危重儿的血糖监测及临床分析

目的:分析危重儿血糖与危重程度及预后的关系,评价危重儿血糖监测的临床意义。方法:对50例危重儿(不含极危重儿)、28例极危重儿和30例非危重患儿进行血糖监测,并进行对比观察和分析。结果:危重儿组、极危重儿组血糖异常发生率显著高于非危重儿组;极危重儿组血糖异常发生率显著高于危重儿组。血糖异常以高血糖为主。高血糖越显著,持续时间越长,且难纠正者,预后差。结论:危重病儿高血糖水平与病情的严重程度及预后显著相关,对危重儿应密切监测血糖变化,及早发现和尽快纠正高血糖或低血糖,改善预后。     

Does long-term glucose infusion reduce brain damage after transient cerebral ischemia?

A recent study reported that hyperglycemia of a brief duration worsens, and of long duration reduces, ischemic brain damage. To test whether this is a valid conception, we induced 10 min of transient forebrain ischemia, recorded postischemic seizures, and evaluated brain morphology. The results showed that administration of glucose 2 h before ischemia aggravated brain damage, induced seizures, and caused animal death in the same manner as was previously observed when glucose was given 30 min before ischemia. Thus, the conclusion that the influence of glucose on an ischemic transient is dependent upon the duration of hyperglycemia is unsubstantiated.     

重组人生长激素在严重延迟复苏病人中的应用

目的:探讨重组人生长激素(rhGH)在严重延迟复苏治疗中的作用。方法:依据应用rhGH与否,将62例严重延迟复苏病人分为rhGH治疗组(GH组,n=26)及非rhGH组(NGH组,n=36),GH组每晚20:00皮下注射重组人生长激素(rhGH,0.2~0.4IU.kg-1.d-1)进行治疗,NGH、GH两组其余治疗方案均相同。观察两组创面愈合时间,前白蛋白水平,rhGH应用前后空腹微量血糖、尿糖、血清胰岛素水平。结果:(1)GH组供皮区、植皮区、深II度、浅II度创面及创面平均愈合时间较NGH组缩短(P<0.05)。(2)两组血浆前白蛋白明显下降,以NGH组下降更为明显(P<0.05)。(3)两组空腹血糖、胰岛素水平均明显升高,但胰岛素以GH组升高更为明显(P<0.05)。(4)13例(20.9%)尿糖明显升高,尿糖阳性多为一过性。GH组中尿糖升高以≥+++为主,与NGH组比较P<0.05。结论:rhGH有助于改善严重延迟复苏烧伤患者的营养状况,促进烧伤创面及供皮区创面愈合,起到良好代谢调理和免疫调控作用。但应用时需注意存在高糖血症及尿糖升高的倾向。     

深低温停循环手术中血糖的变化及控制效果

【目的】本研究通过即刻血糖监测，观察需在深低温停循环（deep hypothermia cardiac arrest，DHCA）下行胸主动脉瘤手术的非糖尿病患者术中血糖的变化。【方法】选择20例需在DHCA下行胸主动脉瘤手术的非糖尿病患者，随机分为两组，每组10例，实验组使用胰岛素控制血糖，对照组观察血糖变化，不控制血糖。【结果】（1）两组患者的一般情况及CPB时间、主动脉阻断时间、停循环时间、鼻咽温、肛温以及各种麻醉药的用量没有显著性差异（P〉0．05）。（2）对照组CPB开始后血糖有上升趋势，至DHCA前为（8±1．4）mmol／L，但与基础值比较无统计学差异，至DHCA后15min时血糖水平明显高于基础值（P〈0．01）。（3）实验组术中血糖波动较小，在DHCA前、胸骨合拢时及入ICU后2h这3个时间点血糖水平低于基础值（P〈0．05）。【结论】（1）在深低温停循环手术中，血糖水平会明显上升，并维持高水平一直到术后。（2）应用本文的血糖控制方案，可以使DHCA相关的高血糖基本得到控制，且不引起术后低血糖的发生。     

