Effects of Chemical Sympathectomy on Contralateral Testicular Histology and Fertility in Unilateral Vasectomy

Unilateral obstruction or injury to the vas deferens can result in significant injury to the contralateral testicle. Although various pathways have been proposed, the mechanism of contralateral testicular deterioration remains controversial. The present animal study was performed to evaluate the effects of unilateral vasectomy on ipsilateral and contralateral testicular histology and fertility in rats that were chemically sympathectomized neonatally. The study comprised 40 male albino rats: 20 received a placebo and the other 20 underwent chemical sympathectomy neonatally. When 60 days old, each group of 20 rats was divided into two groups that underwent either a sham operation or an operation to create unilateral left vasectomy. Eight weeks after surgery, each male rat was housed with two known fertile female rats for 25 days, and then their testes were harvested. Mean seminiferous tubular diameters (MSTD) and mean testicular biopsy scores (MTBS) were determined for each testis. Although MSTD and MTBS were not significantly different between groups, chemical sympathectomy prevented the decrease in total fertility rates of the rats with unilateral left vasectomy in our study. Prevention of this decrease by chemical sympathectomy suggests that the sympathetic nervous system may play a role in the testicular degeneration associated with vasectomy.     

The effect of lesions of the sympathoadrenal system on training induced adaptations in adipocytes and pancreatic islets in rats

Physical training increases insulin stimulated glucose uptake in adipocytes and decreases insulin secretion from pancreatic islets. The mechanism behind these adaptations is not known. Because in acute exercise adrenergic activity influences both adipocytes and pancreatic islets, the sympathetic nervous system was examined as the possible mediator. Rats were either adrenodemedullated or sham adrenodemedullated and underwent either unilateral abdominal sympathectomy or were sham sympathectomized. Resting plasma adrenaline concentration in adrenodemedullated rats was 32% of the concentration in sham adrenodemedullated rats (P<0.0001) and muscle noradrenaline content in sympathectomized leg was 9% of content in sham sympathectomized leg (P<0.0001). After operations rats were either swim trained for 10 weeks or remained sedentary. Insulin stimulated 3-O-[¹⁴C]methylglucose transport was measured in adipocytes from epididymal fat pads, and insulin secretion and glucose metabolism were measured in glucose stimulated pancreatic islets. Training increased insulin stimulated glucose transport in adipocytes (P<0.0001) and decreased their size (P<0.0001), but neither adrenodemedullation nor sympathetic denervation affected these parameters significantly. Training decreased insulin secretion (P<0.01) and increased glucose oxidation (P=0.02) and utilization (P=0.08) in pancreatic islets, but none of these parameters was affected significantly by adrenodemedullation. It is concluded that adrenergic activity is not important for the training induced decrease in size and increase in insulin stimulated glucose transport of adipocytes. Neither is an intact adrenal medulla necessary for training-induced adaptations in pancreatic beta cell function. Finally, in response to training, β cell insulin secretion and glucose metabolism changed in opposite directions.     

Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho-adrenal system

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.     

ADMA对交感神经损毁自发性高血压大鼠血压和肾功能的作用

目的:探讨不对称二甲基精氨酸(ADMA)对交感神经损毁自发性高血压大鼠(SHR)血压和肾功能的作用。方法:新生雄性SHR随机分成交感神经损毁组和对照组,采用单硫酸胍乙啶损毁新生SHR的交感神经。12周后测量常温下鼠尾血压;代谢笼法收集大鼠尿液,检测去甲肾上腺素(NE)排泄量;高效液相色谱法检测肾脏NE和ADMA含量;比色法检测大鼠肾脏一氧化氮(NO)含量;Western blot法测定内皮型一氧化氮合酶(e NOS)的表达;通过检测肾小球滤过率(GFR)评价肾脏功能。结果:与对照组相比,交感神经损毁组尿NE排泄量以及肾脏NE和ADMA含量均明显降低,肾脏NO含量和e NOS表达显著升高,收缩压和舒张压明显降低(P0.05),24 h尿微量白蛋白、尿钠量和GFR未见明显差异。结论:抑制交感神经系统可引起ADMA和NE释放减少,NO合成和e NOS表达升高,从而对血压产生调节作用;但交感神经系统对ADMA生成的调控并不是通过影响肾脏功能来实现的。     

