Aging changes agonist induced contractile responses in permeabilized rat bladder

Aging alters bladder functions where a decrease in filling, storage and emptying is observed. These changes cause urinary incontinence, especially in women. The aim of this study is to examine how aging affects the intracellular calcium movements due to agonist-induced contractions in permeabilized female rat bladder. Urinary bladder isolated from young and old female Sprague-Dawley rats were used. Small detrusor strips were permeabilized with β-escin. The contractile responses induced with agonists were compared between young and old groups. Carbachol-induced contractions were decreased in permeabilized detrusor from old rats compared to young group. Heparin and ryanodine decreased carbachol-induced contractions in young rats where only heparin inhibited these contractions in olds. Caffeine-induced contractions but not inositol triphosphate (IP₃)-induced contractions were decreased in old group compared to youngs. The cumulative calcium response curves (pCa 8–4) were also decreased in old rats. Carbachol-induced calcium sensitization responses did not alter by age where GTP-β-S and GF-109203X but not Y-27632 inhibited these responses. Carbachol-induced contractions decrease with aging in rat bladder detrusor. It can be postulated as IP₃-induced calcium release (IICR) is primarily responsible for the contractions in older rats where the decrease in carbachol contractions in aging may be as a result of a decrease in calcium-induced calcium release (CICR), rather than carbachol-induced calcium sensitization.     

Regional patterns of bone loss and altered bone remodeling in response to calcium deprivation in laboratory rabbits

Summary This study explores the effects of a calcium-deficient diet on patterns of bone remodeling, and examines regional differences in the amount of bone lost. Skeletally mature female rabbits (n=6) were fed a calcium-deficient diet (0.10% Ca²⁺ and 0.50% P) for 14 weeks. A separate group of rabbits (n=4) were fed a maintenance diet (1.2% Ca²⁺ and 0.45% P). Bone mineral content, serum calcium, and serum phosphorus were measured each week during the experimental period. Following sacrifice, the L₃ vetebra, femoral head, proximal tibial metaphysis, and tibial midshaft were analyzed histomorphometrically. Rabbits had 20% less vertebral bone after only 14 weeks of a calcium-deficient diet. As in human postmenopausal osteoporosis, bone loss in calcium-deficient rabbits occurs in the trabecular bone of the lumbar spine before that in the trabecular bone of the lower extremity. Calcium-deficient diets alone do not lead to increased osteoid volume or thickness. Because bone loss is relatively rapid and because the pattern of loss is similar in some respects to that found in humans, adult rabbits may provide an attractive model of calcium deficiency osteoporosis in a skeletally mature mammal in which remodeling is predominant over modeling.     

氢氧化钙预防根管治疗期间急症的临床观察

目的 观察氢氧化钙根管内封药对预防根管治疗期间急症的临床疗效。方法 使用氢氧化钙及传统根管内消毒药物樟脑对氯酚、甲醛甲酚根管内封药，观察疼痛指数并比较其根管治疗期间急症的发生率。结果 氢氧化钙封药后根管治疗期间急症的发生率最低，与传统药物相比，其差异有统计学意义。结论 氢氧化钙根管内封药。对预防根管治疗期间的急症有较好的作用。     

自固化磷酸钙人工骨修复骨缺损的临床应用

目的:探讨自固化磷酸钙人工骨(CPC)填充修复骨缺损的临床效果。方法:骨缺损94例,男59例,女35例;年龄11~72岁,平均39.4岁。骨缺损部位:胸腰椎38例,跟骨25例,胫骨15例,股骨7例,肱骨近端3例,桡骨远端5例,近节指骨1例。骨缺损原因:骨折塌陷复位后骨缺损63例,骨髓炎20例,骨囊肿6例,骨纤维异常增殖症4例,内生软骨瘤1例。骨缺损范围为1cm×1cm~4cm×20cm,用CPC填充修复,CPC充填量为3~42g,其中单纯CPC填充修复74例(胸腰椎骨折行椎体成形38例,骨折复位后空腔充填25例,良性骨肿瘤病灶刮除后充填11例),载药CPC填充修复骨髓炎20例。结果:所有患者均获随访,随访时间14~48个月,平均29.6个月。全部患者术后未见过敏或毒性反应,无皮疹或高热,血钙、磷、碱性磷酸酶均正常,切口无瘙痒感。随访时X线片显示,植入CPC与宿主骨接触紧密,界面处未见间隙存在,骨缺损处的解剖形状完全或大部分恢复,未见脱落现象,随访时部分患者CPC部分降解成骨。9例发生术后伤口渗出,为淡黄色清亮稀薄分泌物,细菌培养阴性,经换药后伤口愈合良好。结论:CPC填充修复骨缺损安全有效,并发症少,是理想的骨替代品,载药CPC是治疗骨髓炎的理想方法。     

Gating modifier toxins of voltage-gated calcium channels.

Some of the most potent and specific inhibitors of voltage-gated calcium channels are peptide toxins that inhibit channel function not by occlusion of the channel pore, but rather by interfering with the voltage dependence and kinetics of channel opening and closing. Many such gating modifier toxins conform to the inhibitor cystine knot structural family and have primary sequence or functional mechanism similar to toxins that target voltage-gated sodium or potassium channels. This review introduces known gating modifiers of calcium channels, discusses the selectivity, binding sites, and mechanism of the toxin-channel interaction, and reviews the usefulness of these toxins as research tools and as the basis for novel calcium channel pharmacology and therapeutics.     

