不同剂量糖皮质激素对重症支气管哮喘的疗效观察

目的 观察不同剂量的糖皮质扩素对重症支气管哮喘的疗效。方法 观察组１６例采用小剂量激素（地塞米松２０ｍｇ／ｄ）治疗,对照组１６例使用较大量激素（地塞米松４０ｍｇ／ｄ）治疗。基他治疗措施及方法基本桢。结果 两组病人症状均在１～２ｄ缓解,动脉血ＰａＯ２恢复正常所需时间两组无差异（Ｐ〉０．０５）。结论 对重症哮喘者早期应用小剂量激素、氩茶碱持续静脉点滴,可避免大剂量应用产生的副作用,可收到较好效果。     

肝素与糖皮质激素在急性肺损伤中的治疗对比

目的 :了解急性肺损伤 (AL I)常见治疗中肝素与糖皮质激素对炎细胞的影响。方法 :用油酸尾静脉注射制作小鼠AL I损伤模型 ,观察其周围血白细胞及肺组织病理改变。结果 :AL I时肺系数损伤组明显高于除肝素组的其他组 ,周围血中性粒细胞 /淋巴细胞 (N/L)比率在 AL I时明显增加 ;肝素组在损伤 6 h后可见 N/L 降低 ,糖皮质激素则使其增高。组织切片见激素治疗组中每高倍视野内的多形核细胞数 (PMN)、肺水肿程度明显低于肝素组与损伤组 ;肝素治疗组中虽然肺水肿程度与损伤组无差异 ,但微小血栓明显少于损伤组与激素组。结论 :激素通过抑制 PMN在肺内的聚集而减少肺损伤 ;肝素则通过调节凝血机制保护肺脏     

Glucocorticoids attenuate haloperidol-induced catalepsy through adrenal catecholamines

Summary To examine the influence of adrenal secretions on neuroleptic induced catalepsy, we studied the effect of adrenocorticoids, noradrenaline (NA) or adrenaline (AD) on haloperidol (HAL) induced catalepsy in adrenalectomised (ADX) and sham-adrenalectomised (sham-ADX) rats. HAL (1 mg/kg, i.p.) induced a greater degree of catalepsy in ADX rats as compared to sham-ADX rats. Corticosterone (CORT, 1–2 mg/kg, s.c.) or dexamethasone (1–2 mg/kg, s.c.) attenuated the HAL catalepsy in sham-ADX but not in ADX rats. Further, when the HAL (1 mg/kg) catalepsy score was maximal (at 120 min), the rats were subjected to cold stress (3 °C for 10 min) or treated with NA, AD (2 g/kg, i.v.) or CORT (2 mg/kg, s.c.). After cold stress procedure or CORT treatment, the catalepsy was significantly reduced in sham-ADX but not in ADX rats, whereas NA or AD infusion caused an immediate but short lasting significant decrease in HAL catalepsy in both sham-ADX and ADX rats. The anticataleptic effect of NA or glucocorticoids was blocked by an ₁adrenoceptor blocker, prazosin.These findings suggest that peripheral noradrenergic and adrenergic mechanisms play an important role in the neuroleptic induced catalepsy. Such mechanisms may mediate the anticataleptic action of glucocorticoids.     

短程糖皮质激素治疗流行性乙型脑炎76例

目的：探讨糖皮质激素治疗流行性乙型脑炎的疗效。方法：采用地塞米松针剂加入液体静脉滴注,并配合物理降温、镇静止痉、脱水、给氧、扩容、纠酸、防治感染,加强护理等常规综合治疗。结果：治愈６９例（９０８％）,好转３例（３９％）,死亡４例（５３％）。结论：在常规综合治疗基础上应用激素治疗乙型脑炎疗效显著提高。     

Short-Term Effect of Vitamin K Administration on Prednisolone-Induced Loss of Bone Mineral Density in Patients with Chronic Glomerulonephritis

Glucocorticoid-induced osteoporosis has been reported to be caused by enhanced bone resorption and suppressed bone formation. To clarify whether administration of vitamin K, which enhances bone formation, prevents prednisolone-induced loss of bone mineral density (BMD), a randomized, prospective, controlled study was conducted on 20 patients with chronic glomerulonephritis scheduled for treatment with prednisolone. All patients were initially treated with 0.8 mg/kg body weight/day of prednisolone (maximum of 40 mg) for 4 weeks, tapering to 20 mg/day over approximately 6 weeks. Ten patients received prednisolone alone (Group 1), and the other 10 patients received prednisolone plus 15 mg of menatetrenone, vitamin K, three times per day (Group 2). BMD of the lumbar spine measured by dual-energy X-ray absorptiometry (DXA) and biochemical markers of bone metabolism in blood and urine were evaluated before and 10 weeks after administration of prednisolone alone or with menatetrenone. In Group 1, treatment with prednisolone significantly reduced BMD of the lumbar spine from 1.14 ± 0.12 to 1.10 ± 0.11 g/cm² (P= 0.0029). Serum intact osteocalcin and procollagen type I C-peptide (PICP) concentrations, biochemical markers of bone formation, were markedly reduced. A biochemical marker of bone resorption, urinary excretion of deoxypyridinoline, was significantly reduced. In Group 2, prednisolone-induced reduction of BMD was prevented by menatetrenone administration (1.09 ± 0.09 to 1.07 ± 0.07 g/cm², P= 0.153). Menatetrenone prevented reduction of PICP concentration by prednisolone but not in serum intact osteocalcin concentration and urinary excretion of deoxypyridinoline. Thus, treatment with prednisolone resulted in loss of BMD of the lumbar spine associated with suppression of both bone formation and bone resorption. Menatetrenone is a useful agent in preventing prednisolone-induced loss of BMD. Received: 7 July 1998 / Accepted: 13 August 1999     

