铁骨晶对大鼠钙代谢、骨密度的影响及临床观察

本实验以铁骨晶（多肽钙），进口脱脂奶粉，活性钙冲剂，贝壳钙为钙源添加于大鼠正常饲料中。观察结果表明：上述４组钙的吸收率分别为６４．４％，６９．１％，５９．９％，５１．６％；钙的储留率分别为８９．８％，９３．３％，８５．２％，７９．０％；钙的存留率分别为４３．６％，４９．０％，３２．４％，２６．８％；股骨指数分别为７．０２×１０（－３），６．４３×１０（－３），６．８４×１０（－３）。６．８８×１０（－３）；折断力（牛顿）分别为６０．５４±１２．５５，４６．８１±９．３２，４３．２６±１６．６２，３８．２４±１０．７９。同时以铁骨晶为钙源对７０例（５～６岁）儿童进行了血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ及生长发育的检测。铁骨晶组的身高，体重，胸围分别比对照组增加。铁骨晶组血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ也均有较好的改善。这表明铁骨晶具有较好的促进钙吸收利用作用，同时能增加骨强度作用。     

佳钙宝及其它钙剂中钙吸收利用率的对比研究

佳钙宝系由海洋生物加工而成的补钙剂。钙的主要形式为醋酸钙和少量柠檬酸钙、苹果酸钙。用佳钙宝及其它几种常用市售补钙剂（活性钙、葡萄糖酸钙、乳酸钙、磷酸氢钙）进行了３０天的大鼠喂养和３天代谢试验，结果显示，佳钙宝中钙的吸收率和储留率分别为６９．２％和９５．１％，均高于其它钙剂（Ｐ＜０．０５）。佳钙宝组大鼠股骨重量（湿重）和股骨含钙量分别为０．８２±０．０４（ｇ）和８４．５±６．２（ｍｇ），均明显大于其它各组（Ｐ＜０．０５）。佳钙宝可作为补充机体钙的良好来源     

蓇密牌钙片对大鼠骨密度的影响研究

目的研究瞢密牌钙片对大鼠骨密度的影响。方法选用雌性Wistar大鼠50只，随机分成5组；每周量身长；给予该产品4周后，进行3天代谢实验；实验结束时，进行股骨骨密度测定和骨钙含量的测定。结果低、中剂量实验组的身长和身长净增加值显著高于低钙对照组（P〈0．05或P〈0．01）。各剂量实验组大鼠股骨中心矿物质含量和骨密度显著大于低钙对照组（P〈0．01或P〈0．05），高剂量实验组大鼠的股骨中心矿物质含量和骨密度显著高于碳酸钙对照组（P〈0．05）。高剂量实验组大鼠的股骨远心端骨矿物质含量和骨密度显著大于低钙对照组（P〈0．01）。中、高剂量实验组大鼠的股骨钙含量及总钙量显著大于低钙对照组（P〈0．01）。中、高剂量组、碳酸钙对照组大鼠钙的表观吸收率显著低于低钙对照组（P〈0．01）。中、高剂量实验组和碳酸钙对照组大鼠钙的存留率显著低于低钙对照组（P〈0．01）。结论认为瞢密牌钙片有增加大鼠骨密度的作用。     

螺旋藻对模拟失重大鼠钙代谢和骨矿盐密度影响的初步研究

目的：研究螺旋藻对模拟失重大鼠钙代谢和骨矿盐密度的影响。方法：30只雄性SD大 鼠随机分为3组（每组10只）：A组：地面自由活动组（饲喂普通饲料）：B组：模拟失重普通饲料组；C组：模拟失重螺旋藻组，实验期21d。结果；B组大鼠饲料钙的表观吸收率、后肢骨密度（BMD）、骨钙含量以及骨钙素（BGP）的水平显性低于A组，血钙水平明显高于A组；C组饲料钙的表观吸收率、骨密度、骨钙含量以及骨钙素水平较B组高，血钙水平显性低于B组。结论：螺旋藻可以减少模拟失重大鼠后肢骨质的丢失，提高骨骼BMD，增加骨形成，对骨代谢产生一定的有益影响。     

