庆大霉素引起急性肾毒性临床分析

目的强调重视庆大霉素肾毒性问题。方法回顾分析庆大霉素引起急性肾功能衰竭（ARF）12例患者资料。结果10例治愈,2例好转。结论医务人员应严格掌握庆大霉素临床特点、用药适应证及合理用药,强调用药期应进行肾功能监测,早期、及时血液透析是提高ARF治愈率的关键。     

庆大霉素致急性肾衰1例报告

病例报告患者,男性,24岁,农民,住院号8920。因咽痛、寒战、高热2天,伴恶心、呕吐、腰腹剧痛、小便困难10小时,于1992年2月16日入院。患者入院前10小时在乡卫生所静滴10%萄葡糖盐水500ml     

人参总皂甙对缺血性急性肾功能衰竭大鼠肾脏的保护作用

目的 探讨人参总皂甙对缺血性急性肾功能衰竭肾脏的保护作用.方法 采用钳夹右肾蒂1 h再灌注并切除左肾法制备缺血性急性肾功能衰竭大鼠模型,观察再灌注24h后血清BUN、Scr含量,ET-1、NO水平和肾组织病理改变.结果 治疗组大鼠血清BUN、Scr含量与I/R组比较明显下降并有显著差异(P＜0.05),与对照组无差异(P＞0.05);治疗组血清NO水平与I/R组比较明显提高亦有显著差异(P＜0.05);肾组织病理示:治疗组肾小管病变明显轻于I/R组(P＜0.01).结论 人参总皂甙对缺血性肾功能衰竭肾脏有明显保护作用,其对NO水平的调节可能是这一保护作用的机理之一.     

外敷庆大霉素致急性肾功能衰竭1例

1 临床资料 患儿,男,1岁7个月,因烫伤8 d,浮肿少尿3 d入院。入院前8 d,患儿不慎被开水烫伤颈、胸、腹部后出现皮肤潮红,继而出现水泡、脱皮。急到某县医院治疗(具体不详),病情好转,3 d后出院。患儿一般情况好,精神食欲好,无呕吐、腹泻,小便量多。出院回家后     

尿磷酸二酯酶Ⅰ预示庆大霉素肾脏损害的研究

本文采用大鼠庆大霉素中毒模型检测尿磷酸二酯酶Ⅰ（ＰＤＥＩ），Ｎ－乙酰－β－氨基葡萄糖苷酶（ＮＡＧ），碱性磷酸酶（ＡＬＰ），β２－微球蛋白（β２－ＭＧ）的变化及大鼠肾脏组织病理学改变。结果表明，治疗剂量庆大霉素对肾脏具有损伤作用，中毒剂量损伤明显加重。尿ＰＤＥＩ变化趋势显示变动辐度大，持续时间长的特性     

鱼胆中毒误用庆大霉素的教训

目的分析鱼胆中毒误用庆大霉素的教训,以避免误诊误治加重肾脏损害.方法回顾性对比分析35例鱼胆中毒的治愈率及肾功能损害情况.结果35例鱼胆中毒未用庆大霉素22例患者全部治愈,13例误用庆大霉素的患者中2例死于急性肾功能衰竭,1例转为慢性肾功能衰竭.未用与使用庆大霉素患者的治愈率比较,经卡方法计算确切概率,P＜0.05.肾功能损害程度,血液透析次数,用庆大霉素组明显高于未用庆大霉素组,P＜0.01.结论鱼胆中毒后再误用庆大霉素更加重急性肾功能衰竭的恶化.     

庆大霉素致急性肾功能衰竭临床分析

庆大霉素因抗菌谱广，疗效可靠，价格低廉在临床上广泛使用，但其导致急性肾功能衰竭国内外有不少报道。本文分析12例庆大霉素致急性肾功能衰竭的病历，讨论防治方法，以引起对庆大霉素肾损害的重视。     

川芎嗪防治庆大霉素致急性肾功能衰竭的药理机制研究

腹膜内注射庆大霉素，建立大鼠急性肾功能衰竭的动物模型，观察川芎嗪对急性肾衰的防治效果，并初步探讨了其作用机制。结果表明：川芎嗪可改善实验动物的肾功能，降低肾小管损害，促进肾髓质ＰＧＥ２分泌，升高ＰＧＩ２／ＴＸＡ２比值，减少该模型肾皮质丙二醛含量。提示川芎嗪可能通过影响肾髓质前列腺素分泌而对急性肾衰产生防治作用，还可能与减少肾皮质氧自由基的产生有关。     

