急性脑卒中与脑心综合征

目的探讨急性脑卒中后脑心综合征（Cerebral-cardiac syndrome，CCS）的发病率、临床特点、发病机制、防治措施、预后及其相关因素。方法对324例急性脑卒中后脑心综合征患者入院后作心电图（ECG），心肌酶谱动态观察并结合临床资料进行回顾性分析。结果急性脑卒中后脑心综合征发生率为31．5％，91％的患者于脑卒中后数小时至1周内发生，出血性脑卒中CCS发生率远高于缺血性脑卒中（P〈0．05），非大脑半球（脑干、小脑、基底节）卒中者远高于大脑半球卒中者（P〈0．01）。CCS心电图主要表现为心律失常、心肌缺血和类心肌梗死。心肌酶谱异常率为46．1，52．9％合并低钾血症和／或低钠血症。死亡率31．3％，明显高于未合并CCS的脑卒中患者（14．1％）（P〈0．05）。结论CCS发生与脑卒中类型及部位、低钾、低钠等因素有关，预后都较未合并CCS脑卒中者差。其发病机制可能为脑卒中直接或间接导致植物神经功能紊乱，神经体液功能紊乱有关。CCS患者须加强心脏功能监护，积极防治脑心综合征。     

急性脑血管病的脑心综合征

目的：探讨急性脑血管病（ACVD）的脑心综合征的发生机理及防治措施。方法：对104例ACVD患者入院后作心电图（EKG）、心肌酶谱动态观察,并结合临床资料进行分析。结果ACVD患者EKG改变占50％－86％,心肌酶谱均有不同程度增高,以脑出血量明显,可见ACVD患者急性期极易产生脑心综合征。只要防治及时,病情可好转,结论：ACVD患者需加强心脏功能监护,积极防治脑心综合征。     

急性脑卒中并脑心综合征临床分析

目的探讨急性脑卒中并脑心综合征(CCS)的临床特点及发病机制。方法对136例CCS患者的临床资料进行回顾性分析、探讨。结果 210例急性脑卒中病人,136例并发脑心综合征,发生率64.8%;出血性卒中、近中线结构卒中及意识障碍卒中发生率高;心脏损害以ST-T段改变、心律失常、心肌酶升高、心功能衰竭最常见。结论 CCS发生率高,对急性脑卒中应监测心肌酶、注意心电图演变、监测心功能;对疑心功能障碍者行中心静脉压、心脏射血分数、心脏B型钠尿肽测定,对及早发现心功能衰竭有益。     

脑心综合征心电图改变相关因素与机制探讨

目的：探讨脑卒中时心电图改变的相关因素,心电图异常率不一的原因及心电图改变的机制。方法：对185例既往无心脏病与无心电图异常史的脑心综合征进行回顾性分析,组间对照采取χ^2检验。结果：心电图异常率：昏迷或嗜睡组＞清醒组;丘脑、基底节组＞大脑及其他部位组;CH组＞CI组;高血糖组＞血糖正常组;死亡组＞好转组(P均＜0.005)。结论：心电图改变的相关因素有意识障碍程度、脑卒中部位与性质、高血糖、病情危重程度。多因素导致脑卒中时心电图改变。     

脑出血并发脑心综合征的临床分析

目的探讨脑出血并发脑心综合征的发病率、临床特点及预后。方法收集122例脑出血并发脑心综合征患者的临床资料并进行回顾分析。结果脑出血后并发脑心综合征的发病率23.8%。临床表现主要为心律失常、心电图ST-T改变、心肌酶谱改变及心功能不全。结论脑出血后脑心综合征发病率较高,定时检测心电图及心肌酶谱改变对早期识别与预防脑心综合征、改善患者预后具有积极意义。     

急性脑血管病并发脑心综合征分析

目的探讨急性脑血管病(ACVD)患者并发脑心综合征时心电图变化和机制。方法分析428例ACVD患者常规12导联心电图结果。脑出血142例,脑梗死201例,蛛网膜下腔出血85例。结果 428例ACVD患者异常心电图382例(89.3%),表现为窦性心律失常(窦速、窦缓、窦律不齐)、房性心律失常(房早、房速、房颤)、室性心律失常(室早、室速)、传导阻滞(房室阻滞、束支阻滞),电解质紊乱(低钾),ST段、T波及U波改变,心肌梗死。ACVD心电图改变呈一过性、暂时性,并随病情恢复而好转。结论 ACVD患者应及时并跟踪检查心电图,必要时检查24hholter,可全面掌握脑心综合征所致心肌损害程度,充分认识其危害性并积极干预,能有效降低患者病死率。     