上皮钙粘附素和树突细胞在膀胱癌中的表达及临床意义

目的：探讨膀胱癌中树突细胞（ＤＣ）和上皮钙粘附素（Ｅ－ｃｄ）的表达及其与生物学行为的关系。方法：采用免疫组织化学ＬＳＡＢ法检测Ｅ－ｃｄ和ＤＣ。结果：６９例膀胱癌中３５例Ｅ－ｃｄ正常表达（５０．７％）,２２例ＤＣ正常表达（３１．９％）,Ｅ－ｃｄ正常表达率在Ⅰ,Ⅱ,和Ⅲ级肿瘤中分别为７２．２％,６５．２％和２５．０％,在Ｔｉｓ￣１期和Ｔ２￣４期肿瘤中分别为７８．８％和２５．０％。ＤＣ正常表达率在Ⅰ、Ⅱ     

低钙透析液对腹膜透析患者钙磷代谢的影响

目的横断面研究腹膜透析患者使用低钙透析液的安全性及其影响因素。方法选择西安交通大学医学院第一附属医院肾脏内科腹膜透析超过6个月的患者共39例，其中男24例，女15例，年龄56．49±19．31岁，其中使用常规（ca 1．75mmol／L）透析液8例，低钙（ca 1．25mmol／L）透析液31例，比较两组血清钙、磷、甲状旁腺激素、血压以及使用碳酸钙的情况。结果两组血钙无明显差异；常规透析液组血磷和钙磷乘积高于低钙组，两组iPTH无明显差异。低钙组服用碳酸钙剂量明显高于常规透析液组。低钙组服用碳酸钙与未服用碳酸钙血钙无明显差异，服用碳酸钙组血磷控制较为理想、钙磷乘积更接近正常，未服用碳酸钙组血PTH明显升高。结论腹膜透析患者使用低钙透析液有利于控制血磷和血压，有效预防钙磷乘积升高。提高对碳酸钙的依从性是预防使用低钙透析液后引起继发性甲状旁腺功能亢进的关键。     

调整腹透液钙浓度对尿毒症患者颈动脉粥样硬化的影响

目的观察调整腹透液钙浓度对持续性不卧床腹膜透析（㈣）患者颈动脉粥样硬化的影响。方法在规律性腹膜透析随访的患者中选择30例伴有颈动脉粥样硬化的患者，先予患者继续使用标准钙腹透液6个月后改用低钙腹透液（Baxter PD4：Ca^2＋1．25mmol／L，其余成分不变），同时增加碳酸钙用量，继续观察12个月，回顾分析患者的血清钙、磷、钙磷乘积及甲状旁腺素（iPTH）水平，颈动脉内-中膜厚度（IMT）、颈动脉血流阻力指数（R1）、颈动脉粥样斑块数量和超声分型的变化。同时观察使用低钙腹透液的不适症状。结果在继续使用标准钙腹透液的6个月中，患者血钙水平逐渐增加，颈动脉IMT增厚，RI增加，差异均有统计学意义。换用低钙腹透液治疗3个月后，颈动脉IMT变薄，RI较前明显下降（P〈0．05），血钙、磷及钙磷乘积明显下降（P〈0．01），iPTH明显增加（P〈0．01）。患者碳酸钙的每日口服剂量也由（2．27±0．41）g增加至（3．35±0．22）g（P（0．05）。在随后的9个月中，血钙、钙磷乘积均稳定在正常范围，血磷降至正常，iPTH 150ng／L左右；颈动脉IMT变薄（P〈0．01）、RI下降（P〈0．01），颈动脉粥样硬化斑块的超声分型及数量变化有统计学意义。治疗过程中，1例死亡，2例自行退出，其余患者均未有明显低钙抽搐、低血压等发生。结论低钙透析能显著减轻腹膜透析患者钙磷代谢紊乱对血管的毒性作用，有助于尿毒症患者颈动脉粥样硬化的转归。     

联合应用运动和钙对卵巢切除大鼠骨量减少的影响

目的：了解运动和钙摄入对切除卵巢大鼠骨量和生物力学改变的影响。材料与方法：切除卵巢大鼠分成模型组，补钙组，运动组，运动和服钙联合组，雌激素组、制动组和正常对照组。检测各组骨密度（ＢＭＤ）和生物力学有关指标，并进行比较分析。结果：联合组ＢＭＤ为０．３０６±０．０２６，运动组为０．３０５±０．０２６，显著高于模型组的０．２７５±０．０１８。制动组ＢＭＤ均显著低于各实验组。生物力学实验显示：（１）单纯运动组、补钙组和激素组的弯曲破坏载荷，强度极限，最大桡度比与正常组无显著性差异；而在刚性系数和韧性系数与正常组则有显著性差异；（２）联合组各项指标与正常组无显著性差异；（３）运动和补钙各组之间的各项指标无显著性差异；（４）激素组的ＢＭＤ与正常组无显著差异，但生物力学性能显示韧性差；（５）制动组的各项指标与运动和补钙组有显著性差异。结论：运动对去势后大鼠骨量的维持和生物力学性能的改善有作用，运动和补钙联合应用可通过不同途径发挥作用，联合组ＢＭＤ值最高，生物力学性能最接近正常     