Effects of sympathectomy on experimentally induced pulpal inflammation and periapical lesions in rats

The role of sympathetic nerves in bone physiology is largely unknown. Recent studies have shown a correlation between sympathectomy and bone remodeling. The present experiments were aimed to study the effects of unilateral sympathectomy on bilateral experimentally induced pulpitis and periapical lesions in the rat maxilla and mandible. Adult male Sprague-Dawley rats were used. Experimental rats (n=11) had the right superior cervical ganglion surgically removed (SCGx) and control rats (n=5) had sham surgery. Pulpal inflammation and periapical bone lesions in the maxilla and mandible were created 14 days later in both experimental and control rats by exposing the dental pulp in the first and second molars and leaving them open to the oral microflora. The rats were perfused 20 days thereafter and the jaws processed for immunohistochemistry with neuropeptide Y (NPY) and ED1 as primary antibodies. Sympathectomy resulted in an almost complete loss of NPY-immunoreactive (IR) fibers in the right SCGx jaws. In the non-sympathectomized (non-SCGx) left side and in the control rats, sprouting of NPY-IR fiber was observed in the inflamed pulp tissue adjacent to reparative dentin formation and in the apical periodontal ligament of the partially necrotic first molars. Significantly more ED1-IR osteoclasts were found in the resorptive lacunae lining the periphery of the periapical lesions on the SCGx side compared with the non-SCGx side (P<0.04) and the controls (P<0.03). The size of the periapical lesions were larger on the SCGx side compared with the non-SCGx side (P<0.03) in the mandible, but not in the maxilla. We conclude that inflammation causes sprouting of NPY-IR nerve fibers and that unilateral removal of the SCG increases both the area of the periapical lesions and the number of osteoclasts in the inflamed region.     

Inhibition of neutrophil chemotaxis and activation following decentralization of the superior cervical ganglia.

Recent studies have shown that bilateral decentralization (sympathectomy) of the superior cervical ganglia (SCG) of rats sensitized to the parasite Nippostrongylus brasiliensis attenuated the development of pulmonary inflammation following allergen challenge. Sympathectomy inhibited total leukocyte infiltration into lung lavage fluids, particularly neutrophil infiltration. To define the effects of decentralization of the SCG on neutrophil responses, peripheral blood neutrophils of rats were isolated and tested in in vitro chemotaxis and phagocytosis assays. Neutrophils from rats that were sympathectomized 7 days previously displayed a marked reduction in chemotaxis to N-formyl-methionyl-leucyl-phenylalanine and leukotriene B4 compared to neutrophils from sham-operated or unoperated groups. Although the degree of chemotaxis was greater in blood neutrophils from parasite-infected rats than from uninfected rats, sympathectomy markedly reduced the chemotactic responses of both groups. In addition, neutrophils of sympathectomized rats were unresponsive to lipopolysaccharide-induced metabolic activation as assessed by in vitro phagocytosis and oxidative reduction of nitroblue tetrazolium. Thus, decentralization of the SCG of rats affects the chemotactic responses and functions of neutrophils. Understanding the role of the sympathetic nervous system in modulating the behavior of neutrophils will shed light on the interactions between the nervous and immune systems.     