脑心综合征的临床特征及发病机制

卒中急性期患者可出现继发性心脏损害的症状、体征,以及心电图和心肌酶的变化,这些改变可随卒中症状的改善而逐渐恢复正常或遗留轻度异常,临床上常常称之为脑心综合征,本文就近年来关于脑心综合征的发病机制,临床特征以及转归和治疗方面做些综合阐述。     

急性脑卒中并发脑心综合征临床分析

目的 探讨急性脑卒中并发脑心综合征的发生机制及防治措施.方法 结合临床资料对226例急性脑卒中患者心电图及心肌酶谱进行回顾性分析.结果 脑心综合征发病率为26.5%,出血性脑卒中发病率明显高于缺血性脑卒中(P<0.01);脑心综合征的心电图改变主要表现为ST-T改变、各种心律失常和心肌梗死.合并脑心综合征的脑卒中患者病死率为48.3%,明显高于同期未合并脑心综合征的脑卒中患者(7.2%,P<0.01).结论 急性脑卒中脑心综合征的发生可能与脑卒中类型有关,机制可能与脑卒中直接或间接导致植物神经中枢功能失调、神经体液功能紊乱等有关.     

单胺类递质在大鼠脑出血心脏损伤中的作用

目的:观察脑出血条件下血浆去甲肾上腺素(NE)及血清肌酸磷酸激酶同工酶MB型(CK-MB)含量的变化,探讨脑心综合征发生、发展机制。方法:动态监测大鼠脑出血过程中血浆NE含量、血清CK-MB水平的变化,NE的测定采用高效液相-电化学法,CK-MB的测定采用酶反应速率法。结果:大鼠脑内血肿开始形成的6小时血浆NE、血清CK-MB均显著升高,并以脑出血24小时血肿高峰期时最为显著,随后逐渐下降。结论:外周NE含量升高可能参与脑心综合征的发生发展过程。     

Peripheral axotomy induces only very limited sprouting of coarse myelinated afferents into inner lamina II of rat spinal cord

Peripheral axotomy-induced sprouting of thick myelinated afferents (A-fibers) from laminae III-IV into laminae I-II of the spinal cord is a well-established hypothesis for the structural basis of neuropathic pain. However, we show here that the cholera toxin B subunit (CTB), a neuronal tracer used to demonstrate the sprouting of A-fibers in several earlier studies, also labels unmyelinated afferents (C-fibers) in lamina II and thin myelinated afferents in lamina I, when applied after peripheral nerve transection. The lamina II afferents also contained vasoactive intestinal polypeptide and galanin, two neuropeptides mainly expressed in small dorsal root ganglion (DRG) neurons and C-fibers. In an attempt to label large DRG neurons and A-fibers selectively, CTB was applied four days before axotomy (pre-injury-labelling), and sprouting was monitored after axotomy. We found that only a small number of A-fibers sprouted into inner lamina II, a region normally innervated by C-fibers, but not into outer lamina II or lamina I. Such sprouts made synaptic contact with dendrites in inner lamina II. Neuropeptide Y (NPY) was found in these sprouts in inner lamina II, an area very rich in Y1 receptor-positive processes. These results suggest that axotomy-induced sprouting from deeper to superficial layers is much less pronounced than previously assumed, in fact it is only marginal. This limited reorganization involves large NPY immunoreactive DRG neurons sprouting into the Y1 receptor-rich inner lamina II. Even if quantitatively small, it cannot be excluded that this represents a functional circuitry involved in neuropathic pain.     

Glutamate release by neurons evokes a purinergic inhibitory mechanism of osmotic glial cell swelling in the rat retina: activation by neuropeptide Y

Glial cell swelling is a central cause of ischemic edema in the brain and retina; however, the regulation of glial cell volume by endogenous factors in situ is largely unknown. In slices of the postischemic retina of the rat, the somata of glial (Müller) cells swell upon hypotonic stress that is not observed in slices of control retinas. We describe an endogenous signaling pathway that leads to inhibition of the osmotic glial cell swelling, and that is evoked by the release of glutamate from retinal neurons upon application of neuropeptide Y. Glutamate activates metabotropic glutamate receptors on swollen glial cells, which evokes a Ca2+ -independent purinergic signaling cascade that involves release of ATP, P2Y1 receptor activation, and transporter-mediated release of adenosine. Activation of A1 receptors causes the inhibition of osmotic glial cell swelling, by a protein kinase A-dependent activation of K+ and Cl- channels. It is proposed that the glutamate-evoked purinergic receptor signaling of glial cells is crucially involved in the cell volume homeostasis of the retina, and that this mechanism may contribute to the protective effect of adenosine in the ischemic tissue.     

