Water imbibition in the rat prostate during castration-induced regression

The present study was conducted to examine changes in water concentration in the ventral prostate of adult rats at different intervals following castration. The prostatic dry weight was obtained by drying the fresh prostate at 70 degrees C for at least 110 hr and the prostatic water content was calculated from its wet and dry weight. Under normal conditions, the prostatic water concentration ranges from 81.9 to 82.7% in uncastrated rats. The prostatic water concentration started to increase at 8 hr postcastration (83.1%) but this increase was not statistically significant. By 16 hr postcastration, the prostatic water concentration (83.8%) became significantly higher than that of the uncastrated animals. In rats of day 1 to day 10 postcastration, the prostate contained significantly more water (84.4%-84.7%) than those in uncastrated animals. By day 21 postcastration, the prostatic water concentration (81.5%) was not significantly different from that of uncastrated rats. Unlike the prostate, the skeletal muscle did not significantly change the water concentration following castration. The 51Cr-EDTA space in the prostate was not significantly different in rats before and after castration. These results indicate that water imbibition in the rat prostate is associated with an active period of prostatic regression and that the change in the 51Cr-EDTA space during prostatic regression is not the major cause of water imbibition in the tissue. Therefore, the present findings suggest that castration-induced water imbibition in the rat prostate is caused by an increase in the intracellular water space.     

Regulation of fluid intake in dogs following water deprivation

Whereas water loss in land living animals occurs continuously, water intake takes place discontinuously. At the normal operating set point of plasma osmolality, urine is more concentrated than plasma due to secretion of vasopressin. Thus animals operate around a state of mild dehydration. As water loss occurs, the severity of dehydration and thirst increase in intensity and at some point water intake occurs. Sufficient water is consumed to return plasma osmolality to the normal operating set point. Food intake and water balance are interdependent as food provides the osmoles which determine obligatory renal solute excretion. When dry food with the same osmotic content was substituted for canned food (water content 74%), dogs increased water intake from 24.2 +/- 4.3 to 62.2 +/- 8.8 ml/kg. Urine output and urine osmolality were unchanged, as under conditions of normal hydration, near maximal urine concentration is achieved. Changing water intake is the only available variable to maintain water balance. During water deprivation, the major renal mechanism appears to be natriuresis. In rehydration, satiety mechanisms ensure appropriate water intake and renal sodium conservation restores sodium balance.     

ACUTE EFFECT OF ETHANOL ON RENAL ELECTROLYTE TRANSPORT IN THE RAT

1. Despite human and animal studies, the direct effect of ethanol on renal water and electrolyte transport is poorly understood. The acute effect of increasing plasma concentrations of ethanol was evaluated in a water diuretic anaesthetized rat model which inhibits endogenous arginine vaso-pressin (AVP) release. 2. Ethanol at a plasma concentration of 1.69 ±0.28 mmol/L produced an immediate increase in urine flow (174 ± 11 μL/min pre-ethanol and 189 ± 13 and then 206 ± 12 μL/min during the ethanol infusion; P<0.001) as well as an increase in fractional sodium excretion (0.17 ± 0.04 to 0.28 ± 0.05 and 0.27 ± 0.05%; P<0.001). There was also a brief phosphaturia. These increases in electrolyte excretion had returned to control values by 20 min despite a further increase in the plasma ethanol concentration. 3. The urinary excretion of potassium, calcium and magnesium was not altered nor was glomerular filtration rate or renal plasma flow. 4. Ethanol at a mean concentration of 1.60 mmol/L did not alter the action of a maximal concentration of AVP (75 ng/kg) on water or electrolyte transport. However, the antidiuretic effect of a submaximal concentration of AVP (7.5 ng/kg) was augmented by ethanol at concentrations of 1.63 and 0.98 mmol/L. 5. These studies suggest that the ethanol induced diuresis commonly ascribed to inhibition of AVP secretion may also be due to other intrarenal effects of ethanol, possibly acting within the proximal tubule. These results also confirm recent in vitro findings that while ethanol does not inhibit the action of a maximal concentration of AVP, it does modulate the effects of lower AVP concentrations.     