中等强度运动对去卵巢大鼠骨质疏松及骨形态发生蛋白2信号通路的影响

目的 探讨中等强度运动对去卵巢大鼠骨密度、骨质代谢、骨生物力学及骨形态发生蛋白2(BMP-2)信号通路的影响。 方法 将24只成年雌性SD大鼠随机分为假手术组、手术组与运动组，每组8只，假手术组仅切除双侧卵巢周围脂肪组织，手术组、运动组摘除双侧卵巢，摘除卵巢1周后运动组进行中等强度运动训练，共训练12周。12周后，进行股骨骨密度、生物力学、骨代谢、组织学检测，Western blotting检测股骨组织BMP-2、Runt相关转录因子2（Runx2）、Osterix及Smad1/5/8蛋白表达。 结果 手术组、运动组血钙、血磷、血抗酒石酸酸性磷酸酶(TRACP)浓度高于假手术组(P<0.05)，而运动组上述指标低于手术组(P<0.05)。手术组和运动组骨密度低于假手术组(P<0.05)，而运动组高于手术组(P<0.05)。手术组和运动组骨组织生物力学性能低于假手术组(P<0.05)，而运动组高于手术组(P<0.05)。组织学显示，运动组骨质疏松程度轻于手术组，骨组织内BMP-2表达量多于手术组。手术组和运动组BMP-2、Runx2、Osterix及Smad1/5/8蛋白表达低于假手术组(P<0.05)，而运动组上述蛋白表达高于手术组(P<0.05)。 结论 中等强度运动可改善去卵巢大鼠股骨的骨密度、生物力学性能与骨代谢，这一作用可能与BMP-2信号通路有关。     

Immunoglobulin producing cells in the rat dental pulp after unilateral sympathectomy

Recent studies show that sympathetic nerves participate in immunomodulation. We investigated the effects of unilateral sympathectomy on recruitment of cells expressing kappa and lambda (kappa and lambda) light chains in the rat dental pulp. Superior cervical ganglion was removed in experimental rats (n=10) while control rats (n=8) received sham surgery. Following perfusion 18 days later, mandibular jaws were processed for immunohistochemistry and electron microscopy. Sympathectomy results in recruitment of cells expressing kappa and lambda light chains into the dental pulp (P=0.005). Electron microscopy revealed these cells to be mainly plasma cells and Mott cells. We conclude that neural imbalance caused by unilateral sympathectomy recruits immunoglobulin producing cells in the dental pulp. Our results are in agreement with a model of immune regulation in which the sympathetic nervous system exerts a tonic regulatory effect over lymphocyte proliferation and migration.     

The effect of lumbar sympathectomy on fiber composition, contractility of skeletal muscle and regulation of central circulation in dogs

It has been speculated upon that the sympathetic activity might be of significance for fiber composition in skeletal muscle and by similar features indirectly affecting muscle contractility and regulation of circulation. To further study this hypothesis unilateral lumbar sympathectomy from L-2 and down was applied on 5 female dogs. After 14 weeks the gracilis muscle on the sympathectomized and the control side as well were examined for their muscle fiber compositions, endurance capacity and how heart rate and blood pressure responses were affected. Muscle fiber composition decreased to 28% slow twitch fibers as compared to 41% on the control side (p less than 0.01). The relative cross-sectional area of the fast twitch fibers increased simultaneously from 57 (control side) to 71% (p less than 0.05). Endurance performance measured as contraction time at 50% of peak tension decreased from 55 to 29 s (p less than 0.05). On an individual bases including both control and sympathectomized muscles it was found that heart rate increased with percent fast twitch muscle fibers (p less than 0.01) and a tendency was present for a similar relationship between blood pressure and fiber types (p less than 0.1).     