糖皮质激素诱导性股骨头坏死模型的血管改变

目的　探讨在糖皮质激素诱导股骨头坏死过程中血管形态的改变与髓腔内脂肪填塞的关系。　方法　 12～ 18个月龄的健康日本大耳白兔 5 2只 ,按 2 5mg·kg-1·d-1注射地塞米松建立股骨头坏死模型 ,通过血管铸型扫描电镜观察、墨汁灌注切片光镜观察及图像分析等方法观察用药中和停药后股骨头病理和血管形态的变化。　结果　用药 2周出现股骨头髓腔内脂肪填塞 ,窦状隙血管因脂肪细胞压迫变细 ,血管铸型、墨汁灌注切片显示了血管表面压迹。病变随用药时间的延长而加重 ,窦状隙血管逐渐失去其结构特征。图像分析示股骨头内血管面积进行性下降 ,8周约为对照组的1/ 4。停药 6周负重区髓腔内仍存在明显脂肪化 ,血管纤细、稀少。实验 4周 ,股骨头内出现典型骨坏死灶。随时间的延长 ,坏死灶增大、股骨头坏死程度加重。　结论　髓腔内脂肪填塞是导致糖皮质激素诱导性股骨头坏死中缺血损害的重要病理因素之一 ,尤其在股骨头坏死的早期起着非常重要的作用     

Glucocorticoids exacerbate insult-induced declines in metabolism in selectively vulnerable hippocampal cell fields

Glucocorticoids (GCs), the adrenal steroids released during stress, can compromise the ability of hippocampal neurons to survive necrotic neurological insults. This GC-induced endangerment has energetic facets, in that it can be attenuated with energy supplementation. In the present report, we studied the effects of GCs on the metabolic response of specific hippocampal cell fields to necrotic insults. We used silicon microphysiometry, which allows indirect measurement of metabolism in real time in tissue explants. Aglycemia caused a significant decline in metabolism in dentate gyrus explants, but not in CA1 or CA3 explants. When coupled with our prior report of cyanide disrupting metabolism only in CA1 explants, and the glutamatergic excitotoxin kainic acid disrupting metabolism only in CA3 explants, this demonstrates that microphysiometry can detect the selective regional vulnerability that characterizes the hippocampal response to these necrotic insults. We then examined the effects of GCs on the response to these insults, monitoring explants taken from rats that were adrenalectomized, intact, or treated with corticosterone (the GC of rats) that produced circulating levels equivalent to those of major stressors. Increased exposure to GCs worsened the decline in metabolism in dentate gyrus explants induced by hypoglycemia, and in CA1 explants induced by cyanide (after eliminating the effects of glial release of lactate for the support of neuronal metabolism). Thus, GCs worsen the metabolic consequences of necrotic insults in hippocampal explants.     

气道局部治疗对气道黏液高分泌干预作用的对比研究

目的探讨常用局部治疗性药物对慢性气道黏液高分泌作用的机制和特点。方法用超声雾化吸入中性粒细胞弹性蛋白酶(NE)复制慢性支气管炎动物模型,分别吸入糖皮质激素布地奈德(budesonide)、胆碱M受体阻断剂异丙托溴铵以及两者配伍联用进行干预,用酶联免疫吸附试验(ELISA)及斑点印迹法分别检测大鼠支气管肺泡灌洗液(BALF)中黏蛋白(MUC)的含量和MUC5ACmRNA表达水平。结果NE能显著增加气道MUC和MUC5ACmRNA的表达(P<0.01);普米克令舒和异丙托溴铵均可降低MUC和MUC5ACmRNA的表达(P<0.05),两者联用可增强抑制黏蛋白的效应(P<0.01)。结论NE是慢性气道黏液高分泌发生的重要因素;布地奈德和异丙托溴铵可抑制MUC基因及转录水平的表达,且两者联用有协同效应。     

自噬对糖皮质激素作用下MC3T3-E1成骨细胞增殖的影响

背景:目前,糖皮质激素(GCs)作用下成骨细胞自噬与其增殖能力的关系尚存争议.目的:探讨自噬对GCs作用下MC3T3-E1成骨细胞增殖能力的影响.方法:不同浓度(0、10-8 M、10-6 M、10-4 M)的地塞米松(DXMS)分别作用于MC3T3-E1成骨细胞,CCK-8检测不同时间(12 h、24 h、48 h)...     

HSP90和P23蛋白量和细胞亚定位在多发性骨髓瘤患者中的临床价值

目的：寻找预测MM患者GC敏感性指标。方法以MM患者作为研究对象,采用ELISA法检测MM患者血清HSP90浓度,Western Blot检测MM患者PBMNC中P23蛋白表达,探讨其与GC抵抗的关系。结果（1）MM患者血清HSP90含量明显比正常人高（P＜0.05）,且GC敏感组患者较GC抵抗组患者高（P＜0.05）,但各组P23血清浓度之间差异无统计学意义（P＞0.05）;（2）P23蛋白低表达患者和P23蛋白高表达患者治疗有效率分别为86%和33%,二者相比差异具有统计学意义（P＜0.05）,在5年随访中,前者生存率高于后者（P＜0.05）;（3）HSP90和P23蛋白在MM1.S、MM1.R细胞株以及GC敏感和抵抗的MM患者均位于胞浆内,无定位意义。结论血清HSP90和P23蛋白表达能预测MM患者对GC的敏感性和生存情况,可用此指标指导临床用药。