Electrocrystallization of calcium carbonate on carbon-based electrodes

Calcium carbonate was deposited by electrochemical reduction of oxygen to hydroxyl ions at various carbon-based electrodes. Although some vaterite was observed during earlier stages of the electrodeposition, the predominant polymorph during later stages was calcite. The average crystal size reached a value of 15 μm after 10 h at a glassy carbon electrode but the crystal growth rate was substantially accelerated when oxygen was catalytically reduced. The same average size of the calcite crystals in this case (Pt/C electrode) was reached within a period of 1.5 h. Efficient removal of CaCO₃ from water was demonstrated when using a porous aerogel carbon electrode and a potential sufficiently negative to promote reduction of water molecules within the pores.     

The Effects of Zero Magnesium Dialysate and Magnesium Supplements on Ionised Calcium Concentration in Patients on Regular Dialysis Treatment

The effect of oral magnesium carbonate aluminium hydroxide onserum ionised calcium, total calcium, aluminium and magnesium,was assessed in 31 patients with chronic renal failure, duringand after one haemodialysis. The behaviour of ionised calcium and total calcium was the samein both groups. Each showed a slight fall during dialysis, whichwas not significant. Serum total calcium was 0.2–0.3 mmol/l(0.8–1.2 mg/dl) greater throughout the period of dialysisin the group taking aluminium hydroxide. Serum magnesium andaluminium were both lower in the group treated with magnesiumcarbonate. In the group taking magnesium carbonate, serum magnesium concentrationsfell markedly during dialysis, but otherwise were maintainedwithin the reference range by the use of a magnesium-free dialysate.These results show the effectiveness of magnesium carbonateoral phosphate-binding agents and zero magnesium dialysate inreducing serum aluminium without affecting the behaviour ofserum calcium fractions during dialysis.     

Direct cadiac electorphysiologic effects of sufentanil and vecuronium in isolated guinea-pig hearts

Sufentanil and vecuronium are commonly used simultaneously in anaesthesia. Bradycardia and asystole have been described immediately after the administration of these two compounds. Therefore, the purpose of the present study was to evaluate the direct cardiac effects of sufentanil and vecuronium in all parts of the cardiac pacemaker and conduction system.
The electrophysiological effects of sufentanil and vecuronium were studied in isolated spontaneously beating guinea-pig hearts perfused by the method of Langendorff. At a concentration of 0.1 μmol/1 sufentanil a significant reduction of the spontaneous sinus rate, prolongation of atrioventricular, intraventricular and His' bundle conduction could be observed. The highest concentration of 10 μmol/1 of sufentanil led to an overall slowing of conduction velocity and to an profound slowing of spontaneous sinus rate. AV nodal as well as atrial and ventricular refractoriness were markedly prolonged at this high concentration of sufentanil. In contrast, during perfusion with vecuronium at a concentration of 0.1 μmol/1 up to 10 μmol/1 no significant effects on cardiac conduction and pacemaker activity could be observed.
In conclusion, the electrophysiological effects of sufentanil are comparable to that of unspecific calcium antagonists. Therefore, especially in patients with a preexisting damage of the cardiac conduction system, the indirect effect of the combination of sufentanil and vecuronium which is predominantly responsible for bradycardia and asystole may be worsened by the direct effects of sufentanil.     

Parathyroid hormone decreases in vivo insulin effect on glucose utilization

Hyperparathyroidism is associated with impaired glucose tolerance, and parathyroidectomy may improve carbohydrate homeostasis. It has been suggested that parathyroid hormone (PTH) suppresses insulin secretion but it is unclear whether it also interferes with the peripheral action of insulin. To evaluate in vivo effects of PTH on insulinmediated glucose utilization, 15 male Sprague Dawley rats were continuously infused with rat PTH (1–34) using an Alzet miniosmotic pump at a rate of 0.03 nm/hour. Controls were infused with the vehicle alone. Following 5 days of PTH infusion, plasma calcium (Ca) levels were higher in the PTH-infused rats (12.3±0.2 versus 9.9±0.1 mg/dl, P<0.01). On the 5th day, glucose (700 mg/kg) and insulin (0.175 U/kg) were given as a bolus infusion through the left femoral vein, blood samples were obtained from the right femoral vein, and plasma glucose and insulin were measured at basal (0 minutes) and at 2, 5, 10, and 20 minutes postinfusion. Basal, nonfasting glucose levels were higher (166±4 versus 155±4 mg/dL, P<0.04) in the PTH-infused rats but their insulin levels were similar to those of controls (6.5±0.6 versus 5.6 ±0.5 ng/ml). Postinfusions and maximal (2 minutes) glucose and insulin levels were similar in both groups. However, although insulin levels were similar in both groups at all measured time points, glucose levels at 20 minutes were higher in the PTH-treated rats (205±13 versus 173±9; P<0.03). Also, calculated glucose disappearance rates (Kg) were decreased in the PTH-infused rats (4.05±0.3 versus 4.63±0.8; P=0.054), suggesting an impaired peripheral effect of insulin on glucose utilization. To gain insight into the potential contribution of the hypercalcemia or the PTH to these abnormalities, correlation evaluations were performed. Only in PTH-infused rats did plasma Ca correlate with plasma glucose at 0 and 20 minutes (r=0.6, P=0.02; r=0.7, P=0.01) and with the area under the glucose curve (r=0.6, P=0.03) during the glucose-insulin infusion. Also only in PTH-infused rats did PTH correlate with 0 (P=0.07) and 20-minute (P=0.02) plasma glucose levels. There was no correlation between either Ca or PTH and basal insulin levels or the area under the insulin curve in either group. Consequently, we suggest that in the rat, PTH infusion associated with hypercalcemia impairs insulin effect on glucose utilization in vivo and this defect may be induced by the Ca, PTH, or both.This study was presented in part at the 76th Annual Meeting of the Endocrine Society, Anaheim, CA, USA, June 1994.