芪月降脂片中黄芪甲苷的含量测定

[目的 ]研究芪月降脂片中黄芪甲苷的含量测定方法 .[方法 ]用甲醇提取、水饱和正丁醇萃取、大孔吸附树脂处理供试品后 ,以双波长薄层扫描法测定黄芪甲苷的含量 .[结果 ]黄芪甲苷的平均回收率为 10 4 18% ,RSD为 3 2 5% .[结论 ]双波长薄层扫描法较为简便、经济且重现性较好 ,可用于制剂中黄芪甲苷的质量控制     

复方决明子口服液的制备工艺研究

目的 :用正交法优选复方决明子口服液的最佳工艺条件。方法 :以决明子中蒽醌的含量及浸出物的含量为指标 ,应用L9(3′)正交试验法优选复方决明子口服液的最佳工艺条件。结果 :最佳提取条件为 :加 1 0倍量水 ,煎煮 3次 ,每次 1 .5h。结论 :优越工艺验证表明 ,最佳提取工艺为A1 B2 C1 。说明优选工艺稳定可靠。     

高危出血患者应用吉派林抗凝血液透析疗效观察

目的：观察危重型肾功能衰竭合并高危出血患者选择抗凝药物进行血液透析治疗的效果。方法：应用吉派林(低分子肝素钠)作为抗凝剂进行血液透析。结果：129例病人进行血液透析386次，均没有出血发生。结论：吉派林在高危出血患者血液透析中使用方便，安全，效果良好。     

头孢哌酮钠在醋酸钠平衡液中的稳定性

考察了头孢哌酮钠在醋酸钠平衡液中的稳定性。二药配伍后，置室温（２５℃）及３７℃水浴中，６ｈ内溶液无颜色改变，亦无沉淀、气体产生，头孢哌酮钠均在初始浓度的９５％以上。     

丙戊酸钠与尼莫地平治疗偏头痛的疗效比较

目的：观察丙戊酸钠与尼莫地平治疗偏头痛的疗效有否差别。方法：偏头痛１２９例，随机分为丙戊酸钠治疗组６６例（男性１７例，女性４９例；年龄２５±ｓ７ａ），丙戊酸钠开始剂量为０．２ｇ，ｐｏ，ｔｉｄ，以后根据发作频率及程度逐渐增量，最大量１．４ｇ／ｄ，共用３ｍｏ；尼莫地平对照组６３例（男性１８例，女性４５例，年龄２７±６ａ），尼莫地平３０ｍｇ，ｐｏ，ｔｉｄ，共用３ｍｏ。结果：丙戊酸钠组总有效率为８３％。尼莫地平组为８５％，２组无明显差异（Ｐ＞０．０５）．未见严重不良反应。结论：丙戊酸钠与尼莫地平治疗偏头痛安全有效、疗效相似。     

Interaction of Nucleoside Analogues with the Sodium–Nucleoside Transport System in Brush Border Membrane Vesicles from Human Kidney

The therapeutic efficacy of nucleosides and nucleoside analogues as antitumor, antiviral, antiparasitic, and antiarrhythmic agents has been well documented. Pharmacokinetic studies suggest that many of these compounds are actively transported in the kidney. The goal of this study was to determine if therapeutically relevant nucleosides or analogues interact with the recently characterized Na⁺-driven nucleoside transport system of the brush border membrane of the human kidney. Brush border membrane vesicles (BBMV) were prepared from human kidney by divalent cation precipitation and differential centrifugation. The initial Na⁺-driven ³H-uridine uptake into vesicles was determined by rapid filtration. The effect of several naturally occurring nucleosides (cytidine, thymidine, adenosine), a pyrimidine base (uracil), a nucleotide (UMP), and several synthetic nucleoside analogues [zidovudine (AZT), cytarabine (Ara-C), and dideoxycytidine (ddC)] on Na⁺–uridine transport was determined. At a concentration of 100 µM the naturally occurring nucleosides, uracil, and UMP significantly inhibited Na+-uridine transport, whereas the three synthetic nucleoside analogues did not. Adenosine competitively inhibited Na+-uridine uptake with a K _i of 26.4 µM (determined by constructing a Dixon plot). These data suggest that naturally occurring nucleosides are substrates of the Na⁺–nucleoside transport system in the renal brush border membrane, whereas synthetic nucleoside analogues with modifications on the ribose ring are not. The K _i of adenosine is higher than clinically observed concentrations and suggests that the system may play a physiologic role in the disposition of this nucleoside.     