孕鼠高血糖对胎鼠胰岛功能的影响

目的　探讨孕鼠高血糖对胎鼠胰岛β细胞分泌胰岛素功能的影响。方法　２８ 只妊娠 Ｓ Ｄ 大鼠随机分成两组,实验组在妊娠晚期持续性静脉输注高渗葡萄糖;对照组同期输注无菌蒸馏水。采用胎鼠胰岛细胞进行胰岛素抽提实验、胰岛素释放试验及灌流试验,研究胎鼠胰岛β细胞功能的变化。结果　实验组胎鼠每个胰腺内胰岛素平均水平为（３ ３２９ ．８１ ±１６３ ．３９）ｎｇ;单位重量胰腺组织胰岛素水平为（１５８ ．５６ ±２３ ．３４）ｎｇ／ｍｇ。对照组胎鼠胰腺内胰岛素平均水平为（２ ３９０ ．０４ ±１５１ ．３９）ｎｇ ;单位重量胰腺组织胰岛素水平为（１２５ ．７９ ±１７ ．９７）ｎｇ／ｍｇ 。两者比较,差异有显著性（ Ｐ＜ ０ ．０５） 。在低糖或高糖 Ｈａｎｋｓ 液中温育胰腺组织２ 小时,实验组胎鼠胰岛素释放量：低糖时为（２４ ．２２ ±４ ．６３）ｎｇ／ｍｇ ;高糖时为（７３ ．７３ ±５ ．９４）ｎｇ／ｍｇ 。对照组胎鼠胰岛素释放量：低糖时为（２０ ．５２ ±２ ．３１）ｎｇ／ｍｇ ;高糖时为（５３ ．３５ ±７ ．５３）ｎｇ／ｍｇ 。两组比较,差异有显著性（ Ｐ＜ ０ ．０５） 。在胰岛素灌流试验中,实验组胎鼠胰岛素分泌时相高峰出现早且峰值高于对照组。结论     

早期糖尿病视网膜病变与全身因素关系的探讨

１２２例（２４４只眼）检眼镜下未查见视网解膜病变的Ⅱ型糖尿病患者，眼底光血管造影发现有病变者６６例（１３２只眼）。包括毛细血管荧光素渗漏，毛细血管扩张，微血管瘤，黄斑及视网膜水肿和毛细血管闭塞，采用多因素逐步回归法对早期糖尿病视网膜病变与全身因素的关系进行分析，结果表明：与空腹血糖、甘油三脂、病程和眼灌注压呈显著正相关，与眼压，发病年龄呈显著负相关。     

高血糖大肠癌病人的围手术期处理

目的：探讨高血糖大肠癌病人围手术期的处理方法。方法：对1997～2002年外科治疗的70例高血糖大肠癌(空腹血糖大于6．1mmol／L)病人作回顾性分析。结果：70例病人均作择期手术，术后并发症发生率：吻合口瘘占8．8％(3／34)。切口感染20．6％，肺部感染、泌尿系感染均为2．9％。无酮症酸中毒发生，无手术死亡。术后平均住院19d。结论：高血糖大肠癌病人的外科治疗必须作好围手术期处理。只要严格控制血糖、选择合理的术式和时机就完全可以达到理想的外科治疗效果。     

