高原低氧大鼠肺组织超微结构及其低氧诱导因子1α的表达

背景：低氧诱导因子1α可介导哺乳动物细胞适应低氧环境。 目的：观察高原低氧对大鼠肺组织超微结构的影响及其低氧诱导因子1α表达变化。 方法：将SD大鼠分别为进行高原低氧干预1,2,3和30 d,并设置对照组。4个高原低氧组由海拔5 m的西安地区途中耗时1 d带到海拔2 700 m的青海格尔木地区、途中耗时2 d带到海拔5 000 m的唐古拉地区,途中耗时3,30 d分别带到海拔4 500 m的西藏那曲地区。 结果与结论：光镜及电镜观察显示,急性高原低氧2 d组肺组织出现明显的高原肺水肿,急性高原低氧30 d组低氧诱导因子1α mRNA的表达明显增高(P < 0.01),高原肺水肿现象则明显减轻。结果证实,低氧习服后肺组织低氧诱导因子1α mRNA表达的提高有利于减轻高原肺水肿。     

NF-κB的活性和iNOS基因表达在低氧性肺动脉高压中的变化

目的：探讨NF-κB的活性及iNOS基因表达在低氧性肺动脉高压（HPH）发病过程中的变化。方法：复制低氧性肺动脉高压大鼠模型，用免疫组化、原位杂交、半定量逆转录-聚合酶链式反应（RT-PCR）和Western blot等方法进行检测。结果：iNOS mRNA在腺泡内肺动脉（IAPA）的表达，低氧28 d（H28d）组染色强于正常（N）组、低氧5 d（H5d）组和低氧14 d（H14d）组。半定量RT-PCR证实低氧肺组织iNOS mRNA含量在H28d组分别是N组、H5d组和H14d组的2.1倍、1.9倍和1.8倍。H28d组肺组织NF-κB的核染色增多，I-κBα的含量在N组、H5d组和H14d组分别是H28d组的2.7倍、2.8倍和2.5倍。结论：在HPH中NF-κB的激活可能与低氧肺血管构建及iNOS mRNA的表达有关。     

一氧化碳饱和血红蛋白通过抑制TREM-1/TLR4通路发挥对高原低氧心脏损伤的保护作用

目的：探究一氧化碳饱和血红蛋白（CO-HBOC）能否通过抑制TREM-1/TLR4通路调节免疫,减轻炎症反应,发挥对高原低氧心脏损伤的保护作用。方法：30只雄性C57/BL6小鼠随机分为常氧生理盐水（NS）组、高原低氧生理盐水（HS）组和高原低氧CO-HBOC(HC)组。低氧组置于低压低氧动物实验舱模拟海拔5 500 m高原环境。实验舱运行时间为24 h/d,控制昼夜比约12 h∶12 h,连续低氧处理7 d;NS组置于相同条件的常压常氧环境下饲养。在建模过程中,HC组给予0.3 g Hb/kg/d CO-HBOC连续处理3 d,NS组和HS组给予等量生理盐水。采用心肌酶和心肌组织HE染色分析评估心肌组织损伤程度,qPCR和ELISA分别检测心肌组织和血浆中IL-1β、TNF-α表达,Western blot检测心肌组织髓源细胞表面触发受体1(TREM-1)、Toll样受体4(TLR4)表达。结果：(1)HS组小鼠CK-MB、LDH较NS组明显升高,但CO-HBOC处理后小鼠心肌损伤减轻;(2)HE染色显示HS组小鼠较NS组出现明显心肌细胞水肿、核坏死、灶状变性并伴有炎症细胞浸润,而H...     