Regeneration of submandibular gland autografts in sympathectomized rats

This morphologic study compares the regenerative response in submandibular gland (SMG) autografts placed in the tongues of previously sympathectomized rats to autografts placed in tongues of sham-sympathectomized rats. We hypothesized that sympathectomy would alter the process of cellular proliferation and inhibit cytodifferentiation in regenerating SMG autografts. Either 1 week, or 8 to 11 weeks following the SMG autografting procedure, the rats were sacrificed and their tongues were removed and sectioned in a cryostat. Frozen tissue sections containing the SMG autografts were either reacted for cholinesterase activity, treated with a glyoxylic acid mixture to induce histofluorescence, or stained for histologic examination. In addition, 3H-thymidine labeled and unlabeled cells were counted in autoradiographs of 1-week autografts, and these counts were used to calculate labeling indices. The 1-week SMG autografts from both the sympathectomized and the sham-sympathectomized rats were similar in histologic appearance, and neither group of autografts contained cholinesterase-positive or monoaminergic nerve fibers. The 8- to 11-week autografts from sympathectomized and sham-sympathectomized rats contained cholinesterase-positive fibers, but monoaminergic fibers were present in the autografts only from the sham-operated rats. Acinar cells were observed in one-third of the 8- to 11-week autografts of both the sympathectomized and sham-sympathectomized rats. This finding suggests that sympathectomy did not prelude cytodifferentiation in the autografts. The autoradiographic data revealed no statistically significant difference between the mean labeling indices of the 1-week autografts from the sympathectomized and sham-sympathectomized rats, which suggests that sympathectomy also did not alter the level of cellular proliferation in the autografts.     

Effect of chronic cervical ganglionectomy on the spontaneous variability of internal carotid blood flow in the conscious rat

The role of sympathetic innervation in the control of spontaneous fluctuations of cerebral blood flow is still poorly understood. In conscious, unrestrained rats, blood flow velocity (pulsed Doppler) was measured in both internal carotid arteries 1 week after either excision of the right superior cervical ganglion (n = 8) or sham surgery (n = 6). Using Fourier-based techniques, spectral power of each carotid blood flow (CBF) was computed over the whole recording period (246 min), which was segmented into nine consecutive 27.3 min periods. Variability of CBF (spectral power) was ～40% higher (P < 0.02) on the denervated than on the intact side at frequencies <1 Hz. Coherence between left and right CBFs was similar in the two groups of rats, except in the 0.01-0.1 Hz frequency range where it was lower (P < 0.05) in rats with unilateral sympathectomy (0.54 ± 0.03) than in intact rats (0.74 ± 0.06). In this frequency range, mathematically removing the influence of arterial pressure had little effect on coherence between CBFs in both groups of rats, so that coherence remained significantly lower in rats with unilateral sympathectomy (0.52 ± 0.03) than in intact rats (0.70 ± 0.06). This study indicates that sympathetic innervation has an overall buffering influence on CBF variability. This modulatory role is especially important in a frequency range corresponding to slow fluctuations of CBF (lasting from 10 to 100 s), which are essentially unrelated to fluctuations of arterial pressure.     

Cardiac contractility,cAMP concentration,cAMP-dependent protein kinase,and phosphorylase activation during acute pressure overload

The relationship between increases in myocardial contractility and cAMP and protein kinase activity were studied for hearts of normal rats and those with altered sympathectic capacity produced by the combined treatments of adrenalectomy, and 6-hydroxydopamine and propranol injections. Increases in myocardial contractility, evaluated from intra-ventricular pressure changes, were produced by occlusion of the ascending aorta for 15, 20, or 25 s. Resting peak left ventricular pressure and the rate of rise of left ventricular pressure were lower (p<0.05) in sympathectomized animals, however, aortic occlusion abolished these differences. Time to peak tension and the relationship between end-diastolic pressure and developed pressure were unchanged by sympathectomy. ATP and CP concentrations in freeze clamped samples of the myocardium were lower (P<0.05) in both groups after aortic occlusion whereas lactate was elevated (P<0.05). Sympathectomy delayed and reduced the magnitude of the increase in the phosphorylasea/a+b ratio produced by aortic occlusion. Myocardial cAMP concentration was increased in the normal rats but decreased in sympathectomized animals after aortic occlusion. cAMP-dependent protein kinase activity followed the pattern of cAMP. The results demonstrate that heart possesses the capacity to increase its contractility to an acute, short-term overload even when devoid of sympathetic control.This work is supported by Research Grant HLI 18527 from the National Institutes of Health     