The effect of high sodium intake on bone mineral content in rats fed a normal calcium or a low calcium diet

The effect of high sodium intake on bone mineral content of rats fed a normal (0.6% Ca) or a low (0.02% Ca) calcium diet was studied. Rats on a normal calcium diet given 1.8% sodium chloride to drink showed persistent and significant hypercalciuria and subnormal bone mineral content. Total calcium content of femur was significantly lower after 4 months (p<0.02) and 12 months (p<0.001). In rats maintained on a low calcium diet (0.02% Ca), a high sodium diet for 8 weeks caused a significant loss of calcium in bone similar to that seen in animals fed a normal calcium diet for 4 months. We conclude that high sodium intake reduces bone mineral content, especially if the diet is low in calcium.     

Effects of acetylsalicylic acid on electromechanical activity ofin vivo rabbit ileum

Aspirin has antisecretory and ulcerogenic properties in the gastrointestinal tract. The aim of this study was to determine the effects of acetylsalicylic acid (ASA) on the electrical and mechanical activity of the ileum in anesthetized New Zealand White rabbits. Ileal electromechanical activity was recorded from serosal electrodes and a miniature intraluminal balloon. Thirty minutes after injection of ASA (30, 60 and 100 mg/kg intravenous) significant and dose-dependent increases in the percentage of slow waves with action potentials were observed when compared with saline-injected animals. The onset of action potentials correlated with phasic increases in intraluminal pressure, indicating the onset of circular muscle contractions. Injection of 15 mg/kg ASA, sodium salicylate (100 mg/kg intravenous) or saline had no effect on baseline action potential activity. Prostaglandin E ₂ (PGE ₂)(5 and 10 g/kg intravenous) significantly increased slow-wave frequency and decreased ASA-induced action potential activity. This study demonstrates that (1) ASA, but not sodium salicylate, stimulates phasic ileal action potential and contractile activity and (2) in ASA-treated animals, PGE ₂ produces differential effects on in vivoslow-wave frequency and action potential activity.     

Differing time courses between Δlactate and mitochondrial respiration during coronary occlusion and after reperfusion in canine hearts

Summary The present study was designed to clarify whether or not a difference between arterial and venous lactate (lactate) levels is useful for evaluation of mitochondrial function in ischemia-reperfused myocardium. In the first experiment, 12 dogs were divided into 2 groups: 10-min occlusion of the left anterior descending coronary artery (LAD) followed by 10-min reperfusion, or 30-min occlusion followed by 40-min reperfusion, were performed. The lactate levels in the femoral artery and the great cardiac vein were measured enzymatically. Lactate was reversed immediately after occlusion. Ten min and 20 min were required for the recovery of lactate in the 10-min-occlusion with 10-min-reperfusion, and 30-min-occlusion with 40-min-reperfusion groups, respectively. In the second experiment, 36 dogs were divided into 6 groups: 10-min occlusion of LAD; 10-min occlusion with 10-min reperfusion; 30-min occlusion; and 30-min occlusion with 10-, 20-, or 40-min reperfusion were performed. Mitochondria from normal and occluded or reperfused areas were prepared, and the respiratory function of the mitochondria was measured polarographically. No significant decreases in the mitochondrial function were observed in the 10-min-occlusion, and 10-min-occlusion with 10-min-reperfusion groups. On the other hand, respiratory function of mitochondria was impaired by 30-min occlusion and was not improved by 10- or 20-min reperfusion. Significant recovery in the mitochondrial function was observed after 40-min reperfusion. That is, differing recovery time courses between lactate and the mitochondrial function were observed.     

Antiserotonergic inhibition of calcitonin-induced increase of β-endorphin,ACTH, and cortisol secretion

Summary In a previous study we observed that calcitonin increases -endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor).Fourteen healthy subjects, aged 30–60 years were investigated. All the subjects received 100IU Salmon calcitonin Sandoz i.v. at 8a.m. (time 0). Plasma -endorphin, ACTH and cortisol were estimated every 30min from – 30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at – 30 min and calcitonin i.v. at time 0. -endorphin, ACTH and cortisol levels (Mean ±SEM) rose significantly after calcitonin (peak value at 30–90 min) from 5.2 ±0.7 to 15.1±2.6 pmol/l; from 43.0±2.7 to 70.7±4.1 pg/ml and from 10.6±1.5 to 19.6 ±2.1 g/100 ml respectively (p< 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time – 30 did not alter the response of -endorphin, ACTH and cortisol to calcitonin (infused at time 0).Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin.We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.