金钱草颗粒剂质量标准的研究

目的 探讨金钱草颗粒剂的质量标准。方法 采用TLC对金钱草颗粒剂处方中的柴胡、延胡索及大黄进行定性鉴别;采用HPLC对其主药金钱草中的槲皮素进行定量分析。结果 该方法定性鉴别薄层色谱特征明显,专属性强;样品中槲皮素在1.896 0~30.336 0 μg·mL_^-1内线性关系良好(r=0.999 8),平均回收率为97.73%,RSD=1.34%。结论 用该方法作定性、定量分析简便、快速、专属性强,可有效控制制剂的质量。     

排石汤质量标准研究

目的:建立排石汤的质量标准。方法:采用薄层色谱(TLC)法对方中金钱草、石苇、甘草进行定性鉴别;采用高效液相色谱(HPLC)法对槲皮素和山柰素进行定量测定。结果:TLC特征斑点明显、专属性强。槲皮素、山柰素的检测浓度分别在3.888～38.88μg.mL-1(r=0.9997)、7.104～56.832μg.mL-1(r=0.9998)范围内与各自峰面积积分值呈良好线性关系;二者平均回收率分别为99.62%、99.78%,RSD分别为1.25%、1.72%(n=6)。结论:所建标准可用于排石汤的质量控制。     

金胆胶囊质量标准的研究

目的建立金胆胶囊质量标准。方法采用TLC法对处方中金钱草、虎杖、龙胆、猪胆膏进行定性鉴别,并用HPLC法对制剂中山柰素、槲皮素进行含量测定。结果薄层色谱特征明显,阴性无干扰。山柰素在0.018μg~0.539μg,槲皮素在0.00538μg~0.1614μg范围内呈良好的线性关系(r=0.9999),平均加样回收率分别为101.1%、91.3%,RSD分别为1.4%、1.9%(n=5)。结论本方法具有简便易行、重现性好,结果可靠、专属性强等特点,可用于该制剂的质量控制。     

鸡骨草肝炎颗粒的薄层鉴别和绿原酸、槲皮素的测定

目的 建立鸡骨草肝炎颗粒的定性、定量方法.方法 采用薄层色谱法定性鉴别处方中的鸡骨草,采用HPLC法测定制剂中的绿原酸和槲皮素.结果 鸡骨草薄层鉴别方法分离度好、专属性强、简单可行;绿原酸和槲皮素的线性范围分别为0.0046～0.0276 μg·μl-1(r=0.9999)、0.0015～0.0084 μg·μl-1(r=0.9991),平均加样回收率分别为98.02%、97.91%,RSD=1.8%、1.1%.结论 所建方法可控制鸡骨草肝炎颗粒的质量.     

肾石颗粒中金钱草及鸡内金的薄层色谱法定性鉴别

目的定性鉴别肾石颗粒中两主药金钱草、鸡内金。方法采用薄层色谱法对制剂中的金钱草、鸡内金进行定性鉴别。结果薄层色谱中样品斑点显色清晰,分离度好。结论本方法灵敏、准确,专属性强,重现性好,可作为该制剂的质量控制方法。     

金胆片质量标准的研究

目的:提高完善金胆片的质量标准。方法:采用薄层色谱法对方中的金钱草进行了定性鉴别,并采用高效液相色谱法对龙胆中的龙胆苦苷进行了含量测定。结果:定性定量方法简便,准确,专属性强,重现性好。结论:提高后的质量标准可更有效的控制该产品的质量。     

双黄解毒乳膏质量标准研究

目的:建立双黄解毒乳膏的质量标准。方法:采用薄层色谱法对制剂中的黄芩和关黄柏进行定性鉴别;采用高效液相色谱法对制剂中的黄芩苷含量进行定量分析。结果:定性鉴别方法能同时鉴别黄芩、关黄柏,专属性强,分离度好。黄芩苷进样浓度在80.0～400.0μg·mL-1范围内与峰面积积分值呈良好线性关系(r=0.9998);平均回收率为97.3%,RSD=1.3%(n=9)。结论:所建标准可用于双黄解毒乳膏的质量控制。     

肾石通颗粒质量标准研究

目的制定肾石通颗粒质量控制方法。方法采用TLC法对方中的扁艹蓄、牛膝进行定性鉴别;采用比色法对方中金钱草的总黄酮进行含量测定。结果本品定性鉴别薄层色谱特征明显,专属性强;总黄酮在0.008~0.048g·L-1,范围内具有良好的线性关系(r=0.9996),平均回收率为101.31%。结论该方法可以准确地进行定性、定量检测,有效地控制肾石通颗粒的质量。     

