偏头痛患者血浆内皮素与环核苷酸水平的变化

目的;研究偏头痛病人血浆内皮素和环核苷酸在发作期和间歇期的水平变化,探讨这些生化因素在偏头痛发生与发展中的作用。方法：空腹抽取偏头痛发作期及间歇期患肘静脉因4ml,测定血浆内皮素及环核苷酸水平,并随机用健康人对照。结果：偏头痛病人发作时,血浆内皮素水平显高于对照组（P＜0．01）及间歇期（P＜0．05）,环磷酸腺苷明显升高（P＜0．01）,环磷酸鸟苷明显下降（P＜0．05）。结论：偏头痛的发病与血浆内皮素密切相关,发作时明显升高。偏头痛存在自主神经功能失调,表现为交感神经功能亢进,副交感神经功能低下。     

偏头痛患者血浆内皮素与降钙素相基因关肽水平检测的临床意义

目的 探讨偏头痛患者血浆内皮素与降钙素基因相关肽变化的临床意义.方法 检测51例偏头痛患者发作期与间歇期的EF-1与CGRP的数值,并与对照组进行比较分析.结果 检测结果发现偏头痛者血浆内皮素高于对照组,而降钙素基因相关肽低于对照组;发作期与间歇期比较,内皮素与降钙素基因相关肽均有显著差异(P＜0.01).结论 检测结果提示偏头痛患者血管内系统存在异常,对偏头痛的临床诊断具有重要意义.     

偏头痛患者血清一氧化氮测定的临床意义

目的：研究偏头痛发作与患者血清一氧化氮（NO）和环磷酸鸟苷（cGMP)变化的关系及其临床意义。方法：用荧分光光度法和放射免疫法分别检测32列偏头痛发作期、25例间歇期和30例正常人血清中NO2和cGMP的含量。结果：偏头痛发作期患者血清中NO2和cGMP的含量明显高于间歇期和正常对照组（P＜0．01）。偏头痛间歇期患者血清中NO2和cGMP的含量仍高于正常对照组（P＜0．01）。结论：NO和cGMP的变化可能参与偏头痛的病理生理过程。     

偏头痛患者血小板活化状态的观察

本文测定了３８例偏头痛病人和相应对照组的血小板内游离Ｃａ～（２＋）浓度和血小板聚集率的变化。结果显示：偏头痛患者血小板内游离Ｃａ～（２＋）浓度明显高于对照组，并且偏头痛发作期组明显高于偏头间歇期组（Ｐ＜０．０５），与对照组比较，偏头痛间歇期组血小板聚集率无明显变化（Ｐ＞０．０５），偏头痛发作期组血小板聚集率明显增加（Ｐ＜０．０５）。提示血小板外Ｃａ～（２＋）内流和血小板聚集率增强参与了偏头痛的症状发作．有效地抑制血小板Ｃａ～（２＋）内流对预防和治疗偏头痛将起到重要作用。     

偏头痛患者TCD、MRA及其相关生化因子变化的意义

目的：观察颅内血管形态、血管舒缩变化,相关生化因子的变化与偏头痛的关系和在评价临床意义中的价值。方法：30例临床确诊为偏头痛的患者,经颅多谱勒（TCD）和复式彩码双功能多谱勒测定颅内外血流情况、头颅磁共振血管像（MRA）探查颅内血管形态,此外,采用放免等方法测定发作间歇期血小板5－羟色胺（5－HT）、β－内啡肽（β－EP）、神经降压素（NT）、精氨酸加压素（AVP）和血栓烷A2（TXA2）含量,并与20例健康对照组进行比较。结果：偏头痛间歇期双侧大脑中动脉（MCA）和基底动脉（BA）血流速度明显增高（P＜0．01）,颞浅动脉（STA）没有显著性变化（P＞0．05） ;MRA显示6例患者颅内动脉异常;血浆5－HT、NT含量偏头痛显著高于对照组（P＜0．01）,血浆β－EP、AVP、TXB2偏头痛组显著低于对照组（P＜0．05）。结论：偏头痛患者可能有先天血管发育异常,发作期间歇期颅内动脉存在血流速度增快,血浆5－HT、β－EP、NT、AVP和TXB2与偏头痛发病有关。     