Effects of monosodiuml-glutamate administration on neuropeptide Y-containing neurons in the rat hypothalamus

Immunocytochemical localization of neuropeptide Y (NPY) was performed in the hypothalamus of rats of which the arcuate nucleus had been destroyed with monosodiuml-glutamate in the neonatal period. The treatment produced a disappearance of most of the NPY cell bodies normally found in the arcuate nucleus. The concentration of fibers was decreased in the paraventricular nucleus, but not in the other hypothalamic nuclei. The treatment also induced the appearance of a large number of immunoreactive cell bodies in the paraventricular nucleus. These results strongly suggest that arcuate NPY neurons are projecting to the paraventricular nucleus and that the arcuate nucleus probably exerts some inhibitory tonic influence on NPY paraventricular neurons.     

Inhibition of sexual maturation in male rats by melatonin: evidence linking the mechanism of action to changes in the regulation of hypothalamic neuropeptide y

Activation of gonadotrophin-releasing hormone (GnRHJ pathways is a pivotal event in the process of sexual maturation, however the regulatory influences that precipitate this change and lead to the onset of puberty remain poorly understood. Recent studies indicate that neuropeptide Y (NPY) may participate in the regulation of luteinizing hormone secretion by modulating the pattern of GnRH secretion and by directly altering the pituitary responsiveness to GnRH stimulation. To determine whether NPY plays a role in puberty-associated changes in hypothalamic function, levels of NPY-like immunoreactivity (NPY-IR) were measured in a fragment of the hypothalamus encompassing the median eminence and medial portion of the arcuate nucleus (ME-AN), and also in the remainder of the hypothalamus from male rats of different ages. To identify changes in hypothaiamic NPY linked to the process of sexual development, the effect of delaying sexual maturation by daily afternoon administration of 100 μg melatonin (MT) from 20 to 40 days was investigated. In the hypothalamus and ME-AN, total NPY content increased progressively with age. Expressed as a concentration (fmol/μg extracted protein), peak values for the ME-AN (55.4 ± 7.0) were observed at 30 days of age followed by a decline to lower levels (30.2 ± 1.9) at 40 days. Daily afternoon administration of MT from 20 days of age resulted in significant increases (P<0.01) in the levels of NPY-IR in the ME-AN compared to control values at 30 and 40 days of age. MT was without effect on NPY-IR levels in the remainder of the hypothalamus. When MT was administered in the early morning, a procedure which does not delay sexual maturation, NPY-IR values for the ME-AN region were not different from control rats indicating that the MT-induced changes in NPY were related to the effects on sexual maturation. Using pituitary luteinizing hormone content and seminal vesicle weight as indices of sexual development, significant inverse correlation coefficients (P<0.001) between these parameters and the NPY concentration in the ME-AN were observed (r =-0.79 and -0.70, respectively). From published data it is not possible to conclude whether the main effects of NPY are exerted at the hypothalamic or pituitary level. However, the changes in the NPY content of the ME-AN observed during the onset of puberty, and the influence of MT on these changes, support assertions that NPY is involved in the regulation of sexual maturation.     

