马桑内酯对培养的大鼠大脑皮层神经元γ─氨基丁酸、生长抑素分泌的影响

本文利用培养的大鼠大脑皮层神经元,在不同浓度马桑内酯（５μｍｏｌ／Ｌ～２５０μｍｏｌ／Ｌ）作用后１２、２４、４８小时,应用双抗夹心法检测各时间点培养上清中γ－氨基丁酸和生长抑素含量。结果表明,各浓度中以２５μｍｏｌ／Ｌ马桑内酯作用最明显,在此浓度作用后１２小时,γ－氨基丁酸分泌受抑（抑制率为８．３％）,生长抑素分泌则增加（增加率为２０．４％）。作用后２４、４８小时,γ－氨基丁酸分泌进一步受抑（抑制率为１０．６％、１４．５％）,而生长抑素分泌则呈现增加幅度降低趋势（增加率为１１．７％、８．２％）。与未加药组相比,γ－氨基丁酸在三个时间点均有统计学意义（Ｐ＜０．０５）,而生长抑素只在加药后１２小时有统计学意义（Ｐ＜０．０５）、本文对马桑内酯作用后两种神经递质变化的意义进行了讨论。     

体外培养大鼠星形细胞的缺糖缺氧性损伤及药物的保护

本实验用大鼠星形细胞体外培养模型,观察了细胞在不同条件下乳酸脱氨酶（ＬＤＨ）的漏出。发现当去掉葡萄糖后,细胞缺氧５和７ｈ后ＬＤＨ漏出明显增加,５ｂ为５９．７±２５．３Ｕ／ｍｇ蛋白（对照组２４．７±１６．３,Ｐ＜０．０５）,７ｈ为６８．３±８９Ｕ／ｍｇ蛋白（对照组３９．９±２１２,Ｐ＜０．０１）。用３－氧－甲基－［１－￣３Ｈ］－Ｄ－葡萄糖摄取法测量细胞体积,结果显示缺糖缺氧５ｈ后细胞明显肿胀,从对照组的４．１±１．２增加到８．１±３．２μｌ／ｍｇ蛋白（Ｐ＜０．０１）。丹参有效成分７６４－３在０．５至５０μｍｏｌ／Ｌ时能减少缺糖缺氧细胞ＬＤＨ漏出;在５０μｍｏｌ／Ｌ时能减小缺糖缺氧细胞的体积。谷氨酸受体拮抗剂ＤＮＱＸ（６,７－ｄｉｎｉｔｒｏｑｕｉｎｏｘａｌｉｎｅ－２,３ｄｉｏｎｅ）５０μｍｏｌ／Ｌ能减轻星形细胞肿胀和ＬＤＨ漏出。     

α_1肾上腺素能受体介导去甲肾上腺素促大鼠培养心肌细胞蛋白质合成效应

在无血清和含１．０％、５．０％血清培养的新生大鼠心肌细胞标本上,去甲肾上腺素（ＮＥ,２．０μｍｏｌ／Ｌ）使细胞蛋白质含量（Ｌｏｗｒｙ法）分别比相应对照组增加４０％、２６％、１９％（Ｐ均＜０．０１）;细胞３Ｈ－亮氨酸参入量与ＮＥ浓度呈正性剂量依赖性,最大效应浓度为２０．０μｍｏｌ／Ｌ;无血清培养体系中,０．２、２．０、２０μｍｏｌ／Ｌ的ＮＥ使参入量分别比对照增加１７．８％、３５３％、３７．７％;１．０％血清培养体系中分别比对照增加１６．２％、２７．９％、３１．６％（Ｐ均＜０．０５）;哌唑嗪（２．０μｍｏｌ／Ｌ）可阻断ＮＥ的促蛋白质合成作用,心得安（２．０μｍｏｌ／Ｌ）则无此效应。提示在无血清或低浓度血清培养体系中,ＮＥ可促进心肌细胞蛋白质合成,增加细胞蛋白质含量,该作用可能是通过α１肾上腺素能受体介导。     