静注庆大霉素致急性肾衰1例

患者 ,男 ,4 1岁 ,体重 82kg ,教师。 2 0 0 3年 4月 30日上午 ,以“急性化脓性阑尾炎”收住我院普外科。入院体检 :T38.1℃ ,R 2 0次 /min ,BP 10 0 / 80mmHg ,心肺功能未见异常。肝、肾功能 :ALT 30 .6IU·L-1,BUN 3.5mmol·L-1,Cr10 2 .4 μmol·L-1。 4月 30日下午 4点 30分 ,术前常规给予5 %葡萄糖注射液 5 0 0mL加庆大霉素 (批号 0 2 110 8) 16万uivdqd ;5 %葡萄糖氯化钠注射液 10 0mL加阿莫西林 2 .0givd ,bid ;0 .5 %甲硝唑注射液 10 0mLivdbid抗感染治疗。术后 ,5月 1日早晨 2点 ,患者自述排尿困难 ,晚上插导尿管引流尿液 …     

抗结核药物致大鼠肾脏损害电镜研究

目的观察透射电镜下不同抗结核药物对SD大鼠肾脏超微结构的改变。方法健康成年SD大鼠(清洁级)152只,体重250～300g,雌雄各半,随机分为8组。对照组:0.9%氯化钠溶液;H(INH)组:异烟肼;R(RFP)组:利福平;Z(PZA)组:吡嗪酰胺;HR组:异烟肼+利福平组;HZ组:异烟肼+吡嗪酰胺组;RZ组:利福平+吡嗪酰胺组;HRZ组:异烟肼+利福平+吡嗪酰胺组。大鼠用药的常规剂量:每公斤体重人的常用剂量乘以5.5倍。标本制备:根据各组的不同要求,每天对大鼠进行一次灌胃,10d后断头取血,分离肾脏,戊二醛固定后做电镜检查。结果肾小球细胞部分线粒体溶解、髓样变,粗面内质网脱颗粒,滑面内质网池扩张;肾近曲小管上皮细胞核固缩,细胞器减少。异烟肼、利福平、吡嗪酰胺均可引起大鼠肾脏的损害,多种药物联用比单药应用损害更明显(P<0.01)。结论电镜诊断对抗结核药物所致大鼠肾脏损害有重要价值。     

RENAL BLOOD FLOW IN OBSTRUCTIVE JAUNDICE: AN EXPERIMENTAL STUDY IN BABOONS

1. The distribution of intrarenal blood flow has been measured using the ¹³³Xe-washout technique in thirteen baboons 2 weeks after ligation of the common bile duct. 2. In comparison with eight sham-operated baboons, there was a significant decrease in the percentage distribution of blood flow to the cortex, although the rate of flow was unchanged. These changes were accompanied by a significantly increased flow rate and percentage distribution of flow through the juxtamedullary circulation. 3. In a further five baboons treated in the same way, various doses of noradrena-line were infused into the renal artery. In these animals there was an enhanced pressor response to noradrenaline, and this effect was completely abolished by an α-adrenoreceptor blocking agent (phenoxybenzamine). The β-adrenoceptor blocking drug (propranolol) had no such effect. 4. This enhanced response was not seen when noradrenaline was infused into three sham-operated baboons. 5. These observations suggest that the alterations in renal perfusion in obstructive jaundice may be due to an increased renovascular sensitivity to circulating catecholamines and an enhanced α-drenoceptor activity.     

激光心肌血管重建加心脏网膜固定术治疗缺血性心脏病的实验研究

２６条杂交犬分为３组：对照组（ｎ＝１０）、激光心肌血管重建术组（ｎ＝８）和激光心肌血管重建＋心脏网膜固定术组（ｎ＝８）。分别监测了ＥＫＧ（ＳＴ—Ｔ）、心输出量、放射性同位素８６Ｒｂ摄取分数和组织学检查等，结果显示激光打孔后ＳＴ—Ｔ改变恢复、心输出量增加、心肌血供增加，以激光心肌血管重建术＋心脏网膜固定术组最好。激光孔道以及新生的血管和形成的网膜－心肌侧支循环，都能为缺血心肌提供血液和改善心功能。     