垂体腺瘤中NPY的表达和细胞定位

目的探讨不同病理类型垂体腺瘤中NPY的表达水平及其在瘤细胞中的定位特点。方法收集我科2003年~2005年诊治的垂体腺瘤57例。所有病例均经手术和病理确诊。肿瘤标本进行NPY免疫组化染色。6例垂体瘤标本进行免疫电镜研究。结果本组34/57例垂体腺瘤的NPY呈阳性表达,占59.65%。NPY阳性表达率在促性腺细胞腺瘤中最高达91.7%,生长激素腺瘤和促肾上皮质激素腺瘤次之均为66.7%,零细胞腺瘤和混和性腺瘤均为50%,泌乳素腺瘤表达率最低25%。NPY在不同类型垂体腺瘤中的表达差异有统计学意义(P<0.05)。NPY在亚细胞水平的定位:4/6例(GH腺瘤2例,GH-PRL混合性腺瘤1例,PRL腺瘤2例和促性腺细胞腺瘤1例)NPY免疫电镜结果呈阳性,胶体金颗粒呈散在或小簇状分布,主要存在于胞质中分泌颗粒上,此外,粗面内质网和细胞基质中也偶见散在的胶体金颗粒,其余细胞器很少有非特异吸附的胶体金颗粒。2例PRL腺瘤偶见NPY阳性颗粒。结论①不同类型垂体瘤的NPY表达各有差异。②促性腺细胞腺瘤中的NPY表达水平较高,泌乳素腺瘤中NPY表达较低。     

脑出血大鼠脑组织神经肽Y水平的变化及意义

目的 :探讨脑出血过程中中枢神经系统神经肽Y(NPY)含量的动态变化及意义。方法 :采用胶原酶和肝素联合注入尾状核的方法建立大鼠脑出血模型 ,测定出血前、出血后 30min ,6、1 2、2 4、48及 72h血肿周边、下丘脑及脑干NPY的活性。结果 :脑出血后血肿周边、下丘脑及脑干NPY的含量同步升高 ,并于 2 4h达峰值 ,48～ 72h开始回落 ,但仍显著高于出血前 (P <0 0 1 )。结论 :脑出血过程中 ,脑组织NPY活性增强 ,导致局部脑血流量减少 ,最终加重神经细胞损害     

Neuropeptide Y reduces orthodromically evoked population spike in rat hippocampal CA1 by a possibly presynaptic mechanism

Application of the brain neuropeptide Y (NPY) to rat hippocampus in vitro reversibly reduced the amplitude of the CA1 population spike evoked by stratum radiatum stimulation. Threshold for the effect was 10(-8) M. NPY had similar effects on single pulse- and paired pulse-evoked population spikes. Antidromic population spikes, evoked from the alveus, were unaffected by NPY. Thus, NPY appears to modulate excitatory transmission in the hippocampus by a presynaptic mechanism.     

Distribution of VIP- and NPY-like immunoreactivities in rat main olfactory bulb

The distribution of vasoactive intestinal peptide (VIP)- and neuropeptide Y (NPY)-like immunoreactivities in the Sprague-Dawley rat main olfactory bulb was analyzed using the peroxidase-antiperoxidase light microscopic immunocytochemical technique. VIP-like immunoreactivity was most prominently localized within a large number of intermediate-sized neurons whose perikarya and extensively branched varicose processes remained confined to the external plexiform layer (EPL). A few small short-axon type neurons in the mitral cell layer and granule cell layer (GRL) and even fewer large neurons in the glomerular layer (GL)/EPL border region contained immunoreactivity for VIP as well. Neuropeptide Y-like immunoreactivity (NPY-I) was principally localized within sparsely distributed large multipolar neurons of the deep GRL and within axons distributed with diminishing density from deep to superficial GRL. In addition, dense NPY-I was localized within very few large superficial short-axon type neurons of the GL/EPL border region. The restricted laminar and cellular distribution of NPY-I and VIP-I suggests that both peptides may act to modulate granule cell activity, and therefore, indirectly, olfactory bulb output.     

脑缺血再灌注心肌损伤老龄大鼠神经肽的变化

目的 从内皮素（ET）,降钙素基因相关肽（CGRP）,神经肽Y（NPY）,神经降压素（NT（的变化方面研究老龄大鼠脑缺血再灌注心肌损伤的机制。方法 青年（5月龄）和老龄（20月龄以上（大鼠均为分为模型组和正常对照组,观察大鼠全脑缺血30min 再灌注60 min后心肌组织病理形态和血浆,脑组织中ET,CGRP,NPY含量。结果 脑缺血再灌注心肌组织出现明显的病理改变,老龄大鼠较青年大鼠严重,青年对照组和青年模型组,老龄对照组脑组织中NPY低于青年对照组和老龄西药组,结论 脑缺血再灌注心肌损伤与以ET占优势的CGRP与ET的平衡失调有关,由于老龄大鼠ET与CGRP间平衡失调和NPY的增龄变化使脑缺血再灌注后这些病理改变较青年大鼠更为明显。