糖足颗粒质量标准研究

目的建立糖足颗粒的质量标准。方法采用薄层色谱法对糖足颗粒中的黄芪、防己、当归3味主要中药进行定性鉴别,以高效液相色谱法对其主药赤芍中的芍药苷进行含量测定。结果定性鉴别分离度好,专属性强;芍药苷在0.504～5.040μg内线性关系良好,r=0.9998（n=6）,平均回收率为97.74%,RSD为0.72%（n=6）。结论本法可靠,准确,专属性强,可有效控制糖足颗粒的质量。     

艾可合剂质量标准研究

目的建立艾可合剂的质量标准。方法采用TLC法定性鉴别艾可合剂中白芍、赤芍及枳壳;采用HPLC法,以乙腈-水为流动相梯度洗脱,对艾可合剂中柴胡皂苷a进行定量分析。结果定性鉴别分离度好,专属性强;柴胡皂苷a在0.513～3.078μg范围内线性关系良好（r=0.9999）,平均回收率为99.5%（RSD=0.95%）。结论所建立的方法准确可靠、重复性好,可有效控制艾可合剂的质量。     

男性不育症患者精浆酸性磷酸酶对精浆生化指标的影响

目的研究男性不育症患者精浆酸性磷酸酶对精浆生化指标的影响。方法以539例男性不育症患者为研究对象,根据精浆酸性磷酸酶水平分为观察组和对照组,精浆酸性磷酸酶〉48．8U／mL为正常组,〈48．8U／mL为对照组,对两组患者精浆生化指标进行比较分析,通过相关性分析比较539例患者精浆酸性磷酸酶与精浆生化指标的相关性。结果观察组精浆锌明显低于对照组,精浆弹性蛋白酶明显高于对照组,曲组相比差异有统计学意义（P〈0．05）,精浆酸性磷酸酶与精浆锌的相关系数为0．612,呈明显正相关（P〈0．05）,与精浆弹性蛋白酶的相关系数为-0．325,呈明显负相关,而与精浆α-糖甘酶及果糖无相关性（P〉0．05）．结论联合检测精浆酸性磷酸酶、锌及弹性蛋白酶对于前列腺相关炎性疾病的诊断及治疗疗效的判定有重要的临床应用价值。     

Differences in the binding of drugs to plasma proteins from newborn and adult man. I

Summary The binding of various drugs to plasma proteins from adult and cord plasma was determined by equilibrium dialysis. For almost all the drugs binding to cord plasma was lower than to plasma from adults. No evidence was found that the difference in binding was due to the different protein concentration in cord and adult plasma or to an influence of substances in ultrafiltrates of the plasmas.     

Increases in plasma kallikrein-like and pancreas kallikrein-like substances after administration of pancreas or plasma kallikrein

Differences between the concentration of a kallikrein-like substance in blood obtained by the peptide-MCA method and that obtained by the TAME (N-tosyl-l-arginine methyl ester) method by administering pancreas kallikrein to rabbits have been recognized already and the existence of a Substance X was evaluated. In the present study, it was revealed that administration of pancreas kallikrein resulted in inactivation of kallikrein in the substrate in gut homogenates and homogenates of various organs except for the pancreas. In the pancreas homogenate, inactivation was not observed. On the other hand, there was a possibility that at least part of Substance X existed due to plasma kallikrein. Thus, the concentration of plasma kallikrein in plasma after administration of pancreas kallikrein was determined. A pattern similar to the concentration curve of Substance X was obtained. Thus, it was clarified that plasma kallikrein-like substance, at least, increased when pancreas kallikrein was administered. On the contrary, when plasma kallikrein was administered to the rabbit duodenum, the concentration of pancreas kallikrein-like substance in plasma increased. It was also clarified that plasma kallikrein-like substance increased in vitro by adding pancreas kallikrein to the blood or plasma, whereas the in vitro addition of plasma kallikrein to the blood induced its decomposition and a slight increase in pancreas kallikrein-like substance, and the addition of plasma kallikrein to the plasma induced an increase in plasma kallikrein and a slight increase in pancreas kallikrein-like substance.     

