血清亚硝酸盐的快速测定

目的：建立一种无需去蛋白的血清亚硝酸盐的快速测定方法。方法：加入蛋白活化剂后，直接用Ｇｒｉｅｓ试剂显色分光光度测定。结果：方法的检测下限为０．２μｍｏｌ／Ｌ，相对标准差为５．１３％～８．８６％，回收率为９４．５％～９９．８％（平均为９７．８％）。血清ＮＯ－２浓度为１４．３８±０．２５μｍｏｌ／Ｌ时，批内变异系数为１．７５％，ＮＯ－２浓度为５．６９±０．２５μｍｏｌ／Ｌ时，批间变异系数为４．４６％。测定５５例正常人血清，得到血清中ＮＯ－２浓度的平均值分别为５．３６±２．１６ｕｍｏｌ／Ｌ；对糖尿病病人血清测定结果表明，亚硝酸盐浓度明显高于正常人。与去蛋白的Ｇｒｉｅｓ试剂分光光度法比较，结果无统计学差异。结论：用蛋白活化剂替代蛋白沉淀剂，减少操作步骤和干扰，测定准确、简便、快速，适用于血清中ＮＯ－２的测定。     

急性有机磷中毒患者的血钾变化及临床意义的探讨

目的：探讨急性有机磷中毒患的血清钾变化及其临床意义。方法：对68例发病6小时内的急性有机磷中毒的患入院后测定血清钾，并根据不同的中毒程度、中毒方式、发病时间分组在比较，并设正常对照组对照。结果：中毒各组均有明显的低钾血症，与对照组比较均有显性意义（P＜0．01）,且重度中毒组与中、轻度组比较亦有显性意义（P＞0．05），但两种不同的中毒途径与不同的中毒时间的组间血清钾的比较无显性意义（P＞0．05）。结论：急性有机磷中毒可致明显的低钾血症，中毒越重，低钾血症越明显。在发病早期应注意监测血清钾的变化，及时纠正低血钾，预防或减轻中毒后严重合并症的产生。     

常见阴离子对血清氯离子选择性电极法测定的影响

目的:研究离子选择性电极在测定血清氯时的影响因素。方法:用E-555电解质分析仪测定氟化钠、溴化钠、碳酸氢钠、硫氰化钾、碘化钾、铁氰化钾、硫化钠以及叠氮钠溶液,并将溴化钠、硫氰化钾、碘化钾、铁氰化钾、硫化钠、叠氮钠分别加入Cl~-均值为100mmol/L的混合血清中观察其具体的干扰情况。结果:所测8种物质中氟化钠、碳酸氢钠的影响较小,而溴化钠、铁氰化钾、碘化钾、铁氰化钾、硫化钠、叠氮钠的影响较大。结论:溴离子、碘离子、硫离子、氢氰根离子、叠氮钠对离子选择性电极法影响性较大,我们在工作中应加以重视。     

Altered calcium metabolism in red blood cells of hypertensives: Persistent marker or sequel of essential hypertension?

Summary The characteristics of the increased calcium (Ca) influx observed in metabolically depleted red blood cells (RBCs) of hypertensive patients were investigated. Twenty-four normotensives, 16 untreated essential hypertensives, and 10 essential hypertensives under sufficient blood pressure control by 50–100 mg/day atenolol were studied. Free intracellular concentrations of Ca, sodium (Na), and potassium (K) were assessed using ion-selective electrodes in freeze-thawed RBCs, which were metabolically depleted by 30 mM desoxy-glucose at 37°C for 48 h. In the treated hypertensives values for Ca and K at 24 and 48 h were not different from values for the normotensives, whereas elevated Ca was found in RBCs of untreated hypertensives. Na in treated hypertensives was significantly increased at 0 and 48 h, thus, being similar to values for untreated hypertensives. Additionally, RBCs of six normals were stressed in a glass/teflon potter. Before metabolic depletion electrolytes were not affected by this procedure, while Ca at 24 and 48 h of metabolic depletion increased to significantly higher values for the hypertensive patients as compared to the controls. These results suggest that the altered Ca metabolism in the RBCs of hypertensives may reflect a secondary phenomenon due to the mechanical damage to RBCs by the elevated blood pressure.     

Special Pharmacokinetic Considerations in Children

Summary: Pediatric patients have greater degrees of pharmacokinetic variability and unpredictability than adults. This variability results from the effects of pharmacogenetics, age and growth, prior and current comedication, and disease. Newborns with seizures have the least predictable dosage requirements, and their needs change as drug-eliminating mechanisms mature in the neonatal period. Infants have the highest relative capacities to eliminate antiepileptics of any age group and require the largest relative doses. In addition to age-related trends, children demonstrate the same drug-specific, pharmacokinetic phenomena that adults do, including nonlinear phenytoin elimination, nonlinear valproate binding, and autoinduction of carbamazepine. Intercurrent illness and drug interactions further modify the age-related pharmacokinetic patterns in children and make dosage requirements even more unpredictable. Recent studies have shown that febrile illness can affect drug elimination, sometimes decreasing drug levels by 50% or more. Intermittent treatment with benzodiazepines administered either orally or rectally can be an important adjunct and help minimize this type of problem for children with marginally controlled epilepsy. Intermittent benzodiazepines are also helpful for children who have febrile seizures and who need only occasional antiepileptic protection.     