Contribution of excitatory amino acids to morphine-induced metabolic alterations

Previous studies have indicated that excitatory amino acids are involved in the analgesic and addictive properties of morphine. However, their role in the morphine-induced alterations in glucose metabolism is not known. This study assessed the contribution of NMDA receptor activation to the morphine-induced hormonal and metabolic alterations in conscious unrestrained chronically catheterized rats. Whole body glucose flux was assessed with a primed constant intravenous infusion of [3-³H]glucose in rats pretreated with the NMDA-receptor antagonist MK-801 (0.25 mg/kg, intraarterial) or an equal volume (1.5 ml) of sterile saline (0.9% ) administered 15 min prior to i.c.v. injection of H₂O (Con; 5 μl) or morphine sulfate (80 μg). No significant alterations were noted in metabolic and hormonal parameters of H₂O injected rats. i.c.v. morphine increased the plasma glucose concentration (60%), hepatic glucose production (R_a; 60%) and whole body glucose utilization (R_d; 53%), but did not alter the glucose metabolic clearance rate (MCR). MK-801 alone resulted in transient hyperglycemia (25%), stimulation of glucose R_a (60%) and glucose R_d (53%), and a significant (30%) increase in MCR. MK-801 pretreatment blunted the morphine-induced hyperglycemia and the increased glucose R_a and R_d. Morphine increased the plasma concentration of epinephrine (4-fold), norepinephrine (2-fold) and corticosterone (67%); however, no alterations in plasma insulin and glucagon were detected. MK-801 pretreatment, blunted the morphine-induced increase in corticosterone and norepinephrine, and elicited a significant rise in insulin concentrations. These results indicate that activation of the NMDA receptors contributes to the morphine-induced hyperglycemia and hormonal alterations. Furthermore, this response appears partially mediated by activation of sympathetic outflow and suppression of insulin release, which is blunted by inhibition of NMDA receptors.     

Mechanical hyperalgesia in rats with chronic perfusion of lumbar dorsal root ganglion with hyperglycemic solution

In diabetes, chronic systemic hyperglycemia is associated with pain and other symptoms of peripheral neuropathy. Evaluation of mechanisms causing these symptoms is complicated because of the overlap between the systemic effects of hyperglycemia and its toxic effects within the peripheral nervous system. To address this problem we developed a technique for chronic local in vivo perfusion of rat lumbar dorsal root ganglion (DRG) with a hyperglycemic solution. Osmotic pumps were filled with 30 mM glucose in physiological buffer and implanted in normal adult rats. The output of the catheter attached to the pump was positioned in a hole drilled through the right transverse process of the L₅ vertebrae to perfuse the corresponding DRG. Repetitive tests of foot withdrawal to mechanical stimuli have shown that chronic hyperglycemia localized to the L₅ DRG causes hyperalgesia in the hind limb innervated by perfused ganglion but not in the contralateral limb. Control experiments (DRG perfusion with 5 mM glucose or 5 mM glucose+25 mM mannitol solution) have shown that hyperglycemia-induced hyperalgesia can not be attributed to surgery-related injury or hyperosmolality of the ganglion-perfusing solution. These data demonstrate direct functional toxicity of hyperglycemia in the peripheral nervous system. This technique provides a new approach for in vivo study of chronic effects of physiologically active factors on DRG neuron function.     

Presentation of striatal hyperintensity on T1-weighted MRI in patients with hemiballism-hemichorea caused by non-ketotic hyperglycemia: report of seven new cases and a review of literature

Recent studies have shown unique clinicoradiologic characteristics in patients with hemiballism-hemichorea (HB-HC) caused by non-ketotic hyperglycemia; however, there is still a limited number of patients being reported. We report 7 patients (3 males and 4 females) with this type of dyskinesia, whose ages ranged from 60 to 84 years. Brain CT of these patients showed hyperdensity in the contralateral striatum, corresponding with MRI studies that showed an increased signal intensity on T1-weighted images and a decreased signal on T2-weighted images. After metabolic control had been achieved, the hyperkinetic state of these patients abruptly ceased. Follow-up neuroimaging studies in 2 patients documentied complete resolution of the striatal hyperintensity on brain CT and MRI after 3 months and 6 months, respectively. A review of patients with HB-HC caused by non-ketotic hyperglycemia reported formerly and in the present study shows that the dyskinesia tends to occur in aged diabetic patients. The age of patients with dyskinesia secondary to cerebral infarction is generelly much lower. We also found that 86 % (30 out of 35 cases) patients reported with HB-HC caused by non-ketotic hyperglycemia were Asians. The prognosis of the dyskinesia was excellent, and the radiological abnormalities are completely reversible. Received: 2 November 2000 / Received in revised form: 1 February 2001 / Accepted: 3 March 2001