SNP抑制5-HT诱导的胞内游离钙浓度升高和内钙释放

用Ｆｕｒａ － ２／ＡＭ 荧光测量技术研究了５ － 羟色胺（５－ ＨＴ） 诱导的大鼠尾动脉平滑肌细胞胞内钙升高和一氧化氮（ＮＯ） 的抑制效应。实验表明, 胞外０ｍ ｍｏｌ／ Ｌ Ｃａ２ ＋ 时胞内静息［Ｃａ２ ＋ ］ ｉ 为２０ ．２±８ ．６ｎｍｏｌ／Ｌ（ｎ ＝ ８） 。１０μｍｏｌ／Ｌ ５－ ＨＴ 可诱导出胞内钙库释放引起的瞬态［Ｃａ２ ＋］ｉ 升高,其峰值达２４５ ．７ ±７１．６ｎｍｏｌ／ Ｌ（ｎ ＝ ６） 。１０ － ７ ｍｏｌ／Ｌ 硝普钠（ＳＮＰ） 可抑制５－ ＨＴ 诱导的［Ｃａ２ ＋］ｉ 升高,其峰值浓度降为７５．１±３５ ．９ｎｍｏｌ／Ｌ（ｎ ＝ ５） 。当细胞浴液含２．５ｍ ｍｏｌ／Ｌ Ｃａ２ ＋ 时,静息［Ｃａ２ ＋］ｉ为１１２ ．８ ±１０ ．３ｎｍｏｌ／ Ｌ（ｎ ＝ ５） , 这时１０μｍｏｌ／ Ｌ ５ － ＨＴ 可诱导［Ｃａ２ ＋ ］ ｉ 的峰值为２５２ ．３ ±８０ ．６ｎｍｏｌ／Ｌ（ｎ ＝ ４） ,以及其后平台浓度为１４３ ．０ ±３７ ．６ｎｍｏｌ／Ｌ（ｎ ＝ ４） ,略大于［Ｃａ２ ＋］ｉ 为１１２．８ ±１０ ．３ｎｍｏｌ／Ｌ 的静息浓度,为外钙内流引起。１０ － ７ ｍｏｌ／Ｌ ＳＮＰ 也可抑制５－ ＨＴ 诱导［Ｃａ２ ＋ ］ｉ 平台相浓度。平台浓度由１４３ ±４７     

γ—氨基丁酸（GABA）对离体大鼠卵巢颗粒细胞孕酮分泌的影响

本文观察了ＧＡＢＡ对大鼠分散颗粒细胞生孕酮的影响。结果表明：当ＧＡＢＡ浓度为１０＾－＾６ｍｏｌ／Ｌ时明显促进颗粒细胞基础孕酮分泌（Ｐ＜０．０５）。但更高浓度（１０＾－＾５ｍｏｌ／Ｌ）时则表现抑制ＨＣＧ刺激孕酮生成的效应（Ｐ＜０．０２）。提示颗粒细胞的激素分泌功能可能受到ＧＡＢＡ的调控。     

2.5次微分伏安法对生物品中丙二醛的测定

以０．１ｍｏｌ／ＬＮＨ４Ｃｌ溶液为介质,用２．５次微分伏安法测定了丙二醛,线性范围为１．０＊１０＾－６至１．０＊１０＾－３ｍｏｌ／Ｌ,检测限达１．０＊１０＾－７ｍｏｌ／Ｌ。并测定了细胞培养液介质中新生ＳＤ大鼠室肌细胞样品的丙二醛。     

