间接免疫荧光法检测婴幼儿急性下呼吸道合胞病毒感染的特异性IgM

本文对1984年1～3月和1985年3～8月共107例急性下呼吸道感染的住院患儿,采用间接免疫荧光法检测其急性期血清抗RSV特异性IgM抗体,并与病毒分离和/或中和试验比较,敏感性为82.1％,特异性为71.8％。RSV感染患儿发病后3天内大多数病例即可从血清中检测出RSV-IgM,因此该法具有早期诊断价值。     

Intrathecal fentanyl prolongs sensory bupivacaine spinal block

The purpose of investigation was to study the effect of intrathecal fentanyl on the onset and duration of hyperbaric bupivacaine-induced spinal block in adult male patients. Fortythree patients undergoing lower extremity or genitourinary surgery were enrolled to receive either 13.5 mg hyperbaric bupivacaine 0.75% + 0.5 ml CSF it, (Group I) or 13.5 mg hyperbaric bupivacaine 0.75% + 25 μg fentanyl it, (Group II) according to a randomized assessor-blind protocol. The onset and duration of sensory block were assessed by pinching the skin with forceps in the midclavicular line bilaterally every two minutes for first twenty minutes and then every five to ten minutes. Similarly, the onset and duration of motor block were assessed and graded at the same time intervals using the criteria described by Bromage. The time required for two sensory segment regression and sensory regression to L₁ dermatome was 74 ± 18 and 110 ± 33 min vs 93 ± 22 and 141 ± 37 min in Groups I and II, respectively (P < 0.05). Intrathecal fentanyl did not enhance the onset of sensory or motor block, or prolong the duration of bupivacaine-induced motor spinal block. Fewer patients demanded pain relief in the fentanyl-treated group than in the control group in the early postoperative period (19% vs 59%; P < 0.05). Episodes of hypotension were more frequent in the fentanyl-treated group than in the control group (43% vs 14%; P < 0.05). We conclude that fentanyl, 25 μg it, prolonged the duration of bupivacaine-induced sensory block (sensory regression to L₁ dermatone) by 28% and reduced the analgesic requirement in the early postoperative period following bupivacaine spinal block.     

雷公藤双层栓的研制

介绍了雷公藤双层栓的制备和质量检查。雷公藤双层栓的上层为空白层,下层为含药层。空白层可有效地阻止后端所释药物向上扩散,从而避免相当部分药物经门肝系统吸收,因此可明显提高其生物利用度。     

动脉粥样硬化形成和消退的形态学研究

本文报告动脉粥样硬化(AS)形成和消退研究的部分工作。在复制AS形成和消退模型的基础上,研究了AS形成和消退中的内皮细胞、平滑肌细胞和单核细胞的改变。     

Brain natriuretic peptide enhances the endothelium-independent cAMP and vasorelaxant responses of calcitonin gene-related peptide in rat aorta

Calcitonin gene-related peptide (CGRP) causes vasorelaxation in rat aorta involving endothelium/nitric oxide (NO)-dependent elevations of both cAMP and cGMP levels. When endothelium is removed, preincubation with exogenous NO uncovers and potentiates direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP. This enhancing effect of NO potentially involves elevation of cGMP and inhibition of Type III (cGMPinhibitable) phosphodiesterase, causing accumulation of cAMP. However, NO may have other actions. The aim of the present study was to determine if brain natriuretic peptide (BNP), which elevates cGMP levels independent of NO, could enhance cAMP accumulations and vasorelaxations induced by CGRP in rat aortic rings denuded of endothelium. When added separately, neither CGRP (100 nM) nor BNP (10 nM) altered cAMP levels. When added in combination, CGRP (100 nM) and BNP (10 nM) significantly elevated cAMP levels (from control of 0.95 ± 0.08 to 1.53 ± 0.09 pmol/mg protein) at 2 min. BNP (10 nM) elevated cGMP levels 10-fold at 2 min and this response was not altered by co-administration of CGRP (100 nM).Pretreatment with BNP at concentrations as low as 1 nM in endothelium-denuded aortic rings greatly enhanced the direct vasorelaxant effects of CGRP (100 nM) (from control of 0% to 57.6 ± 6.8% relaxation of phenylephrineprecontractions). Our findings indicate that BNP enhances direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP in rat aorta, thus supporting the concept that cGMP inhibits cAMP metabolism and enhances CGRP-induced responses in aortic smooth muscle cells.     

钙拮抗剂TMB-8抑制BHQ,NE和KCl引起的培养乳牛基底动脉单个平滑肌细胞内游离钙的升高

用AR CM MIC阳离子测定系统,测量单个细胞内游离钙浓度([Ca²⁺]i),研究8-(N,N-二乙胺)-n-辛基 3,4,5-三甲氧基苯甲酸酯(TMB-8)对培养乳牛基底动脉平滑肌[Ca²⁺]i的作用。在细胞外钙浓度为1.3mmol·L^-1时,TMB-8(30μmol·L^-1)可明显抑制BHQ,NE及KCl引起[Ca²⁺]i的升高。在细胞外钙为零+EGTA 0.1mmol·L^-1时,TMB-8(10,30及100μmol·L^-1)可浓度依赖性地降低静息[Ca²⁺]i,TMB-8(30μmol·L^-1)可几乎完全阻断BHQ及NE引起[Ca²⁺]i的增加。研究表明TMB-8降低培养乳牛基底动脉平滑肌[Ca²⁺]i的机制,主要是抑制肌浆网Ca²⁺的释放,或增加肌浆网对Ca²⁺的摄入,并由此间接地抑制细胞外钙的内流。     

神经肽Y对免疫细胞活性的影响

神经肽Y（NPY）是广泛分布于中枢神经系统和外周神经各部位的神经肽类物质。本实验观察NPY在体外对几种免疫细胞活性的直接作用。结果表明，NPY对小鼠T淋巴细胞丝裂原反应性和NK细胞的杀伤活性均无明显影响（P＞0．05），对巨噬细胞分泌溶菌酶有明显抑制作用（P＜0．05）；而对B淋巴细胞丝裂原反应性则有明显的促进作用（P＜0．05）。上述结果提示，NPY对部分免疫细胞功能的影响因细胞种类而异。