右侧颈交感干离断对大鼠心肌梗死后炎症反应的抑制作用及对HMGB1/TLR4/NF-κB通路的影响

目的:观察右侧颈交感干离断(TCST)对大鼠心肌梗死后炎症反应的抑制作用及高迁移率族蛋白B1(HMGB1)的表达和TLR4/NF-κB信号通路的影响。方法:结扎左冠状动脉前降支制备急性心肌梗死(acute myocardial infarction,AMI)模型,将造模成功的大鼠随机分为心肌梗死(MI)组和心肌梗死+右侧颈交感干离断(MI+TCST)组,MI+TCST组在左冠状动脉前降支结扎后立即离断右侧颈交感神经干。MI组和MI+TCST组分别按模型制备及干预后1、3、7、14和28 d分为5个亚组,另设假手术(sham)组,只穿线不结扎,每组8只。建模后4周,超声心动图检测大鼠心脏功能,然后处死大鼠,取心脏计算心脏肥厚指数,并取梗死周围心肌组织采用HE染色观察心肌病理形态改变。Real-time PCR法检测不同时点梗死边缘区HMGB1、肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)的m RNA表达。Western blot分析MI后不同时点梗死边缘区HMGB1和TLR4蛋白的表达变化,并进一步分析右侧TCST对HMGB1和TLR4/NF-κB信号通路蛋白表达的影响。结果:与MI组比较,MI+TCST组左心室射血分数(LVEF)和左心室短轴缩短分数(LVFS)显著升高(P0.05),左心室舒张末期内径(LVEDd)、左心室收缩末期内径(LVESd)和心脏肥厚指数显著降低(P0.05),梗死边缘区各时点HMGB1、TNF-α和IL-6的m RNA表达水平显著降低(P0.05)。Western blot检测结果显示,与sham组比较,HMGB1蛋白的表达在MI后3 d开始升高,并于7 d达到高峰,之后逐渐下降,28 d时仍明显高于假手术组(P0.05);TLR4蛋白的表达变化与HMGB1一致。进一步研究发现右侧TCST可显著降低心肌组织HMGB1和TLR4/NF-κB信号通路蛋白的表达(P0.05)。结论:右侧颈交感干离断可改善MI后心室重构,发挥保护心功能的作用,其机制可能与其抑制HMGB1/TLR4/NF-κB信号通路,减轻炎症反应有关。     

Effect of interscapular brown adipose tissue denervation on body weight and feed efficiency in alcohol drinking rats

In rats, chronic alcohol intake increases energy expenditure and enhances interscapular brown adipose tissue (IBAT) mass and activity. It is known that alcohol intake is mainly preprandial. In man, alcohol intake during a meal increases postprandial thermogenesis. Since diet-induced thermogenesis is mediated by the sympathetic nervous system, the effect of IBAT surgical denervation was examined on body weight (BW), food intake (FI) and feed efficiency (FE) in alcohol drinking rats. Alcohol drinking rats gained significantly less BW than water drinking rats; FI was identical and so FE was less in alcohol-treated animals. After sympathectomy, the water drinking group was identical to its own control group for BW gain, FI and FE. BW gain of sympathectomized drinking rats was significantly higher than that of controls. FI and FE were nearly identical. It is concluded that the increase in thermogenesis observed in chronic alcohol-treated rats is partly suppressed by sympathectomy. This increase could also involve other BAT mass and other tissues in the whole rat.     

Does the Tibial and Sural Nerve Transection Model Represent Sympathetically Independent Pain?