细胞自噬在大鼠Ⅱ型肺泡上皮细胞低氧/复氧损伤中的作用

目的探讨细胞自噬在大鼠Ⅱ型肺泡上皮细胞(AECⅡ)低氧/复氧(H/R)中的作用。方法将大鼠AECⅡ分为对照组(C)、低氧/复氧组(H/R)、DMSO溶剂组(HD)、自噬激动剂组(Rap)和自噬抑制剂组(3-MA)。CCK-8法检测细胞活力;反转录RT-PCR检测自噬相关蛋白mRNA表达水平;Western blot检测自噬相关蛋白水平;透射电镜检测细胞超微结构。结果与对照组相比,H/R组细胞活力均有下降,自噬相关蛋白及mRNA表达水平均上调(P0.05),细胞超微结构损伤较严重;与H/R组相比,3-MA组的细胞活力较高,自噬相关蛋白及mRNA表达水平均下调(P0.05)。结论低氧/复氧可激活细胞自噬引发大鼠肺泡Ⅱ型上皮细胞损伤。     

低压性低氧暴露后大鼠骨骼肌过氧化物酶增殖激活受体-δ基因表达上调

目的探讨低压性低氧暴露对大鼠骨骼肌过氧化物酶增殖激活受体8（PPAR-δ）基因表达的影响。方法40只SD大鼠随机均分为平原组（H0组）、缺氧1d组（H1组）和缺氧15d组（H15组）。将缺氧组大鼠置于模拟海拔5，000m低压氧舱内，每天23h。平原组大鼠在平原动物房内饲养。分别于缺氧1d和15d后取双后肢腓肠肌，观察腓肠肌毛细血管密度的变化，用同位素标记法测定脂肪酸氧化率，化学比色法测定非酯化脂肪酸（NEFA）含量，RT-PCR法检测骨骼肌中PPAR-δ以及脂肪酸易位蛋白（FAT／CD36）mRNA表达的变化，并与HO组对照。结果①缺氧暴露15d后骨骼肌毛细血管密度增加。②骨骼肌NEFA含量缺氧组显著高于平原对照组（P均〈0．05），H1显著低于H15（P〈0．05）。骨骼肌脂肪酸氧化率H15显著高于H0和H1（P均〈0．05），H0与H10之间无显著性差异。③骨骼肌H1组PPAR-δ mRNA表达水平较H0和H15组分别下调39．4％和30．0％（均P〈0．05），H0和H15组间无显著性差异。H15组CD36 mRNA表达水平较Ⅲ组上调12．2％（P〈0．05），H0和H15组间以及H0和H1组间无显著性差异。结论慢性高原暴露时骨骼肌PPAR-δ mRNA表达上调，这可能是慢性高原暴露时脂肪酸氧化利用增强及骨骼肌毛细血管密度增加原因之一。     

高原低氧对大鼠心肺组织超微结构的影响

背景：研究表明快速进入高原地区时,机体不可避免地会受到不同程度的损伤,以心肺损伤较显著。 目的：观察低氧习服对高原低氧大鼠心肺组织的超微结构影响。 方法：将SD大鼠分别为进行高原低氧干预1,3和30 d,并设置对照组。3个高原低氧组由海拔5 m的西安途中耗时1 d带到海拔2 700 m的青海格尔木地区、途中耗时3,30 d分别带到海拔4 500 m的西藏那曲地区,观察各时间点心肺标本的组织学变化。 结果与结论：急性高原低氧1,3 d组肺组织显微和超微结构出现明显的间质性肺水肿和肺泡性肺水肿,其心脏组织光镜下大鼠各室壁心肌细胞均可见不同程度的浊肿、空泡变性、溶解坏死及间质水肿等,电镜下可见心肌细胞线粒体肿胀,肌浆网扩张,肌原纤维溶解,细胞内外水肿等,急性高原低氧3 d上述改变右室壁较左室壁明显,而低氧习服后高原低氧30 d组间质性水肿和则肺水肿明显减轻。结果证实,高原急性缺氧可造成大鼠间质性肺水肿和肺泡型肺水肿,并引起以右心室为主的全心性损伤,经过高原低氧习服后心肺组织病变明显减轻。     