大鼠红细胞葡萄糖代谢的异头物选择性

为研究大鼠红细胞对葡萄糖利用的异头物选择性及其作用机制,应用大鼠红细胞,对葡萄糖的两种异头物作了异构化速率、乳酸生成量、内流速度和大鼠红细胞已糖激酶作用下的磷酸化速度等进行了测定．结果指出,３７℃时大鼠红细胞的Ｄ－葡萄糖β－异头物和α－异头物代谢成乳酸的速度分别是０．２７μｍｏｌ／ｇＨｂ（３ｍｉｎ）和０．２１μｍｏｌ／ｇＨｂ（３ｍｉｎ）,即前者快于后者３０％．同时β－Ｄ－葡萄糖向红细胞内转运速度也快于后者：分别是５．０和３．５μｍｏｌ／ｇＨｂ（３ｍｉｎ）．大鼠红细胞已糖激酶的葡萄糖磷酸化速率实验结果指出：β－异头物比α－异头物快３０％;对于该两种异头物已糖激酶的Ｋｍ值均为５３μｍｏｌ／Ｌ．红细胞与α－和β－Ｄ－葡萄糖保温１ｍｉｎ后,其葡萄糖浓度均达到１ｍｍｏｌ／Ｌ左右,说明至少在１ｍｉｎ内对于已糖激酶的磷酸化此两种异头物的葡萄糖浓度均已饱和．这些结果提示,大鼠红细胞葡萄糖利用的β－异头物优选性主要与其磷酸化速度有关,而与其转运速度关系不大．     

大鼠肾上腺单个嗜铬细胞分泌儿茶酚胺的电化学检测

报道以直径７μｍ的碳纤丝制作碳纤电极,在原代培养的大鼠肾上腺单个嗜铬细胞上检测诱发的儿茶酚胺激素分泌。当用微管向细胞吹加１０ｍｍｏｌ／Ｌ乙酰胆碱或６０ｍｍｏｌ／Ｌ氯化钾时,２－５ｓ延迟后记录到数目不等的峰形信号。峰信号上升快（约１ｍｓ）;衰减则较慢,呈指数形状。峰信号的检测要求电极上所加氧化电压足够大。实验表明,以高钾刺激时,该峰信号依赖于外钙（２ｍｍｏｌ／Ｌ）的存在。根据峰信号对应于嗜铬细胞内单个囊泡的儿茶酚胺量子化释放的事实,我们推算每次量子化释放的儿茶酚胺约为１０－２０—１０－１８ｍｏｌ量级。     

运动对大鼠血小板L—精氨酸转运的影响

本工作在游泳大鼠模型上,观察血小板Ｌ－精氨酸（Ｌ－Ａｒｇ）转运特征,并观察凝血酶和ＰＡＦ对血小板Ｌ－Ａｒｇ转运的影响。结果发现,运动大鼠血小板Ｌ－Ａｒｇ转运明显高于未运动对照大鼠,表现在高亲和性最大转运速率（Ｖｍａｘ）明显增高（５０．５６±３．２７ｐｍｏｌ／１０８ｖｓ４５．８４±２．３６ｐｍｏｌ／１０８血小板／ｍｉｎ。Ｐ＜０．０５）,米氏常数亦显著增加（２．１４±０．２３μｍｏｌ／Ｌｖｓ１．４６±０．１３μｍｏｌ／Ｌ,Ｐ＜０．０１）。应用刺激剂凝血酶和ＰＡＦ诱导运动大鼠血小板Ｌ－Ａｒｇ转运速率增加的幅度明显高于未运动对照大鼠（Ｐ＜０．０１）。实验结果表明,运动能增强血小板转运Ｌ－Ａｒｇ的效率。提示,运动可能促进血小板一氧化氮（ＮＯ）生成,抑制血小板聚集,防治血管栓塞性疾病     

