关节腔渗透压调控骨关节炎的研究进展

骨关节炎是一种慢性、进行性、不可逆性的关节退行性疾病,是一种中老年人的常见疾病,被认为是全球致残率较高的疾病之一。近年来,随着经济发展和人口老龄化,骨关节炎的患者数量在不断增加,这也让骨关节炎在临床上得到了极大的重视。而临床上治疗骨关节炎的一个关键性问题是关节软骨的丢失和难以自我修复。渗透压可以通过调节细胞体积和调控离子通道影响软骨细胞的生理代谢,从而影响关节软骨的损伤和修复。这一过程可能在骨关节炎发生发展中起到了重要作用。本文就离子通道、渗透压和骨关节炎三者间的相关性作一综述。     

渗透性脱髓鞘综合征的临床分析

摘 要： 目的了解渗透性脱髓鞘综合征（ODS）的发病机制、诊断、治疗和预防方法。方法报告11例ODS患者，并结合文献进行分析。结果10例患者有明显低钠血症；发病诱因包括药源性3例，营养不良3例，肝移植术后、脑挫裂伤、垂体微腺瘤、糖尿病肾病和妊娠剧吐各1例。存在严重呕吐或进食量极少的患者7例。神经系统表现包括不同程度意识障碍，假性球麻痹，四肢瘫痪，眼球活动障碍，闭锁综合征，精神症状，震颤或手足徐动等不自主运动，肌张力齿轮样增高等帕金森样症状等。头颅MRI显示桥脑或双侧豆状核、尾状核头、丘脑等桥外部位脱髓鞘。单纯CPM 3例，单纯EPM 2例，CPM合并EPM 6例。治疗后10例好转，1例病情获稳定。结论ODS的发病与脑内渗透压平衡失调有关，各种原因引起的低钠血症及其快速纠正容易诱发，临床表现可为单纯CPM、EPM或二者合并存在。随着头颅MRI的应用，可使该病早期诊断，其预后明显改善。避免快速纠正低钠血症是预防的主要措施。     

用M-NRTL模型及平衡空气法交叉验证甘氨酸溶液的渗透压

目的尝试通过药物溶液的浓度计算其渗透压。方法采用M-NRTL模型,由甘氨酸溶液浓度计算其渗透压,并应用平衡空气法测定溶液的渗透压。结果应用双向单侧t检验法和多重检验调整法进行验证,结果显示M-NRTL模型的计算值与平衡空气法的测定值具有等效性。结论可以应用物理模型由药物溶液的浓度计算渗透压值。     

高血压肾病患者尿电导率与渗透压的相关性分析

目的 观察高血压肾病患者的尿液电导率和尿液渗透压的变化,并探讨两者之间的相关性.方法 采用UF-1000i全自动尿沉渣分析仪与渗透压仪分别测定85例临床确诊高血压肾病患者和98例健康体检者(对照组)晨尿的电导率和渗透压值,并对结果进行统计学分析.结果 高血压肾病组患者尿液电导率和渗透压分别为(11.64 ± 3.68) mS/cm和(352.45 ± 91.22) mOSM/kgH2O,均低于对照组的(17.58 ± 4.35) mS/cm和(557.11±131.70) mOSM/kgH2O,差异均有显著统计学意义(P<0.01);两组受检者的尿液电导率与渗透压相关性系数r分别为0.823和0.939,直线回归方程分别是Y=24.01X+73.01和Y=33.13X-25.52.结论 尿液电导率变化可以反映尿液渗透压的变化,能够更加快速地监测高血压肾病患者肾脏浓缩稀释功能.     

Movement disorders and the osmotic demyelination syndrome

With the advent of MRI, osmotic demyelination syndromes (ODS) are increasingly recognised to affect varied sites in the brain in addition to the classical central pontine lesion. Striatal involvement is seen in a large proportion of cases and results in a wide variety of movement disorders. Movement disorders and cognitive problems resulting from ODS affecting the basal ganglia may occur early in the course of the illness, or may present as delayed manifestations after the patient survives the acute phase. Such delayed symptoms may evolve over time, and may even progress despite treatment. Improved survival of patients in the last few decades due to better intensive care has led to an increase in the incidence of such delayed manifestations of ODS. While the outcome of ODS is not as dismal as hitherto believed – with the acute akinetic-rigid syndrome associated with striatal myelinolysis often responding to dopaminergic therapy – the delayed symptoms often prove refractory to medical therapy. This article presents a review of the epidemiology, pathophysiology, clinical features, imaging, and therapy of movement disorders associated with involvement of the basal ganglia in ODS. A comprehensive review of 54 previously published cases of movement disorders due to ODS, and a video recording depicting the spectrum of delayed movement disorders seen after recovery from ODS are also presented.     

Sporadic hypokalemic paralysis caused by osmotic diuresis in diabetes mellitus

A wide variety of neurological manifestations are known in patients with diabetes mellitus. We describe a 40-year-old man who presented with hypokalemic paralysis. On evaluation, we found that the cause of the hypokalemia was osmotic diuresis induced by marked hyperglycemia due to undiagnosed diabetes mellitus. The patient had an uneventful recovery with potassium replacement, followed by glycemic control with insulin. Barring a few instances of symptomatic hypokalemia in the setting of diabetic emergencies, to our knowledge uncomplicated hyperglycemia has not been reported to result in hypokalemic paralysis.     