硝苯地平对大鼠急性胰腺炎时钙向组织内转移和低钙血症的预防作用

目的：探讨大鼠急性胰腺炎时低钙血症的形成机理和硝苯地平对低钙血症的预防作用。方法：将130只SD大鼠随机分成4组：正常对照组（A组）;手术对照组（B组）;急性坏死性胰腺炎组（C组）和硝苯地平预防组（D组）。术后3,6,12h测定血清钙浓度和组织钙含量。结果;D组术后3,6,12h血清钙浓度分别为1．34,1．35,1．32mmol/L与A组接近,各组织钙含量明显降低,与C组比较差异有极显著性（P＜0．01）。结论：钙向组织内转移可能是急性胰腺炎低钙血症的原因或部分原因。钙通道阻滞剂硝苯地平可阻止过多的钙进入细胞内,从而纠正低钙血症。     

同位素稀释技术比较六种不同钙剂的生物利用度

目的测定和比较6种不同的有机和无机钙剂的真正吸收率和生物利用度。方法采用同位素稀释技术。在2w的代谢研究中,60只生长期雄性SD大鼠,肌肉注射45Ca后,分为6组,每组10只,分别饲喂含柠檬酸钙、乳酸钙、醋酸钙、牡蛎壳粉、蛋壳粉和β-磷酸三钙的人工半合成饲料。6种饲料中含钙、磷、镁的量均相同,分别为2.8,5.3和0.65g/kg。结果柠檬酸钙、乳酸钙和醋酸钙等有机形式钙的真正吸收率和生物利用度（真正吸收率分别为98.8,98.3和98.6%;生物利用度分别为96.8,96.0和96.8%）略高于生物碳酸钙类的牡蛎壳和蛋壳（真正吸收率分别为97.7和96.3%;生物利用度分别为95.3和93.8%）以及无机类的β-磷酸三钙（94.9和92.0%）。然而,从实际应用角度衡量,所观察的6种钙剂均显示很高的吸收率和生物利用度。结论可以认为,膳食钙的化学形式并不是影响钙生物利用度的主要因素。     

Risk of Calcium Oxalate Nephrolithiasis after Calcium or Combined Calcium and Calcitriol Supplementation in Postmenopausal Women

Although calcium supplementation can cause hypercalciuria, the risk of nephrolithiasis has been shown to decrease rather than increase among subjects who had a higher calcium intake. Hypercalciuria is also a well-established side effect of calcitriol administration. However, the risk of nephrolithiasis is not well defined. The present study was undertaken to prospectively determine the effect of calcium with or without calcitriol on physicochemical risk factors associated with calcium oxalate nephrolithiasis in Thai postmenopausal women with osteoporosis. Subjects consisted of 53 Thai women more than 10 years postmenopausal who were randomly allocated to receive 750 mg of calcium carbonate supplement alone (n= 28) or 750 mg of calcium carbonate plus 0.5 mg calcitriol (n= 25) daily. Mean ± SEM for age was 65.3 ± 1.1 years, body weight 53.5 ± 1.3 kg. Urine samples for biochemical assays were collected at baseline and 3 months after treatment. Supersaturation for calcium oxalate stone formation was assessed from the 24 h urine constituents by the Tiselius’s index, AP(CaOx). Three months of calcium supplement alone resulted in a modest, but not significant, increase in urinary calcium (baseline, 2.90 ± 0.43 mmol/day; after treatment 3.58 ± 0.54 mmol/day) with no change in urinary oxalate, citrate or magnesium. In contrast, calcium together with calcitriol caused a significant increase in urinary calcium (baseline, 2.87 ± 0.41 mmol/day; after treatment, 4.08 ± 0.57 mmol/day; p<0.05). No significant change in other urine constituents after treatment with calcium and calcitriol was detected. Therefore, AP(CaOx) did not significantly increase either after calcium alone (baseline, 1.17 ± 0.39; after treatment, 1.36 ± 0.28) or after calcium plus calcitriol (baseline, 1.09 ± 0.17; after treatment, 1.09 ± 0.19). However, after treatments, 12 subjects (23%) – 6 receiving calcium supplement alone and 6 receiving calcium plus calcitriol supplement – had high AP(CaOx) values (greater than the upper limit of 95% CI for AP(CaOx) derived from non-stone-forming Thai women). The post-treatment/baseline ratio was 3.21 ± 0.74 for urinary calcium, 1.01 ± 0.19 for urinary oxalate, and 2.23 ± 0.42 (median 1.15) for AP(CaOx). The post-treatment/baseline ratio of calcium, but not for urinary oxalate, had a significant correlation with the post-treatment/baseline ratio of AP(CaOx). Our findings suggest that the alteration in the risk of calcium oxalate nephrolithiasis based on urinary composition is related to the alteration in urinary calcium. The risk of calcium oxalate nephrolithiasis does not increase significantly after calcium or combined calcium and calcitriol supplement in the majority of postmenopausal women with osteoporosis. Received: 10 March 1999 / Accepted: 16 November 1999     