EDRF对PE引起的大鼠主动脉缩血管效应的作用

本文研究ＥＤＲＦ（ｅｎｄｏｔｈｅｌｉｕｍ－ｄｅｒｉｖｅｄｒｅｌａｘｉｎｇｆａｃｔｏｒ,ＥＤＲＦ）对ＰＥ（ｐｈｅｎｙｌｅｐｈｒｉｎｅ）引起的大鼠主动脉收缩反应的影响。内皮完整和去内皮的大鼠主动脉环悬挂于器官浴槽中,测定血管的张力和收缩速度的变化。所有的实验在消炎痛（ｉｎｄｏｍｅｔｈａｃｉｎ,１０μｍｏｌ／Ｌ）存在下进行。用美兰（ｍｅｔｈｙｌｅｎｅｂｌｕｅ,ＭＢ,１０μｍｏｌ／Ｌ）或左旋硝基精氨酸（ＮＧ－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅ,Ｌ－ＮＮＡ,３０μｍｏｌ／Ｌ）处理内皮完整的大鼠主动脉环,ＰＥ的剂量－收缩张力曲线明显左移,ＥＣ３０值均降低５倍,最大反应比率分别为１．６±０．４和１．６±０．５。在去内皮的大鼠主动脉环中,经ＭＢ和Ｌ－ＮＮＡ处理后,仍可见ＥＣ３０下降３倍,最大反应比率均为１．０±０．２。后者可能与血管平滑肌产生少量ＥＤＲＦ有关。我们的结果提示ＰＥ对血管的收缩反应也受血管内皮和平滑肌产生的ＥＤＲＦ的调控     

Angiotensin II Increases Catecholamine Release from Bovine Adrenal Medulla but Does Not Enhance That Evoked by K+ Depolarization or by Carbachol

The effect of angiotensin II on catecholamine release from bovine adrenal medulla has been investigated. In retrogradely perfused, isolated bovine adrenal glands, angiotensin II increased basal efflux of catecholamines, but the presence of angiotensin II did not increase the release of catecholamines evoked either by bolus injections of the secretagogue carbachol or by depolarization with a perfusing solution containing a raised concentration of K+. In chromaffin cells maintained in primary tissue culture, angiotensin II increased 3H release from cells preloaded with [3H]-noradrenaline but did not enhance the release evoked by carbachol or by depolarization with K+. The increase in 3H release evoked by angiotensin II from chromaffin cells in tissue culture was inhibited by its analogue antagonist Sar1,Ala8-angiotensin II (saralasin) and was entirely dependent on the presence of Ca2+ in the experimental medium. These findings suggest that, in the chromaffin cells of the bovine adrenal medulla, angiotensin II acts on specific receptors to cause a calcium-dependent catecholamine release but triggers no additional response that acts synergistically with depolarizing or nicotinic stimuli to augment catecholamine release.     

Modulation of catecholamine release by endogenous adenosine in the rat adrenal medulla

Adenosine was shown to inhibit norepinephrine (NE) release from sympathetic nerve endings. The purpose of this study was to examine whether endogenous adenosine restrains NE and epinephrine release from the adrenal medulla. The effects of an adenosine receptor antagonist, 1,3-dipropyl-8-(p-sulfophenyl) xanthine (DPSPX), on epinephrine and NE release induced by intravenous administration of insulin in conscious rats were examined. Plasma catecholamines were measured by HPLC with an electrochemical detector. DPSPX significantly increased plasma catecholamine in both control rats and rats treated with insulin. The effect of DPSPX on plasma catecholamine was significantly greater in rats treated with insulin. Additional experiments were performed in adrenalectomized rats to investigate the contribution of the adrenal medulla to the effect of DPSPX on plasma catecholamine. The effect of DPSPX and insulin on epinephrine in adrenalectomized rats was significantly reduced compared with that of the controls. Finally, we tested whether endogenous adenosine restrains catecholamine secretion partially through inhibiting the renin-angiotensin system. The effect of DPSPX on plasma catecholamine in rats pretreated with captopril (an angiotensin-converting enzyme inhibitor) was reduced. These results demonstrate that under basal physiological conditions, endogenous adenosine tonically inhibits catecholamine secretion from the adrenal medulla, and this effect is augmented when the sympathetic system is stimulated. The effect of endogenous adenosine on catecholamine secretion from the adrenal medulla is achieved partially through the inhibitory effect of adenosine on the renin-angiotensin system.     