Neuropathic pain can be divided into sympathetically maintained pain (SMP) and sympathetically independent pain (SIP). Rats with tibial and sural nerve transection (TST) produce neuropathic pain behaviors, including spontaneous pain, tactile allodynia, and cold allodynia. The present study was undertaken to examine whether rats with TST would represent SMP- or SIP-dominant neuropathic pain by lumbar surgical sympathectomy. The TST model was generated by transecting the tibial and sural nerves, leaving the common peroneal nerve intact. Animals were divided into the sympathectomy group and the sham group. For the sympathectomy group, the sympathetic chain was removed bilaterally from L2 to L6 one week after nerve transection. The success of the sympathectomy was verified by measuring skin temperature on the hind paw and by infra red thermography. Tactile allodynia was assessed using von Frey filaments, and cold allodynia was assessed using acetone drops. A majority of the rats exhibited withdrawal behaviors in response to tactile and cold stimulations after nerve stimulation. Neither tactile allodynia nor cold allodynia improved after successful sympathectomy, and there were no differences in the threshold of tactile and cold allodynia between the sympathectomy and sham groups. Tactile allodynia and cold allodynia in the neuropathic pain model of TST are not dependent on the sympathetic nervous system, and this model can be used to investigate SIP syndromes.     

肾脏去神经对动脉粥样硬化家兔炎症因子的影响

目的:探讨肾脏去神经(renal denervation,RDN)对动脉粥样硬化(atherosclerosis,AS)家兔肿瘤坏死因子α(TNF-α)、白细胞介素1α(IL-1α)和白细胞介素6(IL-6)的影响。方法:28只雄性新西兰白兔随机分为对照组、RDN后高脂饲养(high-fat diet,HFD)组(RDN组)、假手术后HFD组(假手术组)和单纯HFD组(HFD组),每组7只。测量各组血浆去甲肾上腺素(norepinephrine,NE)、炎症因子及血脂水平;免疫组化检测血管紧张素Ⅱ(Ang Ⅱ)的表达,Western blot检测核因子κB(NF-κB)和血管紧张素Ⅱ 1型受体(AT1R)的表达;real-time PCR检测TNF-α、IL-1α和IL-6 mRNA的表达;光镜下观察肾动脉结构改变和主动脉病理变化。结果:8周后RDN组NE水平明显低于假手术组和HFD组(P0.05);RDN组血浆甘油三酯(TG)水平低于HFD组(P0.05);RDN组的Ang Ⅱ蛋白表达低于假手术组和HFD组(P0.01);RDN组NF-κB蛋白表达低于假手术组(P0.05);RDN组TNF-α和IL-1α的血浆水平低于假手术组和HFD组(P0.05),RDN组IL-6 mRNA的表达低于假手术组(P0.01)。结论:RDN能有效抑制全身交感神经活性,降低血浆TG水平,减轻血管炎症反应,延缓动脉粥样硬化的发展。     

Unilateral but not bilateral olfactory bulbectomy inhibits body weight gain in hamsters.

The relation of the olfactory bulbs and photoperiod to the regulation of body weight was studied in male golden hamsters. Animals underwent sham operation, bilateral olfactory bulbectomy, or unilateral bulbectomy. They were left on long photoperiod for 5 weeks and then were transferred to short photoperiod for 11 weeks. The unilaterally olfactory bulbectomized hamsters gained less weight on long or short photoperiod than the sham operated group, while the bilaterally bulbectomized hamsters gained at least as much weight as the sham group. Thus, we report the novel finding that unilateral but not bilateral olfactory bulbectomy reduces body weight gain in male golden hamsters.     

