用视诱发电位和富里叶变换作视力客观估计

目的:研究用图形视觉诱发电位(PVEP)和离散富里叶变换(DFT)作视力客观估计的方法。方法:检测对象为33只正常眼。用翻转频率为10次/秒,条纹张角分别为30、20、18、12、10、6、4和2弧分的垂直方波光栅图形刺激,记录相应的稳态图形视诱发电位。用离散富里叶交换提取WEP频谱中10Hz成分的幅值。以光栅条纹张角为横坐标、相应的VEP频谱幅值为纵坐标作关系曲线,取阈值附近的近似线性部分的数据点作直线回归,用外推法求得阈值和视力。结果:比较VEP所测之视力与用国际标准视力表所测之视力,可见在本研究中70％的受检眼VEP视力估计较准确。结论:用本研究中的VEP技术客观地测量视力可靠性较高。眼科学报1997;13:59～61。     

In Vivo Studies of Pulsatile Implantable Impeller Assist and Total Hearts

Abstract: A pulsatile impeller assist heart and a total heart were tested as a chronic left ventricular assist device in 5 calves and an acute biventricular assist device in 4 pigs respectively, to evaluate their blood compatibility. During the left ventricular assist experiments, the indicators for hemolysis, thrombogenesis, renal dysfunction, and hepatic dysfunction were measured preoperatively, at the beginning of the pumping, 6 h postoperatively, and every following day. The results demonstrated that the impeller assist heart causes no severe blood damage nor organ dysfunction in the experiments lasting up to 11 days. In biventricular assist experiments, the number of red blood cells, white blood cells, platelets, and the he-matocrit, hemoglobin, free hemoglobin, and lactate dehy-drogenase levels were tested preoperatively at the beginning of the pumping and every 2 h postoperatively. The data remained in acceptable ranges during experiments lasting 6 h. It is confirmed that the authors' impeller assist heart and total heart have the advantages of simplicity, implantability, and pulsatility with good blood compatibility.     

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.     

安吉复口服液的耐缺氧,耐低温和抗疲劳作用

采用缺氧、寒冷和负重游泳等方法,观察了安吉复口服液(0.025、0.1和0.4mg·kg~(-1),ig,qd×14d)对小鼠的耐缺氧、耐低温及抗疲劳作用.结果表明,安吉复口服液0.1、0.4mg·kg~(-1)可延长KCN中毒小鼠的存活时间及延长小鼠在寒冷环境中存活时间,而0.4mg·kg~(-1)可延长常压缺氧条件下小鼠存活时间及延长小鼠负重游泳时间.     

Behavioral, biochemical and neurotoxicological actions of the alpha-ethyl homologue of p-chloroamphetamine

The present set of experiments was designed to examine the effects of extension of the alpha-methyl of p-chloroamphetamine (PCA) to an alpha-ethyl. Therefore, the alpha-ethyl homologue of PCA, 1-(4-chlorophenyl)-2-aminobutane (CAB), was compared to PCA in a number of pharmacological assays. CAB was 2-fold less potent than PCA at inhibiting synaptosomal uptake of [3H]5-hydroxytryptamine ([3H]5-HT), and 5-fold less potent at inhibiting uptake of [3H]dopamine ([3H]DA). In drug discrimination assays, CAB was approximately 3-fold less potent than PCA in animals trained to discriminate 3,4-methylenedioxymethamphetamine (MDMA) or its alpha-ethyl homologue, S-(+)-N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine (S-(+)-MBDB), from saline. Monitoring with in vivo microdialysis, 10 mg/kg of PCA caused a large increase in extracellular DA and a significant decrease in 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum. In contrast, 11 mg/kg CAB caused no increase and 22 mg/kg CAB caused only a slight increase in extracellular DA. Both doses of CAB caused a decrease in extracellular DOPAC. The potential 5-HT neurotoxicity of CAB was examined by measuring monoamine and metabolite levels and [3H]paroxetine binding at one week following acute doses. A 10 mg/kg dose of PCA caused an 80% decrease in cortical and hippocampal serotonergic markers, while an equimolar dose of CAB decreased only hippocampal 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels. However, 22 mg/kg of CAB produced a 20-40% decrease in all serotonergic markers. Thus, extension of the alpha-alkyl significantly decreases the dopaminergic effects of PCA. The similar decrease in relative 5-HT neurotoxicity and the decreased ability to alter dopaminergic systems in vivo and in vitro supports the involvement of DA in the neurotoxicity of PCA.