Fetal adrenal VIP: distribution and effect on medullary catecholamine secretion

Vasoactive intestinal peptide (VIP) was found in the adrenal gland of ovine fetuses at 130-135 days gestation and was shown to stimulate catecholamine secretion. VIP was demonstrated by immunocytochemistry using the indirect antibody-enzyme method. VIP-immunoreactive nerve fibers were observed in the capsule, zona glomerulosa and inner layer of the cortex as well as in the medulla; furthermore small clusters of VIP-containing cell bodies were found at the corticomedullary border. To study the direct effect of VIP on catecholamine release, fetal adrenal medulla was dispersed into single cells and incubated in vitro with VIP for 6 hours. Catecholamine release into the medium was measured at 1, 3 and 6 hours. At 6 hours of incubation, VIP stimulated total catecholamine release from fetal adrenomedullary cells in a dose-dependent manner at concentrations ranging from 10(-8) to 10(-4) M. The release of norepinephrine and epinephrine, but not dopamine, was significantly enhanced. The presence of VIP in the fetal adrenal cortex and medulla, and the ability of VIP to stimulate catecholamine release from fetal adrenomedullary cells in vitro suggest that VIP may be an important modulator of medullary catecholamine secretion during fetal life.     

B and C Types Natriuretic Peptides Modify Norepinephrine Uptake and Release in the Rat Adrenal Medulla

Vatta, M. S., M. F. Presas, L. G. Bianciotti, M. Rodriguez–fermepin, R. Ambros and B. E. Fernandez. B and C types natriuretic peptides modify norepinephrine uptake and release in the rat adrenal medulla. Peptides 18(10) 1483–1489, 1997.—We have previously reported that atrial natriuretic factor (ANF) modulates adrenomedullar norepinephrine (NE) metabolism. On this basis, the aim of the present work was to study the effects of B and C types natriuretic peptides (BNP and CNP) on the uptake, intracellular distribution and release of ³H-NE. Experiments were carried out in rat adrenal medulla slices incubated “in vitro.” Results showed that 100 nM of both, CNP and BNP, enhanced total and neuronal NE uptake. Both peptides (100 nM) caused a rapid increase in NE uptake during the first minute, which was sustained for 60 min. NE intracellular distribution was only modified by CNP (100 nM), which increased the granular fraction and decreased the cytosolic pool. On the other hand, spontaneous as well as evoked (KCl) NE release, was decreased by BNP and CNP (50 and 100 nM for spontaneous release and 1, 10, 50 and 100 nM for evoked output). The present results suggest that BNP and CNP may regulate catecholamine secretion and modulate adrenomedullary biological actions mediated by catecholamines, such as blood arterial pressure, smooth muscle tone, and metabolic activities.     

类α-蝎神经毒素BmKⅠ对离体大鼠心脏收缩力及电活动的特异调控

本研究探讨了一种特异性钠通道调制剂(Buthus martensi Karsch,BmKⅠ)对离体大鼠心脏收缩力及电活动的调制作用.离体心脏灌流实验显示(1)BmKⅠ(0.5-10 μmol/L)剂量依赖地增强大鼠心肌收缩力,左心室最大发展压(LVDPmax)以及dp/dtmax与对照组相比均显著增强(n=6,P＜0.05),同时可触发正性变时作用(n=6,P＜0.05);(2)大剂量BmKⅠ(20μmol/L)引起负性肌力作用及心动过缓;(3)冠脉流量随心脏收缩力的增强反而减小,应用500nmol/L BmKⅠ时冠脉流量由14.5 ml/min降至8.6 ml/min(n=6,P＜0.05);此外,心电图记录表明BmKⅠ(0.5-10μmol/L)可触发心动过速及复杂的心律失常等电活动变化;正常灌流液洗脱后BmKI引起的大鼠心脏收缩力及电活动的改变可部分恢复.由于β-肾上腺素能受体阻滞剂普奈洛尔预先应用抑制了儿茶酚胺类神经递质的释放,提示BmKⅠ引起的大鼠心脏收缩力及电活动的改变不是由于其调节儿茶酚胺类神经递质的释放及随后β-肾上腺素能受体的激活,而可能与其对心肌电压门控钠通道的调控有关.     