Calcium and osteoporosis

The loss of bone which starts at the menopause is self-limiting (exponential) and possibly mainly trabecular. It merges into an age-related linear loss of bone which is probably mainly cortical. The menopause is associated with a rise in obligatory urinary calcium loss resulting from an increase in the filtered load of calcium which may be due to the complexed fraction. The dependence of the urinary hydroxyproline on the urinary calcium and sodium suggests that the bone resorption is a response to calcium losses rather than a primary event. In osteoporotic women, there is a further increase in filtered load of calcium and obligatory calcium loss, frequently coupled with malabsorption of calcium. Urinary hydroxyproline can be suppressed by calcium administration in those with normal absorption and by calcitriol in those with calcium malabsorption. It is known that calcium deficiency causes osteoporosis in experimental animals, but there is controversy about the role of calcium deficiency in the pathogenesis of human osteoporosis. Calcium supplementation inhibits cortical bone loss in postmenopausal women but there is some doubt as to whether it can inhibit trabecular bone loss in women close to the menopause. This may be partly a matter of dose, formulation and time of administration.     

Calcium metabolism and hypertension

Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)     

Calcium and neuronal function

Calcium is unique among metals because its ions have a very large concentration gradient across the plasma membrane of all cells, from 10^–3 M Ca²⁺ outside, to 10^–7 M Ca²⁺ inside. This gradient is maintained by the use of metabolic energy through ion pumping, and its existence allows cells to use transient increases in the intracellular Ca²⁺ concentration as signals, which regulate cell function. In neurones these Ca signals are initiated by electrical activity (action potentials) which open voltage-dependent Ca channels in the plasma membrane, allowing Ca to enter the cell. Intracellular Ca signals can also be produced by transmitters at synapses, which open Ca channels, either directly, or indirectly by causing local depolarization and the opening of voltage-dependent Ca channels. The main effects of Ca signals on neurones are to alter their electrical activity, by modifying the opening and closing of Na and K channels, and to stimulate the release of transmitter substance. Ca has a host of other effects, such as the regulation of metabolic activity, the regulation of cell growth, and the long-term modification of synaptic efficiency, and it is even implicated in the destruction of neurones.     

Calcium pyrophosphate and pseudogout

Calcium pyrophosphate deposition disease (CPDD) is a condition in which calcium pyrophosphate dihydrate crystals are deposited in joint articular cartilage, menisci, and synovium. The main clinical presentations of CPDD are chondrocalcinosis--calcification of cartilage, pseudogout--acute joint inflammation due to crystal-induced synovitis, and pyrophosphate arthropathy--degenerative joint disease similar to osteoarthritis associated with calcium pyrophosphate crystal deposition. The clinical importance of CPDD for the arthroscopist is the ability to recognize the condition so that appropriate treatment can be instituted. Arthroscopy is valuable for diagnosis as well as lavage and intraarticular debridement or meniscectomy. Tissue removed for microscopic examination should be sent to the laboratory in saline, since formalin dissolves the crystals. Postarthroscopy treatment of CPDD should include oral antiinflammatory medication. Asymptomatic chondrocalcinosis does not require treatment.     

Calcium and the anaesthetist

Calcium plays a central role in a large number of physiological actions that are essential for life. It is important therefore that the anaesthetist understands calcium pathophysiology. In this review, the physiology, regulation, clinical features, causes and treatment of alterations in circulating calcium will be discussed. In addition, the effects that acid-base status, massive blood transfusion and cardiopulmonary bypass may have on circulating calcium will be highlighted. Finally, the role that calcium plays in ischaemic/reperfusion injury and myocardial stunning will be summarised.