The Toxic Effects of Serum from Patients with Type 1 Diabetes Mellitus on Mouse Neuroblastoma Cells: A New Mechanism for Development of Diabetic Autonomic Neuropathy

The pathogenesis of diabetic neuropathy is incompletely understood. The possibility that humoral neurotoxic factors contribute as a cause of diabetic neuropathy was tested by application of serum from patients with Type 1 and Type 2 diabetes to mouse neuroblastoma cells, which have the characteristics of adrenergic neurons in culture. Serum from patients with Type 1 diabetes and somatic neuropathy significantly inhibited both proliferation and differentiation of neuroblastoma cells, while serum from patients with Type 1 diabetes but no symptoms of neuropathy and patients with Type 2 diabetes and neuropathy had no effect on proliferation, and serum from Type 2 patients only marginally inhibited differentiation. The effects of Type 1 diabetic serum could be reversed by pre-absorption of the serum to neuroblastoma cells, and were independent of glucose levels. Immunoglobulins precipitated from the sera mimicked the effects of whole sera. These results suggest that Type 1 diabetes mellitus causes a change in serum composition, possibly related to autoimmunity, that is capable of contributing to adrenergic autonomic neuropathy in diabetic patients.     

Serum modulates cyclic AMP-dependent morphological changes in cultured neurohypophysial astrocytes

The effects of serum on the morphological plasticity exhibited by pituicytes in explant cultures of the neurohypophysis of adult rats have been examined. Cultured pituicytes are normally nonstellate, protoplasmic, amorphous cells (< 25% are stellate with a distinct cell body and phase bright processes). After incubation (90 min) of pituicyte cultures in a HEPES buffered salt solution (HBSS) supplemented with isoproterenol or forskolin, the fraction of stellate pituicytes significantly increased. The increase in the fraction of stellate cells induced by isoproterenol was not reversed by subsequent incubation in isoproterenol-free HBSS for 90 min. In contrast, after stellation was induced in cultures by exposure to forskolin (90 min), the fraction of stellate cells was significantly reduced if these cultures were incubated in forskolin-free, serum (0.5%) supplemented HBSS for the same duration. Serum also blocked the increase in the fraction of stellate pituicytes induced by forskolin. These experiments suggest that serum components may have a significant role in controlling the plasticity of neuroglial relations in the neurohypophysis priviously demonstrated in vivo.     

The effects of brisk walking on markers of bone and calcium metabolism in postmenopausal women

Weight-bearing exercise has been shown to maintain or increase bone mass in younger as well as older individuals but the mechanisms by which mechanical loading affects bone metabolism are not known in detail. Twelve postmenopausal women participated in a single bout of brisk walking (50% of VO_{2 max}) for 90 minuttes. Calciotropic hormones and markers of type I collagen formation (PICP) and degradation (ICTP) were measured before the exercise, and 1, 24, and 72 hours following the exercise. Total body bone mineral content (BMC) and density (BMD) were measured by dual energy X-ray absorptiometry (DXA). Brisk walking did not induce any significant changes in the concentrations of ionized calcium, parathyroid hormone (PTH), calcitonin, or osteocalcin. A significant increase of PICP was noted 24 and 72 hours (P<0.01) after exertion and a significant decrease in the concentration of serum ICTP at 1 hour (P<0.05) was followed by an increase at 72 hours (P<0.001). There was no significant difference between the increases in the concentrations of PICP and ICTP at 72 hours. Strong inverse correlations between the basal levels of PTH and BMD (r=−0.78;P<0.01) as well as between osteocalcin and BMD (r=−0.83;P<0.01) were noticed. The changes in serum levels of bone collagen markers indicate an altered bone collagen turnover due to this moderate endurance exercise. The results also support the fact that serum levels of PTH as well as those of osteocalcin are associated with total body BMD in postmenopausal women.     

冠心病中血糖与血清微量元素间的关系分析

对７５例冠心病患者依血糖水平分两组，进行１２种血清微量元素测定，旨在探讨微量元素与冠心病及糖尿病间的相互关系。结果发现锌、铬、锰、硒、钴元素高血糖组较对照组血清水平为低，呈非常显著差异（Ｐ＜０．０ｌ）；铜、镍元素增高，差异显著（Ｐ＜０．０５）；而锶、铁、砷、铅、铝元素两组间无显著差异（Ｐ＞０．１）。表明部分微量元素与冠心病及血糖间存在着密切联系。     

Niflumic acid-induced increase in potassium currents in frog motor nerve terminals: effects on transmitter release

The actions of the nonsteroidal antiinflammatory drug niflumic acid were studied on frog neuromuscular preparations by conventional electrophysiological techniques. Niflumic acid reduced the amplitude and increased the latency of endplate potentials in a concentration-dependent manner. Neuromuscular junctions pretreated with niflumic acid (0.05–0.5 mM) showed much less depression than control when they were stimulated with trains of impulses. Inhibition of acetylcholine release was reverted by raising the extracellular Ca²⁺ concentration but not by simply washing out the preparations with niflumic acid-free solutions. Pretreatment with indomethacin (0.1 mM), another nonsteroidal antiinflamatory drug, did not affect the niflumic acid-induced inhibition of evoked responses. Niflumic acid (0.1 mM) did not change the amplitude of miniature endplate potentials and had a dual action on the frequency of miniatures: it decreased their frequency at 0.1 mM whereas it produced an enormous increase in the rate of spontaneous discharge at 0.5 mM. Niflumic acid (0.1–1 mM) reversibly increased the amplitude and affected the kinetics of presynaptic voltage-activated K⁺ current and Ca²⁺-activated K⁺ current in a concentration-dependent manner. Niflumic acid (0.1–1 mM) irreversibly decreased the amplitude and reversibly affected the kinetics of the nodal Na⁺ current. Indomethacin (0.1 mM) had no effect on presynaptic currents. In conclusion, niflumic acid reduces acetylcholine release by increasing presynaptic K⁺ currents. This may shorten the depolarizing phase of the presynaptic action potential and may reduce the entry of Ca²⁺ with each impulse.