模拟高原缺氧不依赖肺动脉高压促进大鼠右心室ACE2的表达

目的： 研究模拟高原缺氧环境下大鼠心脏血管紧张素转换酶2（ACE2）的变化规律及调节因素,初步探讨ACE2与高原心脏病的关系。 方法： 在低氧环境（模拟海拔5 000 m高原、23 h/d）下饲养成年雄性 Sprague Dawley（SD）大鼠,并分为缺氧1、15、30 d组,设立平原对照组;检测各组大鼠右心室ACE2活性,同时测定右心室功能、重量指数以及肺动脉压力变化。在此基础上,我们观察了卡托普利、尼群地平灌胃对慢性缺氧30 d组大鼠右心室ACE2活性的影响。结果： 缺氧30 d 组右心室ACE2 mRNA、蛋白表达显著上调,ACE2活性明显增加,同时伴明显心室肥厚及心功能显著升高。另外,卡托普利、尼群地平虽然显著降低了肺动脉压力以及心脏功能,但对ACE2活性无显著影响。结论： 慢性高原缺氧环境促使心脏ACE2的表达与活性上调,提示ACE2可能与缺氧心脏结构功能变化有关;表达增加是缺氧环境中大鼠右心室ACE2活性升高的原因之一,而肺动脉高压可能并非是缺氧情况下ACE2活性变化的主要原因。     

DDAH2抑制低氧诱导大鼠心肌细胞H9c2(2-1)凋亡

 目的 探讨过表达二甲基精氨酸二甲胺水解酶-Ⅱ（DDAH2）对低氧诱导的大鼠心肌细胞凋亡的抑制作用和是否通过内皮型一氧化氮合酶（eNOS）活化来保护心肌细胞。方法 低氧诱导大鼠心肌细胞H9c2(2-1)36h从而诱导凋亡,同时转染DDAH2真核细胞表达质粒,用WST-1细胞毒试验和流式细胞术检测细胞凋亡,Western blot法检测eNOS磷酸化。结果 低氧组心肌细胞存活率显著性降低;过表达DDAH2基因使低氧下心肌细胞存活率明显地上升。DDAH2过表达组心肌细胞凋亡率为17.38%±1.52%,显著性低于低氧组（27.34%±1.33%）（P<0.05）。转染DDAH2基因可以显著上调低氧组心肌细胞的eNOS磷酸化水平;过表达DDAH2基因的低氧组用eNOS抑制剂L-NAME干预后,凋亡水平明显上升。结论 过表达DDAH2基因上调eNOS磷酸化抑制低氧所致的大鼠心肌细胞H9c2（2-1）凋亡。     

异丙肾性心肌梗死大鼠钙敏感受体的表达和凋亡通路的变化

目的：观察钙敏感受体（CaSR）在异丙肾性心肌梗死大鼠的表达和凋亡通路的变化。方法: 采用连续2 d大剂量异丙肾上腺素（200 mg/kg）皮下注射制备大鼠心肌梗死模型。Wistar大鼠随机分为3组：正常对照组（control）;异丙肾上腺素1 d组(ISO/1d);异丙肾上腺素2 d组（ISO/2d）。采用RT-PCR和Western blotting分别观察CaSR、bax、〖STBX〗bcl-2〖STBZ〗、caspase-3 mRNA和蛋白表达;TUNEL染色观察心肌细胞凋亡情况;光镜和电镜分别观察心肌形态学和超微结构变化;紫外分光法检测乳酸脱氢酶（LDH）、肌酸激酶（CK）、超氧化物歧化酶（SOD）活性和丙二醛(MDA)含量,电化学免疫发光法检测肌钙蛋白（cTnT）水平。结果: 与正常组比较,ISO/1d组：LDH 和CK活性、cTnT水平和MDA含量、细胞凋亡指数以及CaSR、Bax和caspase-3的表达均达高峰,同时SOD活性降低,Bcl-2表达减少,心肌细胞超微结构损伤严重;ISO/2d的心肌损伤指标较ISO/1d组有所减轻。结论: CaSR表达增多可能参与了异丙肾性大鼠心肌梗死的发生,其机制与氧化应激和细胞凋亡有关。     