Neurochemical Characterization of Extracellular Serotonin in the Rostral Ventromedial Medulla and Its Modulation by Noxious Stimuli

Abstract: Using in vivo microdialysis, we have characterized serotonin release from the rostral ventromedial medulla of the freely moving rat. Addition of tetrodotoxin or removal of calcium from the dialysis solution diminished the dialysate serotonin content, suggesting that spontaneous, calcium channel- and sodium channel-dependent neuronal release mechanisms contribute to the extracellular serotonin collected from the rostral ventromedial medulla. Extracellular serotonin concentration was increased by depolarization (with 100 m M potassium) and by the local administration of either a reuptake blocker (citalopram), a monoamine oxidase inhibitor (pargyline), or amphetamine. Serotonin release was reduced significantly by 8-hydroxy-2-(di- n -propylamino)tetralin, suggesting that serotonin_1A receptors may regulate release from rostral ventromedial medulla neurons. Because the basal serotonin concentration in the rostral ventromedial medulla was approximately twofold higher than that collected from the rostral ventrolateral medulla, a region that contains serotonin terminals but many fewer cell bodies, the possibility of release of serotonin from rostral ventromedial medulla neurons is discussed. Finally, intraplantar formalin injection significantly increased serotonin release, suggesting that this neurotransmitter contributes to nociceptive modulation by regulating the outflow of the rostral ventromedial medulla neurons.     

Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1-100 micromol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 micromol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 micromol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1 micromol/L), blocker of small conductance Ca2+-dependent K+ channels, was not able to affect the response to SNP. Ciclopiazonic acid (10 micromol/L) or thapsigargin (0.1 micromol/L), sarcoplasmatic reticulum Ca2+-ATPase inhibitors, decreased the SNP-inhibitory effects. Ryanodine (10 micromol/L), inhibitor of Ca2+ release from ryanodine-sensitive intracellular stores, significantly reduced the SNP inhibitory effects. The membrane permeable analogue of cGMP, 8-bromoguanosine 3',5'-cyclic monophosphate (100 micromol/L), also reduced spontaneous mechanical activity, and its effect was antagonized by ryanodine. The present study suggests that NO causes inhibitory effects on longitudinal smooth muscle of mouse ileum through cGMP which in turn would activate the large conductance Ca2+-dependent K+ channels, via localized ryanodine-sensitive Ca2+ release.     

Catecholamine secretion from the adrenal medulla of the fetus, regulation by hormones

In the ovine fetus, the adrenal medulla activity secretes catecholamines into the circulation under normal and stress conditions. Little is known regarding the endocrine regulation of adrenal medullary catecholamine secretion in the fetus. The present study was undertaken to investigate the direct effects of the hormones prolactin, angiotensin II and cortisol on catecholamine release from fetal adrenal medulla, and to determine whether the effect of the hormones change during development into adulthood. Adrenal medulla from fetal, newborn and adult pregnant sheep was collected, dispersed into single cells and plated. Following preincubation, the cells were treated with ovine prolactin or angiotensin II at 8, 40 and 200 micrograms/ml; or cortisol at 10(-8), 10(-7) and 10(-6)M for 24 h. Catecholamine release into the medium were measured at 3, 6, 12 and 24 h. Ovine prolactin at 8 to 200 micrograms/ml significantly stimulated the release of total catecholamines after 12 h of incubation. The effect of prolactin was dose-dependent such that the magnitude of the response increased and the response time shortened with increasing concentrations of prolactin. In addition, the release of all three catecholamines--dopamine, norepinephrine and epinephrine--was significantly elevated. In newborn cells, only the highest concentration of 200 micrograms/ml ovine prolactin stimulated total catecholamine release at 6 h and 12 h, with significant increases of the three catecholamines at 12 h. In maternal cells, stimulation of catecholamine release was observed also with the highest concentration of prolactin tested (200 micrograms/ml) and after 12 h of incubation, when only the release of epinephrine was significantly enhanced by 324%.(ABSTRACT TRUNCATED AT 250 WORDS)     