提高血流切应力对老年大鼠后肢侧支血管生长的作用

目的　利用老年大鼠股动脉结扎加股动静脉吻合和单纯股动脉结扎的侧支血管生长模型探讨提高血流切应力对老年大鼠侧支血管生长的作用。 方法　老年SD大鼠（24月龄）30只,分为假手术组,结扎组和吻合组。结扎组大鼠行股动脉结扎手术,吻合组大鼠行股动脉结扎加股动静脉吻合手术。大鼠术后存活1周,每组5只大鼠取后肢带侧支血管的肌肉做冰冻切片用于免疫荧光组织化学法检测eNOS,Ki67和MMP2的表达;另外5只使用明胶四氧化三铅进行血管造影再用X线拍照观察侧支血管的生长情况。 结果　与假手术组相比,结扎组的大鼠后肢侧支血管数量增多（P<0.01）,Ki67阳性细胞数量增多（P<0.01）,eNOS的表达显著增强（P<0.001）,MMP2的表达也有所增强（P<0.05）。吻合组与结扎组相比,大鼠的后肢侧支血管数量进一步增多（P<0.01）,Ki67阳性细胞数量明显增多（P<0.01）,eNOS的表达显著增强（P<0.001）,MMP2的表达也明显增强（P<0.01）。 结论　提高血流切应力能促进老年大鼠缺血后肢侧支血管生长。     

Increase of dopamine beta-hydroxylase immunoreactivity in non-noradrenergic nerves of rat cerebral arteries following long-term sympathectomy.

The expression of dopamine beta-hydroxylase (DBH) and tyrosine hydroxylase (TH) immunoreactivity (IR) after short-term (2 days) and long-term (3 weeks) sympathectomy was investigated in rat cerebral vessels, dura mater and pterygopalatine ganglion neurones (which are known to project to cerebral arteries) by immunohistochemistry at both the light and electron microscopical levels. TH-IR, like glyoxylic acid-induced fluorescence, was completely abolished by sympathectomy. By contrast, DBH-IR was localized in nerve fibres, lacking 5-hydroxydopamine (5-OHDA)-labelled vesicles, along cerebral vessels of long-term sympathectomized rats, but not in the dura mater, and in pterygopalatine ganglia, where the number of DBH-IR neurons increased from 27.87% to 54.11%. Since virtually all the pterygopalatine neurons displayed choline acetyltransferase (ChAT)-IR, both in control and sympathectomized rats, it is concluded that long-term sympathectomy caused an increase of the expression of DBH-IR in cholinergic neurones of the pterygopalatine ganglion, without these neurons producing or storing noradrenaline.     

下丘脑室旁核CRH神经元激活在慢性充血性心力衰竭中的交感兴奋作用

目的:观察慢性心衰时下丘脑室旁核(PVN)内促肾上腺皮质激素释放激素(CRH)表达变化及其与交感神经活动之间的关系。方法:健康雄性SD大鼠,冠脉结扎制备心衰模型,侧脑室插管渗透压泵持续给药。假手术组和心衰组给予人工脑脊液0.25μL/h,心衰给药组给予CRH抑制剂αh-CRH 15 mg/h。同时,选取健康雄性体内CRH合成不足的Lewis大鼠与同源纯种Fischer 344大鼠分别制备心衰模型和假手术对照进行对比研究。4周后,测定左室舒张末压(LVEDP)、左室内压最大上升和下降速率(±dp/dtmax)、右心室/体重比(RV/BW)、肺/体重比(lung/BW)、肾交感神经放电活动(RSNA)、血浆去甲肾上腺素(NE)浓度和PVN内CRH阳性神经元数目。血浆促肾上腺皮质激素(ACTH)含量。结果:与假手术组相比,SD心衰大鼠PVN内CRH阳性神经元数目明显增加,血浆ACTH浓度升高,RSNA增强,血浆NE浓度增加,LVEDP、lung/BW和RV/BW增加,±dp/dtmax降低;心衰模型后给予αh-CRH可明显逆转上述各种变化(P0.05)。Fisher 344大鼠心衰组和假手术对照相比,PVN内CRH阳性神经元数目明显增加,血浆ACTH浓度升高,RSNA增强,外周血NE浓度升高,LVEDP、RV/BW和lung/BW增加,±dp/dtmax下降(P0.05)。但Lewis大鼠心衰组和假手术对照相比,以上各指标改变均不明显。结论:慢性心衰时,下丘脑室旁核CRH神经元被激活,激活的CRH神经元可增强外周交感神经活动,加重心功能恶化。