急性脑血管病现变性质量严重程度与血浆内皮素-1浓度的关系

目的：主要是探讨急性脑血管病患者病变性质、严重程度与血浆内皮素－1（ET－1）浓度的关系。方法：应用放射免疫方法测定87例急性脑血管病人血浆ET－1浓度并与42例正常人进行比较。结果：脑出血与脑梗塞组血浆ET－1浓度明显高于对照组（P＜0．001），而脑梗塞组血浆ET－1浓度比脑出血组升高，但未有统计学意义（P＞0．05）。急性脑血管病重型者比轻型者血浆ET－1浓度明显升高（P＜0．01），合并高血压者血浆ET－1浓度较正常对照组显著升高（P＜0．001），而与血压正常组相比较二者无显著性差异（P＞0．05）。结论：提示急性脑血管病患者血浆ET－1浓度升高与病变严重程度、血压升高有一定关系，与病变性质虽无统计学意义，但脑梗死者也较脑出血组升高，表明ET－1作为一种内源性血管活性肽在急性脑血管病的预后和发病机制方面是一种有害的介质。     

偏头痛患者血浆内皮素与降钙素基因相关肽水平检测的临床意义

目的探讨偏头痛患者血浆内皮素与降钙素基因相关肽变化的临床意义。方法检测51例偏头痛患者发作期与间歇期的EF-1与CGRP的数值,并与对照组进行比较分析。结果检测结果发现偏头痛者血浆内皮素高于对照组,而降钙素基因相关肽低于对照组;发作期与间歇期比较,内皮素与降钙素基因相关肽均有显著差异(P<0.01)。结论检测结果提示偏头痛患者血管内系统存在异常,对偏头痛的临床诊断具有重要意义。     

哮喘患者血浆内皮素测定及其临床意义

应用放射免疫方法测定了27例哮喘发作、18例哮喘缓解状态患者血浆内皮素浓度，并与42例正常人进行比较。结果表明，哮喘发作患者血浆内皮素浓度明显高于正常人及哮喘缓解状态者（P值分别为P＜0．01与P＜0．05），而哮喘缓解组与正常对照组间无显著性差异（P＞0．05）。提示血浆内皮素浓度与哮喘发作有关，可能是哮喘发作的中间介质。     

偏头痛患者血清中过氧化物酶体增殖物激活受体γ水平研究

目的：观察不同时期及不同亚型偏头痛患者血清中过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptorγ,PPARγ）水平变化,探讨其与偏头痛的关系及临床意义。方法收集偏头痛患者105例,随机分成偏头痛发作期组（A 组,n＝47）和偏头痛发作间期组（B 组,n＝58）,再根据患者有无先兆症状进一步分成四个亚组,同时选取100例健康者作为对照组。采用酶联免疫法（ELISA）检测受试者血清PPARγ水平,采用SPSS系统软件进行统计分析。结果偏头痛患者发作期PPARγ水平明显低于发作间期及健康对照者（P＜0.01）;发作间期的 PPARγ水平与健康对照者相比无明显统计学差异（P＞0.05）;有先兆与无先兆发作期PPARγ水平比较无明显差异（P＞0.05）;有先兆和无先兆发作间期PPARγ水平无明显统计学差异（P＞0.05）。结论偏头痛发作时血清PPARγ下调,其可能是偏头痛发病的潜在机制之一。有无先兆对PPARγ水平无明显影响。     