miR-323通过FGF9调控缺氧诱导的心肌H9C2细胞凋亡

目的:探讨微小RNA-323(miR-323)对缺氧诱导大鼠心肌H9C2细胞凋亡的影响及其机制。方法:建立缺氧损伤的H9C2细胞模型,在H9C2细胞转染anti-miR-323、pcDNA-FGF9和si-FGF9,并缺氧处理48 h。采用qPCR检测miR-323的表达, Western blot检测成纤维细胞生长因子9(FGF9)、cleaved caspase-3、c-Jun氨基末端激酶(JNK)和p-JNK的蛋白水平,MTT比色法检测细胞活力,流式细胞术检测细胞凋亡。生物学信息预测miR-323的靶基因并用双萤光素酶报告基因进一步验证。结果:缺氧明显降低H9C2细胞12 h、24 h和48 h的细胞活力(P<0.05),显著提高细胞凋亡率和cleaved caspase-3的蛋白水平(P<0.05),效应均呈时间依赖性。缺氧处理的H9C2细胞中miR-323和p-JNK水平上调,FGF9蛋白表达下调(P<0.05)。下调miR-323表达或过表达FGF9显著提高缺氧处理的H9C2细胞活力,降低细胞凋亡率和cleaved caspase-3蛋白的水平(P<...     

施万样细胞对大鼠脊神经节NGF和BDNF表达的影响

目的观察施万样细胞对坐骨神经损伤(sciatic nerve injury,SNI)大鼠脊神经节NGF和BDNF表达的影响,初步探讨施万样细胞对脊神经节的保护作用。方法先将脂肪源性干细胞(adipose-derived stem cells,ADSCs)诱导分化为施万样细胞并对后者进行鉴定,后将二者分别植入脱细胞神经移植物(ANA)中,构建组织工程神经。大鼠随机分为正常对照组、ADSC组和施万样细胞组。后两组建立SNI模型并用相应的组织工程神经桥接损伤的神经。术后4周采用Western Blot和Real-time PCR检测各组大鼠脊神经节神经生长因子(nerve growth factor,NGF)和脑源性神经营养因子(brainderived neurotrophic factor,BDNF)蛋白和m RNA的表达。结果 ADSCs能够诱导分化为施万样细胞并表达施万细胞标记物S100β和GFAP蛋白。施万样细胞组大鼠脊神经节内NGF和BDNF蛋白及m RNA表达量均高于ADSC组(P0.05)。结论施万样细胞可上调脊神经节NGF和BDNF的表达,对SNI所致的脊神经节内神经元损伤有保护作用。     

SHR鼠颈上交感神经节内NPY的差异表达研究

目的　通过对自发性高血压大鼠（SHR）颈上神经节形态学及其内神经肽酪氨酸（NPY）表达变化的研究，探讨NPY在高血压发生发展中的作用。 方法　随机选取成年SHR和WKY各20只，观测颈上交感神经节的位置、形状、大小及重量，采用Real-time PCR技术和免疫组织化学法，检测两组大鼠颈上神经节内NPY mRNA和蛋白的表达。 结果　与同周龄的WKY组大鼠相比较，SHR组大鼠血压明显升高（P<0.05）；Real-time PCR和免疫组化结果显示：SHR颈上神经节内NPY mRNA和蛋白水平均较WKY增加（P<0.05）。 结论　NPY在基因转录和蛋白表达等方面均较WKY上调，并参与高血压的形成。     

