs recovery from hyperglycemia in mice

Administration of antiserum to thyrotropin-releasing hormone (TRH) into the lateral cerebral ventricle of mice significantly attenuated recovery from hyperglycemia induced by treatment with 2-deoxyglucose but had no effect on the plasma glucose of saline-treated mice. TRH, injected centrally together with the anti-TRH antibody, reversed the effect of the antiserum and blocked the development of hyperglycemia. These findings suggest that activation of TRH neurons in the central nervous system may be a physiological event influencing recovery from hyperglycemia.     

急性脑卒中患者应激性高血糖危险因素分析

目的 探讨重症监护室（ICU）急性脑卒中患者应激性高血糖的危险因素。方法对50例急性（发病5d内1非糖尿病脑卒中患者监测血糖7-14d，比较高血糖及正常血糖两组患者年龄、糖皮质激素、临床肺部感染评分等对血糖的影响。结果高血糖组临床肺部感染评分（CPIS）为4．77±2．11，显著高于正常血糖组的3．36±2．36（P〈0．05），急性生理学及慢性健康状况评分（APACHEⅡ）高血糖组为16．23＋5．40，也显著高于正常血糖组的12．43±3．83，有显著性差异（P〈0．01）。结论CHS和APACHEⅡ升高可能是ICU非糖尿病卒中后应激性高血糖的危险因素。