偏头痛患者血浆一氧化氮和内皮素含量的相关性研究

目的观察偏头痛患者急性发作期及缓解期血浆一氧化氮(NO)和内皮素(ET)的含量变化及探讨两者在偏头痛发病机制中的作用.方法应用高效液相色谱分析法测定NO的含量,用放射免疫法测定ET的含量.结果偏头痛患者急性发作期血浆NO和ET含量均显著高于正常对照组(P＜0.05),偏头痛缓解期血浆NO降低,与对照组比较无显著差异(P＞0.05).血浆ET含量也降低,但仍高于正常对照组(P＜0.05).急性发作期血浆NO和ET含量呈显著正相关(r=0.564,P＜0.01).还发现偏头痛患者急性发作期血浆NO和ET比值较对照组降低(P＜0.05),而缓解期较对照组增高(P＜0.05).结论偏头痛患者可能存在血浆NO和ET的动态失衡,影响血管的舒缩功能.     

Neuropeptide Y in Juvenile Migraine and Tension-Type Headache

SYNOPSIS
Neuropeptide Y (NPY) is widely distributed throughout sympathetic nerve endings where it is co-stored and co-secreted with noradrenaline. It is considered a marker of noradrenergic function. To determine the role of NPY in the pathogenesis of juvenile headache, we determined its plasma levels in two groups of young migraine patients (with and without aura), in a group of episodic tension-type headache patients and in a group of age and sex-matched healthy subjects. Significantly lower plasma levels of NPY were evident in the migraine patients with aura (P<0.001) and, to lesser extent, in the migraine patients without aura (P<0.02), both assessed in the interictal period, with respect to the control group. Plasma NPY levels tended to significantly increase during attacks in migraine patients with aura (P<0.0009). A less evident, though significant increase was also present during attacks in migraine patients without aura (P<0.02). No significant variations were observed between headache-free periods and attacks in tension-type headache patients. Reduced NPY levels in the interictal period can be considered further evidence of the derangement of the sympathetic function in the course of migraine, particularly that with aura. The increase in NPY levels during migraine attacks could be an expression of sympathetic activation, even though the functional status of this system is less efficient.     

Intermittent hypoendorphinaemia in migraine attack

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.     

Absence of vasoactive peptide release from brain to cerebral circulation during onset of migraine with aura

In eight patients carotid angiography was required for evaluation of transient neurological attacks. Cerebral blood flow results, angiography and clinical observations subsequently suggested the diagnosis of migraine. We measured plasma concentrations of substance P(SP), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) in repeated blood samples obtained from the carotid artery and the internal jugular vein in conjunction with cerebral angiography followed by 4 to 6 repeated recordings of regional cerebral blood flow (rCBF) with the intracarotid Xenon-133 injection technique. This technique is known to induce attacks of migraine with aura in many sufferers. Four patients developed aura symptoms. In three this was succeeded by throbbing headache, Typical, migraine-related, focal hypoperfusion occurred in conjunction with the aura symptoms. The remaining four patients had no symptoms or rCBF changes. There were no systematic or statistically significant changes over time in arterial-venous plasma concentrations or in the release rates of any of the peptides. All migraineurs had an overall elevated mean CGRP value compared to control values from the literature. The overall plasma levels of the potent vasoconstrictor NPY were higher ( p < 0.10) in the group that developed symptoms and rCBF changes (136 pmol/l) than in the non-symptomatic group (97 pmol/l). The difference in NPY levels could perhaps be associated with the focal rCBF decrease seen in the attack group.     

Mmp-9 immunoreactivity in acute migraine

OBJECTIVE: To examine the role of matrix metalloproteinase 9 (MMP-9) in migraine during headache and asymptomatic periods. METHODS: Thirty-four patients with migraine with and without aura (according to International Headache Society criteria) were studied. Clinical characteristic of headache were recorded. Blood samples for measurement of MMP-9 were drawn during headache attacks and during asymptomatic periods in all patients and in 10 healthy controls. RESULTS: We found higher plasma MMP-9 levels in migraine patients than in control group (129.3 [78.0-258.9] vs. 49.6 [39.1-64.3] ng/mL; P < .001). Migrainous patients showed higher MMP-9 plasma levels during headache attacks than in asymptomatic periods, both in migraine without aura (338.4 [275.1-396.2] vs. 118.2 [75.3-137.5] ng/mL; P < .0001), and migraine with aura (389.3 [273.4-487.1] vs. 139.3 [107.3-191.4] ng/mL; P < .0001). CONCLUSIONS: Our study showed an increased production of MMP-9 during migraine attacks. These data suggest a possible role of inflammation or blood-brain barrier disruption during the migraine attack.     