地塞米松诱导的危重病性肌病大鼠骨骼肌p62和泛素的表达

目的　探讨危重病性肌病大鼠骨骼肌自噬相关因子p62和泛素的表达情况。 方法　将健康SD大鼠分为对照组和实验组;实验组又分为7、9、11 d 3个时相点（n=10）。实验组采用5 mg/kg地塞米松连续腹腔注射,每天1次,对照组腹腔注射等量的生理盐水。采用肌功能缺损评分判定肌功能缺损情况。利用免疫组化和Western blot检测骨骼肌自噬相关因子p62和泛素的表达情况。 结果　与对照组相比,实验组大鼠出现不同程度肌肉功能缺损症状,以11 d时大鼠缺损程度最为严重。免疫组化检测结果显示,对照组骨骼肌纤维可见少量泛素阳性表达细胞,无p62阳性细胞表达,实验组肌纤维胞质中可见明显p62和泛素表达,随时间延长表达量逐渐减少,以11 d时相点降低表达最为明显。 Western blot也证实了同一趋势。 结论　地塞米松诱导的大鼠CIM可能通过抑制p62和泛素的表达从而发挥对细胞自噬的调节作用。     

Origin and peptide content of nerve fibers in the nasal mucosa of rats

Injection of the retrograde neuronal tracer True blue into the anterior-lateral part of the nasal mucosa of rats labeled nerve cell bodies in the superior cervical ganglion, the sphenopalatine ganglion, the otic ganglion and the trigeminal ganglion on the ipsilateral side. In the superior cervical ganglion, the sphenopalatine ganglion and the trigeminal ganglion on the contralateral side, very few nerve cell bodies were labeled, indicating that these ganglia provide minor contributions only. The number of labeled cell bodies indicates that the superior cervical ganglion, the sphenopalatine ganglion and the trigeminal ganglion contribute most to the innervation of the nose, while the contribution from the otic ganglion is minor. Cell bodies in the superior cervical ganglion harbored noradrenaline (NA) or NA/neuropeptide Y (NPY); in the sphenopalatine ganglion vasoactive intestinal peptide (VIP) or VIP/NPY; in the otic ganglion VIP, VIP/NPY or VIP/substance P (SP) and in the trigeminal ganglion calcitonin gene-related peptide (CGRP) or CGRP/SP. The results from denervations and tracer experiments suggest that all NA-containing and the majority of NPY-containing fibers in the nasal mucosa are derived from the superior cervical ganglion (sympathetic nerve supply). VIP- and VIP/NPY-containing fibers originate from the sphenopalatine and otic ganglia (parasympathetic nerve supply). Nerve fibers containing CGRP and CGRP/SP emanate from the trigeminal ganglion (sensory nerve supply).     

Neonatal neuronal loss in rat superior cervical ganglia: retrograde effects on developing preganglionic axons and Schwann cells

Summary Beginning prenatally and during the first week after birth, there is normally a loss of axons in rat cervical sympathetic trunk. To test the hypothesis that this spontaneous axonal loss represents a natural process whereby an excessive number of immature preganglionic axons in the cervical sympathetic trunk adapts to the neuronal population in the superior cervical ganglion, the number of nerve cells in the superior cervical ganglion was reduced in newborn rats by administration of nerve growth factor antiserum, 6-hydroxy-dopamine or postganglionic axotomy. Quantitative ultrastructural studies of these animals at later stages of development revealed that, with each method, the number of preganglionic axons and Schwann cells was reduced to nearly one-third of normal. These findings indicate that the superior cervical ganglion plays an important role in the development of the cervical sympathetic trunk. Removal of ganglionic cells causes a retrograde loss of preganglionic fibres. This process probably represents an exaggeration of the normal mechanism for elimination of redundant axons. Because the changes in axonal numbers are associated with similar reductions in the number of Schwann cells, it can also be concluded that postnatal Schwann cell proliferation is influenced by axonal populations.     

Angiotensin AT1 receptors in paraventricular nucleus contribute to sympathetic activation and enhanced cardiac sympathetic afferent reflex in renovascular hypertensive rats