Intracerebroventricular choline increases plasma vasopressin and augments plasma vasopressin response to osmotic stimulation and hemorrhage

Intracerebroventricular (i.c.v.) injection of choline (50-150 microg), a precursor of the neurotransmitter acetylcholine, produced a time-and dose-dependent increase in plasma vasopressin levels in conscious, freely moving rats. The increase in plasma vasopressin in response to i.c.v. choline (150 microg) was inhibited by pretreatment with the nicotinic receptor antagonist, mecamylamine (50 microg; i.c.v.), but not by the muscarinic receptor antagonist, atropine (10 microg; i.c.v). The choline-induced rise in plasma vasopressin levels was greatly attenuated by hemicholinium-3 (HC-3; 20 microg; i.c.v.), a neuronal choline uptake inhibitor. Choline (50 or 150 microg; i.c.v.) produced a much greater increase in plasma vasopressin levels in osmotically stimulated or hemorrhaged rats than in normal rats. Choline (150 microg; i.c.v.) also enhanced plasma vasopressin response to graded hemorrhage; the enhancing effect of choline was also attenuated by HC-3 (20 microg; i.c.v.). Choline and acetylcholine concentrations in hypothalamic dialysates increased significantly following i.c.v. injection of choline (150 microg). It is concluded that choline increases plasma vasopressin levels by stimulating central nicotinic receptors indirectly, through the enhancement of acetylcholine synthesis and release, and augments the ability of osmotic stimulations or hemorrhage to stimulate vasopressin release.     

Changes of GABA(A) receptor binding and subunit mRNA level in rat brain by infusion of NOS inhibitor

In the present study, we have investigated the effects of prolonged inhibition of nitric oxide synthase (NOS) by infusion of NOS inhibitor, L-nitroarginine, to examine the pentobarbital-induced sleep, modulation of GABA(A) receptor binding, and GABA(A) receptor subunit mRNA level in rat brain. Pre-treatment with L-nitroarginine 30 min before pentobarbital treatment (60 mg/kg, i.p.) significantly increased the duration of sleep in rats. However, the duration of pentobarbital-induced sleep was shortened by the prolonged infusion of L-nitroarginine into ventricle. We have investigated the effect of NOS inhibitor on GABA(A) receptor binding characteristics in discrete areas of brain regions by using autoradiographic and in situ hybridization techniques. Rats were infused with L-nitroarginine (10, 100 pmol/10 microl/h, i.c.v.) for 7 days, through pre-implanted cannula by osmotic minipumps. The levels of [(3)H]muscimol and [(3)H]flunitrazepam binding were markedly elevated in almost all of brain regions including cortex, caudate putamen, thalamus, hippocampus, and cerebellum. However, there was no change in the level of [(35)S]TBPS binding. The levels of beta2-subunit were elevated in the cortex, brainstem, and cerebellar granule layers. By contrast, the levels of beta3-subunit were significantly decreased in the cortex, hippocampus, and cerebellar granule layers in L-nitroarginine-infused rats. Following L-nitroarginine treatment, the levels of alpha6- and delta-subunits which were strictly localized to the cerebellum, were not changed in the cerebellar granule layer. These results show that the prolonged inhibition of NOS by L-nitroarginine-infusion markedly elevates [(3)H]muscimol and [(3)H]flunitrazepam binding throughout the brain, and alters GABA(A) receptor subunit mRNA levels in different directions. Chronic inhibition of NO generation has differential effects on the various expressions of GABA(A) receptor subunits. These suggest the involvement of different regulatory mechanisms for the NO-induced expression of GABA(A) receptor.     

小儿肾积水肾盂成形术后尿理化性质和尿水通道蛋白2改变的研究

目的 探讨小儿单侧先天性肾盂输尿管连接处梗阻(pyeloureteric junction obstruction,PUJO)肾积水术后1周内尿理化性质和尿水通道蛋白2(aquaporins-2.AQP2)的变化.方法 选取14例符合Grignon法四、五级标准的小儿单侧先天性PUJO.肾积水患儿;经肾盂成形术后给予严格设定的补液标准,收集术后第一、三、五、七天积水侧肾脏和对侧无积水肾脏24 h尿液,分别测定排尿量、渗透压、Na+和肌酐,并用酶联免疫吸附法(ELISA)测定尿液中AQP2水平.结果 相对于对侧无积水肾脏,积水侧肾脏梗阻解除术后1周内尿液AQP2显著降低.尿量明显增多.尿渗透压显著降低,Na+排泄分数显著增加;同时术后1周内双侧肾脏尿液AQP2、排尿量和尿渗透压有升高趋势,而积水侧肾脏Na+排泄分数有减少的趋势;积水侧.肾脏术后第五、七天的尿液AQP2.排尿量和尿渗透压较第一天均显著增加(P<0.05).对侧无积水肾脏术后第五、七天的尿液AQP2和尿渗透压较第一天也显著增加(P<0.05).其余指标在术后小同天数之间差异无统计学意义(P>0.05).结论小儿单侧先天性PUJO解除术后1周内积水侧.肾脏的尿液AQP2和尿渗透压均较对侧尤积水肾脏尿液显著减少.提示梗阻解除后尿液中AQP2可能和尿液浓缩能力改变有关.