RENAL UPTAKE AND NEPHROTOXICITY OF GENTAMICIN DURING URINARY ALKALINIZATION IN RATS*

1. Effect of urine pH on accumulation of gentamicin in the renal cortex of rats was studied following constant intravenous infusion, and single or repeated i.v. injections with gentamicin. 2. The cortical uptake of gentamicin was moderately inhibited by urinary alkalinization due to sodium bicarbonate treatment, but was unaffected by acidification with ammonium chloride. The altered urinary pH had no effect on urinary excretion of gentamicin. 3. An alkaline urine induced by acetazolamide injections failed to influence cortical accumulation of gentamicin. This effectmay be ascribed to ‘acidification’ of the proximal tubular fluid after carbonic anhydrase inhibition, even though the final urine was alkaline. 4. Nephrotoxicity resulting from chronic treatment of gentamicin was ameliorated by concomitant sodium bicarbonate administration. 5. In conclusion, the intratubular pH of the proximal tubule is a factor which influences the cortical uptake of gentamicin, probably by means of changing the cationic nature of the molecule and, therefore, reduced binding with the luminal membrane.     

八种海洋生药抗疲劳作用的初步研究

本文通过实验探讨了海洋生物药尖海龙、三斑海马、牡蛎、龟板、刺参、海星黄、螺旋藻、海带的抗疲劳作用。结果表明,这八种生药均能不同程度地延长小鼠负重游泳时间,有效降低游泳后血乳酸含量（P＜0．05或P＜0．01）,证明有推迟运动性疲劳出现和促进疲劳恢复的积极作用。比较实验结果表现,尖海龙抗疲劳作用效果最好。     

亚微米强酸树脂对庆大霉素的吸附特性研究

亚微米强酸树脂对硫酸庆大霉素吸附过程的研究结果表明,最佳ｐＨ为９,温度对吸附影响不大,吸附等温式为ｑ＝０．５７９×Ｃｅ／（０．６３＋Ｃｅ）,标准自由能ΔＦ°＝１１０６Ｊ。选择含６％ＮＨ３的氨水、在ｐＨ１１．０时的解吸效果最好,回收率为９９．５％。     

硝硫氰胺抗日本血吸虫病的研究

硝硫氰胺是抗血吸虫病的一种新药物。本文进一步研究该药物对实验性日本血吸虫病的预防和治疗的作用。实验动物在感染血吸虫尾蚴前后,即使口服500mg/kg/天×2或4天的硝硫氰胺,血吸虫组比对照组仅减少32.3～59%。药物对童虫几乎无作用,而对成虫则有明显的疗效。病鼠一次口服硝硫氰胺40mg/kg,停药后1～8天的肝移率达93.6～100%。各实验治疗组的减虫率为74～100%,但此疗效的高低与剂量和疗程有关。     

LONG-TERM INCREASES IN RENAL SYMPATHETIC NERVE ACTIVITY AND HYPERTENSION

1. Essential hypertensive patients have been characterized by increased sympathetic nerve activity, increased peripheral vascular tone, decreased plasma volume and normal cardiac output when compared with normotensive subjects. Bilateral renal denervation reduces the magnitude or delays the onset of the blood pressure response in numerous models of experimental hypertension regardless of the aetiology of the elevation in arterial pressure. 2. Using a servocontrolled intrarenal infusion system, we have elevated intrarenal noradrenaline concentration via intermittent renal artery infusion without decreasing renal blood flow as a method of simulating selective elevation of renal sympathetic outflow. 3. Chronic intrarenal adrenergic stimulation increased arterial pressure within 24 h and this hypertension persisted for 28 consecutive days. The elevated arterial pressure was not associated with sustained increases in plasma renin activity, aldosterone, circulating catecholamines, arginine vasopressin or significant renal vasoconstriction. Urinary sodium excretion was chronically elevated and the dogs remained in negative sodium balance for the duration of the intrarenal noradrenaline infusion. 4. After 2 weeks of elevated intrarenal neurotransmitter coupled with hypertension, renal vascular reactivity to further adrenergic stimulation was significantly increased because the hypertension was maintained during continual reductions in the daily dosage of neurotransmitter allowed to be infused by the servocontroller. After only 28 days of noradrenaline infusion, renal vascular hypertrophy developed in vessels from 150–300 μm. 5. We conclude that selective and intermittent increases in intrarenal adrenergic neurotransmitter are sufficient to elicit chronic hypertension in the absence of volume expansion. This intrarenal neuroadrenergic hypertension is closely associated with the haemodynamic parameters which characterize a major subset of human essential hypertensives.