Sympathetic activity is enhanced in hypertension, which contributes to the pathogenesis of hypertension and progression of organ damage. The cardiac sympathetic afferent reflex (CSAR) is enhanced in renovascular hypertension and involved in the sympathetic activation. The present study was designed to investigate whether angiotensin II (Ang II) and Ang II type 1 (AT(1)) receptors in paraventricular nucleus (PVN) contribute to the enhanced CSAR and sympathetic outflow in experimental renovascular hypertensive rats. Hypertension was induced by the two-kidney one-clip (2K1C) method. The normotensive rats underwent sham operation (Sham). Acute experimentation was carried out at the end of the 4th week. Under urethane and α-chloralose anaesthesia, the renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in rats with sino-aortic denervation and cervical vagotomy. The AT(1) receptor expression was determined with Western blot. The CSAR was evaluated by the response of RSNA and MAP to epicardial application of 1.0 nmol of capsaicin. The AT(1) receptor expression in the PVN was increased, and Ang II in the PVN augmented the enhanced CSAR and RSNA in 2K1C rats. The effects of Ang II were abolished by pretreatment with the AT(1) receptor antagonist, losartan, in 2K1C rats. Losartan in the PVN normalized the enhanced CSAR and decreased the RSNA and MAP in 2K1C rats. These results indicate that the increased activity of AT(1) receptors in the PVN contributes to the enhanced CSAR and excessive sympathetic activation in renovascular hypertensive rats.     

Synaptically mediated potentials elicited by the stimulation of post-ganglionic trunks in the guinea-pig superior cervical ganglion

Summary Stimulation of a post-ganglionic nerve trunk (internal carotid nerve) leads to synaptic activation of the majority of the sympathetic neurons in the superior cervical ganglion of the guinea-pig. Curarization of the ganglion and the section of the cervical sympathetic trunk eliminate any sign of synaptic activation in the ganglion cells produced by stimulating the internal carotid nerve. Stimulation of other post-ganglionic nerve trunks (superior cardiac nerve) gives rise only to pure antidromic responses in the cells. A compound action potential of considerable amplitude, which is completely cancelled by curarization of the ganglion, may be led off from the superior cardiac nerve after stimulating the internal carotid nerve; no propagated potential in the opposite direction was recorded at all. The conclusion is drawn that pre-ganglionic fibres projecting into the internal carotid nerve give rise to an elaborate system of collateral endings impinging onto most of the ganglion neurons and are responsible for synaptic activation of the ganglion cells observed after stimulating post-ganglionic nerves. The characteristics of action potentials evoked antidromically in the sympathetic neurons are also described.     

[Met5]enkephalin-Arg6-Phe7- and [Met5]enkephalin-Arg6-Gly7-Leu8-immunoreactive nerve fibres and neurons in the superior cervical ganglion of the rat

[Met⁵]enkephalin-Arg⁶-Phe⁷- (MEAP-) and [Met⁵]enkephalin-Arg⁶-Gly⁷-Leu⁸- (MEAGL-) immunoreactivity was studied by indirect immunohistochemistry in the superior cervical ganglion of the rat with specific antisera produced in rabbits against the corresponding synthetic opioid peptides. Several MEAP- and a few MEAGL-immunoreactive principal nerve cells were observed in the ganglion, while the small intensely fluorescent cells appeared as non-reactive. The superior cervical ganglion also contained dense networks of MEAP- and MEAGL-immunoreactive nerve fibres, which often formed basket-like structures around the principal nerve cells and small intensely fluorescent cells. After ligation of the preganglionic nerve trunk with simultaneous transection of the main postganglionic trunks, a distinct accumulation of both MEAP- and MEAGL- immunoreactivity was observed on both sides of the ligature. Ligation of the preganglionic nerve trunk caused a marked decrease in the number of both MEAP- and MEAGL-immunoreactive nerve fibres in the ganglion. Ligation of the main postganglionic nerve trunks with simultaneous preganglionic nerve division resulted in accumulation of MEAP- and MEAGL-immunoreactive material on the ganglionic side of the ligature in both the external and internal carotid nerve. After division of both the pre- and postganglionic nerve trunks, some immunoreactive nerve fibres and principal nerve cells were still observed in the ganglion. A few immunoreactive neurons and nerve fibres were also observed in the ganglion stellatum. A large number of MEAP- and MEAGL-immunoreactive nerve fibres was detected in the spinal cord at the levels C6-Th6. A few neurons in the intermediolateral cell column of the spinal cord at levels C8-Thl showed MEAP- but not MEAGL-immunoreactivity. The cultured superior cervical ganglion contained a few MEAP-immunoreactive neurons, and the fibre outgrowth showed immunoreactivity both to MEAP and MEAGL. In electron microscopy, MEAGL-immunoreactivity in the superior cervical ganglion was localized in nerve fibres containing neurotubules and in principal nerve cells.The present results demonstrate that the rat superior cervical ganglion contains both extrinsic and intrinsic MEAP- and MEAGL-immunoreactive nerve fibres. Most of these fibres are of preganglionic origin. Both the principal nerve and small intensely fluorescent cells are often surrounded by MEAP- or MEAGL-immunoreactive nerve fibres and may receive innervation by these fibres. Several ganglionic neurons projecting to the sympathetic target tissues show MEAP- and/or MEAGL-immunoreactivity. Since MEAP- and MEAGL sequences are included in the proenkephalin A molecule, but not in the other opioid precursor molecules, it is evident that a neuronal system containing proenkephalin-A-derived enkephalins, is present in the rat superior cervical ganglion.     