Mesalazine release from a pH dependent formulation: effects of omeprazole and lactulose co-administration

Aims The plasma binding of the cyclosporin D analogue SDZ PSC 833 was investigated in vitro .
Methods The plasma total binding constant (corresponding to the bound-to-free concentration or binding ratio) was determined at 37°  C by the erythrocyte partitioning technique on plasma samples from three healthy volunteers and three cancer patients. Lipoproteins were also removed from plasma samples from three healthy volunteers by a standard ultracentrifugal technique.
Results SDZ PSC 833 plasma binding was 97.8±1.1% and 97.3±0.2% in samples from three healthy volunteers and three cancer patients respectively. More than 95% of blood SDZ PSC 833 was distributed in plasma. When the original plasma samples of three individuals were delipidated, SDZ PSC 833 binding was strongly decreased (58% bound to plasma proteins) and when lipoproteins were resuspended in the delipidated plasma samples to produce varying lipoprotein plasma concentrations, the binding increased continuously with the fraction of added lipoproteins. When lipoproteins were resuspended to restore the original lipoprotein plasma content, the % plasma-bound SDZ PSC 833 increased to 98.2%, close to the value observed with the original plasma (98.7%).
Conclusions These results clearly indicate that SDZ PSC 833 plasma binding is mainly determined by lipoproteins and that in blood, most of SDZ PSC 833 is distributed in plasma.     

Factors affecting the free plasma fraction of phenytoin in patients with epilepsy

The variability and possible factors modifying the free plasma fraction of phenytoin were investigated in 134 patients with epilepsy undergoing long-term treatment. The total and free plasma concentrations of phenytoin were determined using fluorescent polarisation immunoassay. Concentrations of albumin, bilirubin and creatinine were also obtained. The free plasma concentration was separated by ultrafiltration, at 25 degrees C, using Centrifree((R)) filters. Factors related to the free plasma fraction of phenytoin (free plasma concentration/total plasma concentration) were gender, age, dose, therapeutic regimen, total plasma concentration and the biochemical parameters mentioned. The mean of free plasma fraction was 9.1% with a very high variability (between 3.3 and 37%). No significant relationship was found between the free plasma fraction and dose, age, gender, total plasma concentration or the biochemical data. The only variable with a significant effect (p < 0.05) on the free plasma fraction was polytherapy with valproic acid. The variability in the free plasma fraction of phenytoin was high in epileptic patients, and was poorly related to the clinical or analytical variables studied. In the absence of pathologies that modify phenytoin binding (uraemia, hypoalbuminaemia), the only factor predictive of a possible alteration in the binding of phenytoin to plasma proteins was polytherapy with valproic acid.     

In vivo effects of camostat mesilate on plasma kallikrein, plasma kininase II and renal kallikrein of man

N,N-Dimethylcarbamoylmethyl-4-(4-guanidino-benzoyloxy)phenylacetat e methanesulfonate (camostat mesilate) is reported to be an effective inhibitor of plasma kallikrein. It was shown in vitro to inhibit not only plasma kallikrein, but also renal kallikrein and plasma kininase II. These inhibitory activities, however, were very weak. The inhibition of plasma kallikrein in human plasma was limited in time, since a rapid reactivation of plasma kallikrein was noticed when samples were incubated at room temperature. In order to establish whether camostat mesilate was able to inhibit plasma kallikrein, kininase II and renal kallikrein also in vivo the inhibitory activity of camostat mesilate on these enzymes was studied in 5 healthy volunteers. After an oral intake of a single dose of 600 mg of camostat mesilate, plasma kallikrein was inhibited significantly, while kininase II in plasma was unaffected. Renal kallikrein activity determined by urinary excretion of active kallikrein remained unchanged after camostat mesilate intake. Thus, the results demonstrate that camostat mesilate in vivo inhibits only plasma kallikrein and has no effect on the activity of kininase II or renal kallikrein.     

Pharmacological evidence that the sympathetic nervous system mediates the increase in renin secretion prodsuced by immobilization and head-up tilt in rats

To determine the mechanism by which immobilization and head-up tilt under inactin anesthesia increase plasma renin activity (PRA), the effect of these stimuli on plasma levels of vasoactive intestinal polypeptide (VIP) were measured and the effect of the β-adrenergic blocking drug, propanolol on the response of plasma renin activity determined. Increases in circulating VIP are known to stimulate secretion of renin. After 10 min of immobilization, plasma renin activity was increased and VIP in plasma was unchanged. After 30 min of tilting, plasma renin activity was also increased and VIP in plasma was unchanged. The increases in plasma renin activity were blocked by propranolol. Inactin anesthesia by itself increased plasma renin activity and this response was unaffected by propranolol and associated with a small decrease, rather than an increase in VIP in plasma. The results indicate that the responses of plasma renin activity to immobilization and head-up tilt are due to increased secretion of renin mediated by the sympathetic nervous system. On the other hand, the increase in secretion of renin produced by inactin anesthesia does not appear to be mediated by the sympathetic nervous system. There was no evidence that VIP was responsible for any of the increases.     