血浆神经肽Y含量变化与原发性高血压并发心功能不全相关性研究

目的 探讨血浆神经肽Ｙ（ＮＰＹ）含量变化在原发高血压合并心功能不全中的临床意义。方法 采用放射免疫分析法。结果 原发性高血压并发心功能不全患者血浆ＮＰＹ含量较原发性高血压无心功能不全组显著升高（Ｐ〈０．０１）;且随着心功能不全程度的加重,血浆ＮＰＹ水平明显升高（Ｐ〈０．０５）,两者呈正相关（ｒ＝０．４８５,Ｐ〈０．０５）。结论 血浆ＮＰＹ含理变化在高血压并发心功能不全中可能起着一定的作用。     

针刺对偏头痛大鼠血浆内皮素与神经肽Y变化的影响

目的观察针刺对偏头痛大鼠血浆内皮素(endothelin,ET)和神经肽Y(neuropeptideY,NPY)的影响,并探讨其在偏头痛治疗中的作用。方法将40只大鼠随机分为正常对照组、模型对照组、针刺对照组和治疗组;采用放射免疫法测定颈静脉(externaljugularvein,EJV)血中ET和NPY含量。结果与正常对照组比较,模型对照组ET和NPY水平显著升高(P<0.05);与模型对照组比较,治疗组ET和NPY水平显著降低(P<0.05)。结论针刺治疗偏头痛可能是通过调节ET和NPY等神经递质的含量而发挥作用的。     

Vasoactive peptide levels in the plasma of young migraine patients with and without aura assessed both interictally and ictally

We measured, by RIA methods, ictal and interictal levels of substance P (SP), calcitonin-gene related peptide (CGRP) and neurokinin A (NKA) in the plasma of 30 young migraine patients with aura (MPA) and 45 migraine patients without aura (MWA), and compared the results with those of 30 age-matched controls. There were no significant differences between the levels of these vasoactive peptides in the control group and the levels in both migraine groups studied in headache-free periods. An elevation of CGRP levels in plasma was found during attacks in MPA and, to a lesser extent, in MWA ( p < 0.03 and p < 0.05, respectively). A significant increase in NKA levels was also demonstrated in the MPA and MWA groups ( p < 0.02 and p < 0.04, respectively). These data suggest, although indirectly, that CGRP and NKA could be involved in the pathogenesis of migraine attacks in juvenile migraine patients.     

Neuropeptides in migraine and cluster headache

The cerebral circulation is invested by a rich network of neuropeptide Y (NPY) and noradrenaline containing sympathetic nerve fibers in arteries, arterioles and veins. However, the nerve supply of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) containing fibers is sparse. While noradrenaline and NPY cause vasoconstriction, VIP, SP and CGRP are potent vasodilators. Stimulation of the trigeminal ganglion in cat and man elicits release of SP and CGRP. Subjects with spontaneous attacks of migraine show release of CGRP in parallel with headache. Cluster headache patients have release of CGRP and VIP during bouts. Treatment with sumatriptan aborts headache in migraine and cluster headache as well as the concomitant peptide release.     

Neuropeptides in the cerebral circulation: relevance to headache

The article briefly describes the innervation of the human cerebral circulation by nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gent-related peptide (CGRP). The neuropeptides in human cerebral arteries were characterized by radioimmunoassay in combination with HPLC. These neuropeptides mediate contraction (NPY) and dilatation (VIP, SP, CGRP). In conjunction with spontaneous attacks of migraine or cluster headache, release of CGRP is seen. With the associated symptoms of nasal congestion and rhinorrhea, VIP is released. Successful treatment may abort the peptide release in parallel with disappearance of headache.