Correspondence: Communication between the superior cervical sympathetic ganglion and the inferior laryngeal nerve

Complex arborisations occurs between the inferior ganglion of the vagus nerve and the superior cervical sympathetic ganglion (Braeucker, 1923; Fick, 1926; Siwe, 1931; Hoffman, 1957). The superior cervical sympathetic ganglion sends branches to the internal and the external carotid arteries, the inferior vagal ganglion, the superior laryngeal nerve and the cervical nerves, and provides superior cardiac and thyroid branches as well as the trunk that descends directly to the middle and inferior cervical sympathetic ganglia. There are communications between the vagus nerve (laryngeal branches) and the superior cervical sympathetic ganglion (SCSG). Cannizzaro et al. (1991) and Zerilli et al. (1994) reported abnormalities of sympathetic function among the effects of injury to the superior laryngeal nerve during thyroid surgery. The interconnections between these various nerves are therefore of clinical importance. We document here a rare example of complex communication between the vagus nerve and the SCSG in dissections of 113 adult (78 male, 35 female) Japanese cadavers. Both sides were examined in 88 cases, the right only in 18 and the left only in 7 (i.e. 201 sides in total).     

Reconsideration of the Autonomic Cranial Ganglia: An Immunohistochemical Study of Mid‐Term Human Fetuses

The cranial parasympathetic ganglia have been reported to paradoxically contain the sympathetic nerve marker, tyrosine hydroxylase (TH), in addition to neurons expressing parasympathetic markers such as vasoactive intestinal peptide (VIP) and neuronal nitric oxide synthase (nNOS). However, the distribution of these molecules in the cranial ganglia of human fetuses has not yet been examined. Using paraffin sections from 10 mid‐term human fetuses (12–15 weeks), we performed immunohistochemistry for TH, VIP, and nNOS in the parasympathetic ciliary, pterygopalatine, otic, and submandibular ganglia, and for comparison, the sensory inferior vagal ganglion. The ciliary and submandibular ganglia contained abundant TH‐positive neurons. In the former, TH‐positive neurons were much more numerous than nNOS‐positive neurons, whereas in the latter, nNOS immunoreactivity was extremely strong. No or a few cells in the pterygopalatine, otic, and inferior vagal ganglia expressed TH. Ciliary TH neurons appeared to compensate for classically described sympathetic fibers arising from the superior cervical ganglion, whereas in the submandibular ganglion, nNOS‐positive neurons as well as TH neurons might innervate the lingual artery in addition to the salivary glands. Significant individual variations in the density of all these markers suggested differences in sensitivity to medicine affecting autonomic nerve function. Consequently, in the human cranial autonomic ganglia, it appears that there is no simple dichotomy between sympathetic and parasympathetic function. Anat Rec, 2012. © 2011 Wiley Periodicals, Inc.