血浆中细菌内毒素定量测定方法的研究

目的:建立定量测定血浆中细菌内毒素的实验方法。方法:以内毒素检查用水制备标准曲线,动态浊度法定量测定分别采用3种抗凝剂的抗凝血中细菌内毒素的含量及回收率;以正常人血浆制备内毒素标准曲线,以抗增液复溶鲎试剂,动态浊度法定量测定人血浆中内毒素的含量及回收率。结果:使用肝素钠抗凝的血浆溶液对内毒素测定无干扰,而其他抗凝剂肝素锂、EDTA-K2等有干扰;人血浆经稀释加热处理,配合使用抗增液后制备的标准曲线与使用内毒素用水制备的标准曲线相比,可以更好地测定人血浆中细菌内毒素的含量,且具有较好的重现性;用所建立的方法测定肠癌患者血浆中内毒素的含量,其结果显著高于正常人血浆中内毒素的含量。结论:以肝素钠作抗凝剂,血浆经稀释加热处理并配合使用抗增液可定量测定血浆中细菌内毒素的含量。     

ACTIVATION BY PUFF ADDER VENOM OF INACTIVE RENIN IN NORMAL AND HYPERTENSIVE RAT PLASMA

Inactive renin has been studied extensively in human plasma, but in animal plasma its accurate quantification has proved more difficult, due partly to higher activity of plasma protease inhibitors. Such activity in human plasma can be conveniently destroyed by a metalloprotease in Bitis arietans venom, with concommitant release of endogenous enzyme activities, such as plasma kallikrein, that then activate inactive renin. It was therefore of interest to look for inactive renin in rat and rabbit plasma using this approach, so providing, in addition, a comparison for the disparate data of other groups who have used trypsin or acid for activation. In both rat and rabbit plasma the proportion of inactive renin was 62% of total renin, whereas human plasma contained more inactive renin and a higher proportion, 82%. A higher concentration of venom was required for rat (33 ug venom/ml plasma) and rabbit (4 micrograms/ml) than needed for activation, at a similar rate, in human plasma (1 microgram/ml). When applied to studies of rats made hypertensive and hyper-reninaemic by aortic ligation for 5 days, higher total (active + inactive) renin was observed. The proportion of inactive renin, as a percentage of total renin in plasma collected at this time, was, however, found to diminish significantly. In conclusion, puff adder venom activates inactive renin in rat and rabbit plasma and can be used to study physiological changes in inactive renin in such animal plasma.     

SALIVARY CONCENTRATIONS OF ATRAZINE REFLECT FREE ATRAZINE PLASMA LEVELS IN RATS

The protein binding of atrazine in plasma and its effect on salivary excretion of atrazine was determined in male Sprague-Dawley rats. The degree of protein binding of atrazine was determined at 3 steady-state plasma concentrations, 50, 150, and 250 mug/L, using an ultrafiltration technique. In total, 48 arterial blood samples were collected from 18 rats; 38 of 48 blood samples had their time-matched whole saliva samples. The average protein binding of atrazine ranged from 18% to 37% ; however, it was not significantly different across the 3 steady-state plasma concentrations nor among the individual rats. Overall, 26% of atrazine was bound to plasma proteins and not available for transport from blood into saliva. Protein binding of atrazine in plasma was not correlated with total atrazine plasma concentration nor with free atrazine plasma concentration, which indicates that the protein-bound fraction of atrazine is independent of plasma concentration within the range measured in this study (30-400 mug/ L). The average saliva/ plasma (S/P) concentration ratio of atrazine increased from 0.7 using total atrazine plasma concentration to 0.94 (S/fP) when free atrazine plasma concentrations calculated as 26% of protein binding was used. Salivary concentration was highly correlated with free atrazine plasma concentration. The results suggest that salivary concentration of atrazine not only reflects its total plasma level but accurately measures the portion of atrazine (free atrazine) in plasma, which may be of toxicological significance.