青中年人群微量白蛋白尿患病率与心血管疾病危险因素的关系

目的　探讨微量白蛋白尿患病率与心血管疾病危险因素的关系。方法　选择 775例 (男 32 6例 ,女 4 4 9例 )年龄 2 0～ 5 0岁的社区人群 ,测定其体重指数 (BMI)、血压、空腹血糖、血脂谱 ;收集晨尿检测尿白蛋白、尿肌酐浓度 ,并计算尿白蛋白 /尿肌酐的比率。根据有无高血糖、高血压或高三酰甘油 /低高密度脂蛋白胆固醇 (高TG/低HDL C)血症分为 4组 ,即正常组 (A组 )、1种代谢紊乱组 (B组 )、2种代谢紊乱组 (C组 )及代谢综合征组 (D组 ) ,评价微量白蛋白尿与代谢紊乱的关系。结果　①糖尿病患者微量白蛋白尿的患病率为 2 2 .2 % ,显著高于正常血糖者 (5 .2 % ,P =0 .0 0 2 ) ;高TG/低HDL C血症者微量白蛋白尿的患病率为 8.3% ,显著高于正常血脂者 (4.0 % ,P =0 .0 12 ) ;高血压患者与正常血压者的差异无显著性。②随代谢紊乱加重 ,尿白蛋白浓度显著升高 (协方差分析 ,P <0 .0 1) ,微量白蛋白尿患病率升高 (趋势分析 ,P =0 .0 0 3)。③ 4组间尿肌酐浓度、尿白蛋白 /尿肌酐的差异无显著性。结论　①糖尿病、高TG/低HDL血症人群的微量白蛋白尿的发病率显著升高。②随代谢紊乱加重 ,微量白蛋白尿患病率亦升高     

高效液相色谱法测定微量耳血中头孢他定的浓度

本文介绍采取微量耳血以高效液相色谱法测定头孢他定（Ｃｅｆｔａｚｉｄｉｍｅ）的血药浓度。血样经６％高氯酸沉淀蛋白，流动相为含２５％甲醇的０．０５ｍｏｌ／Ｌ醋酸铵溶液，以冰醋酸调节ｐＨ值至４～５，检测波长为２５４ｎｍ，内标物为头孢唑啉（Ｃｅｆａｚｏｌｉｎ）。经对家兔采取微量耳血测定其血药浓度，可知头孢他定为二室模型，Ｔ＿１／２α为０．１８±０．０５ｈ，Ｔ＿１／２β为１．７５±０．０７ｈ。并对３名住院病人静脉注射１ｇ头孢他定后定时分别取微量耳血进行分析，所得结果与文献基本一致。本文方法简便、快速，结果令人满意。     

2001～2003年上海地区淋病奈瑟菌对抗生素的敏感性测定及质粒分析

目的了解上海地区2001～2003年淋病奈瑟菌(NG)对抗生素的敏感性情况及变化趋势。方法采用琼脂稀释法测定青霉素、头孢曲松、大观霉素、环丙沙星、四环素对742株NG的最小抑菌浓度(MIC)。用纸片酸度法检测β内酰胺酶菌株。用碱裂解方法抽提质粒。结果742株NG检出产青霉素酶菌(PPNG)342株(46.09%);质粒介导高度耐四环素(TRNG)166株(22.37%);耐环丙沙星718株(96.77%);耐大观霉素1株;未发现对头孢曲松耐药菌株;超过20%的菌株同时对青霉素、四环素和环丙沙星耐药;对35株菌株作了质粒分型,含耐药质粒检出率97%,分别带有5.4和7.4kb耐药性质粒。结论淋球菌对青霉素、四环素和环丙沙星3种药物分别有较高比例的耐药率。上海地区治疗淋病应首选大观霉素和头孢曲松。     

氯胺酮对荷包牡丹碱诱导PC12细胞内Ca2+浓度波动方式的影响

目的研究氯胺酮对荷包牡丹碱诱导PCI2细胞内Ca^2＋浓度波动方式的影响。方法使用含25ng／LNGF的DMED培养基在多聚赖氨酸包被的培养皿中培养PCl2细胞；与终浓度10gmol／L的Ca^2＋指示剂Fluo-3 AM ester共孵育30min洗涤后，加入终浓度50gmol／L荷包牡丹碱；在激光共聚焦显微镜选定多个细胞分别测定荧光强度的变化；随后加入氯胺酮，记录细胞荧光强度的改变。在试验结束前依次加入Triton X-100和EGTA分别记录单个细胞最大荧光强度（Fmax）和最小荧光强度（Fmin），以计算细胞内Ca^2＋的相对强度。结果氯胺酮不改变荷包牡丹碱诱导PCl2细胞内Ca^2＋浓度波动的基线，但抑制细胞内Ca^2＋浓度升高的幅度（P〈0．05），缩短相邻波峰间的时间间隙（P〈0．05）。结论氯胺酮不仅改变荷包牡丹碱诱导PCl2细胞内Ca^2＋浓度升高的幅度，而且改变Ca^2＋浓度波动的周期。     

精子质量参数分析的标准化与质量控制的研究进展

精液分析是评价男性生育能力的最基本测试。最近几年,对精液分析标准化的迫切需求已引起男科学家的广泛重视。本文对精子质量参数———精子密度、活动率和形态学分析的标准化及质量控制进行了综述。精子密度分析的关键是计数池的标准化,因此Cell-VU计数池应该是最佳的选择;精子活动率和精子形态学的分析由于主观性太强,CASA系统可能是其标准化的最终选择。精液质量参数分析的质量控制主要是质量控制材料的选择,以及在男科学实验室实施EQC和IQC项目,而一些监测质量控制的图表和计算方法应被相应地建立。