银杏苦内酯B对豚鼠模拟缺血心室肌细胞L-型钙电流及胞内游离钙的影响

应用全细胞膜片钳及激光共聚焦技术 ,研究银杏苦内酯B(ginkgolideB ,GB)对豚鼠心室肌细胞L 型钙电流及胞内游离钙的作用 ,并探讨GB心肌保护作用的机制。实验结果显示 ,在指令电压为 0mV时 ,GB对生理状态下豚鼠心室肌细胞L 型钙电流无明显作用。在模拟缺血状态下 ,L 型钙峰值电流减小 3 7 71% ,但加入 1μmol/LGB后 ,可逆转缺血引起的L 型钙电流的降低 ,与缺血对照组比较 ,有显著性差异 (P <0 0 5 )。 1μmol/LGB能使由于模拟缺血而上移的L 型钙电流 电压曲线回复正常。在生理状态下 ,0 1、1、10mol/LGB分别使心肌细胞内游离钙降低 10 5 8%(n =12 )、17 2 7% (n =12 )、16 3 5 % (n =10 ) ,与对照组相比有非常显著性差异。模拟缺血液灌流 12min时 ,细胞内游离钙浓度增加 2 0 15 % ,在模拟缺血液中分别加入 1μmol/Lnifedipine或 5mmol/LNiCl2 ,结果显示 :模拟缺血液灌流 12min ,与正常对照组相比细胞内钙分别增加 18 18% (P >0 0 5 )与 11% (P <0 0 5 )。在模拟缺血液中加入1mol/LGB灌流 12min时细胞内钙仅增加 9 60 % (n =12 ,P <0 0 0 1) ,与缺血对照组相比有显著性差异 (P <0 0 5 )。结果表明 ,GB可逆转模拟缺血造成L 型钙电流的降低 ,同时可部分减轻由于缺血所造成的细胞内钙的超载     

Role of TrkB expression in rat adrenal gland during acute immobilization stress

Expression of tyrosine receptor kinase B (TrkB), a receptor for brain‐derived neurotrophic factor (BDNF), is markedly elevated in the adrenal medulla during immobilization stress. Catecholamine release was confirmed in vitro by stimulating chromaffin cells with recombinant BDNF. We investigated the role of TrkB and the localization of BDNF in the adrenal gland during immobilization stress for 60 min. Blood catecholamine levels increased after stimulation with TrkB expressed in the adrenal medulla during 60‐min stress; however, blood catecholamine levels did not increase in adrenalectomized rats. Furthermore, expression of BDNF mRNA and protein was detected in the adrenal medulla during 60‐min stress. Similarly, in rats undergoing sympathetic nerve block with propranolol, BDNF mRNA and protein were detected in the adrenal medulla during 60‐min stress. These results suggest that signal transduction of TrkB in the adrenal medulla evokes catecholamine release. In addition, catecholamine release was evoked by both the hypothalamic–pituitary–adrenal axis and autocrine signaling by BDNF in the adrenal gland. BDNF–TrkB interaction may play a role in a positive feedback loop in the adrenal medulla during immobilization stress.