关于高血压卒中急性期的血压调控机制与血压管理的思考

高血压是卒中的主要原因及独立危险因素,有效控制高血压可使卒中发生率减少一半[1]。而卒中急性期的血压管理是决定卒中治疗成败的重要因素。目前高血压脑出血患者急性期的血压控制尚无统一的标准[2],对脑出血后高     

缺血性脑卒中的血压调控

近20年来,抗高血压治疗的最大收益是使卒中发病率降低了35%～50%。在缺血性脑卒中患者中患高血压的比例很高,TOAST研究亦提示腔隙性脑梗死患者中70%以上伴有高血压。由此可见,高血压与脑卒中密切相关,心内科和神经科医生在脑梗死急性期如何调控血压这个问题上一直存在分歧。因此,合理应用降压药,做好缺血性卒中的一级和二级预防以及脑卒中急性期如何合理调控血压是需要探讨的问题。     

动态血压负荷与脑微出血的关系研究

目的 探讨原发性高血压(essential hypeaension,EH)患者动态血压负荷(blood pressure load,BPL)参数与脑微出血(cerebral microbleeds,CMBs)的关系.方法 将原发性高血压患者分为2组:合并CMBs者为A组,其中血压达标者为A1组,血压不达标及未治疗者为A2组;无CMBs者为B组,其中血压达标者为B1组,血压不达标及未治疗者为B2组.全部患者作动态血压测定,比较2组各时域动态血压BPL差异及分级血压负荷(分为1~3级).结果 (1)A2组与B2组比较,24 h、日间及夜间收缩压BPL(SBPL)和舒张压BPL(DBPL)水平均有明显差异;A1组24 h-SBPL明显高于B1组;(2)A组1级高血压SB-PL、2级高血压与3级高血压SBPL、DBPL与B组相比存在明显差异.结论 24 h、日间及夜间的SBPL和DBPL增高与CMBs的发生有密切关系;2级、3级SBPL、DBPL的增加,均可能预示脑微出血的发生.     

脑梗死急性期血压变化与预后的关系及血压管理

目的观察脑梗死患者急性期血压变化与预后的关系以及对血压管理的影响。方法选取2011-02—2012-07我院就诊的脑梗死急性期(24h)患者153例为研究对象,记录患者急性期发病时的血压以及在1~3d后的动态血压监测,所有患者采用日常生活活动能力量表(BI)、改良后Rankin表以及美国国立卫生研究院卒中量表(NIHSS)进行评定。结果研究对象中合并原发高血压104例,入院时急性期血压以重度高血压为主85例(81.73%);未合并49例,入院时急性期血压以低血压为主19例(38.78%)。患者急性期收缩压和舒张压与入院后第3天比较差异有统计学意义(t=4.786、5.697,P0.01),出院时低血压组、正常或轻度血压升高组和重度高血压组日常生活活动能力量表评分差异无统计学意义(P0.05),改良Rankin评分和脑NIHSS评分,正常或轻度血压升高组评分小于其余2组(P0.05)。3组并发症差异无统计学意义(P0.05)。结论脑梗死患者急性期血压过高或过低均可能加重病情,脑梗死急性期注意血压监测以及保持血压正常或轻度升高对患者预后具有重要意义。     

脑梗死急性期患者的高血压分级及其血压变化的分析

目的 观察脑梗死急性期患者的血压变化。方法 对203例脑梗死急性期患者的高血压进行分级，并观察其住院7天内的血压变化。结果 (1)110例人院时血压最高，93例住院后继续升高，其中72例持续到住院3天内下降。(2)单纯收缩期高血压和I级高血压患者血压恢复正常的比例高于Ⅱ、Ⅲ级高血压患者(P＜0．01)。(3)抗高血压治疗与非抗高血压治疗血压恢复正常的比例虽无显著差异，但Ⅲ级高血压，大灶梗死者死亡率高。结论 脑梗死急性期患者的高血压分级有助于合理的个体化抗高血压治疗。     

自发性脑出血急性期血压管理的研究进展

高血压与自发性脑出血的发病、进展和预后息息相关,然而在脑出血治疗的过程中,由于血压对于血肿体积和脑灌注压的影响,是否对脑出血急性期血压给予控制存有争论。本文总结了目前关于脑出血急性期血压控制的主要观点,并对其相关的治疗策略进行综述。     

卒中急性期的血压管理

血压升高是卒中急性期患者的常见并发症对缺血性卒中而言,高血压与脑水肿有关,升高的血压可以避免脑灌注压及脑血流量的降低,而且已有升高血压治疗急性脑缺血的研究报道[1],对于出血性卒中的急性期患者,由于缺乏有力的临床证据,高血压与患者预后的关系目前还不明确.……     

脑卒中急性期血压变化规律及影响因素的研究

目的 观察脑卒中急性期血压变化规律及其影响因素.方法 研究发病24h内入院的急性脑卒中患者704例.监测入院后7d内血压,收集详细病史资料,对病程中伴发疾病进行评分,记录入院后血压的管理方式及干预时间等.运用简单和多因素统计方法进行数据的统计分析.结果 脑卒中急性期血压升高,并且存在自发下降趋势,8h内下降最明显,36h趋于稳定.其中脑梗死患者血压在入院30h内趋于稳定,脑出血患者血压在入院96h内趋于稳定.出血性卒中患者血压要高于缺血性卒中患者.缺血性卒中患者TOAST分型和OCSP分型间血压无显著差异.神经功能缺损程度影响入院时和入院后36h内血压.独立影响入院时收缩压的因素有卒中类型、入院时NIHSS评分、心脏病史、高血压史,其中心脏病史与入院时血压成负相关.独立影响入院时舒张压的因素有卒中类型、年龄、入院NIHSS评分、高血压史.年龄与入院时舒张压呈负相关.独立影响7d内平均收缩压的因素有卒中类型、入院NIHSS评分、伴发疾病评分、心脏病史、高血压史、既往史评分.心脏病史与7d平均血压呈负相关.影响入院7d内舒张压的因素有卒中类型、年龄、伴发疾病评分、入院NIHSS评分、心脏病史.心脏病史和年龄与7d平均舒张压呈负相关.结论 脑卒中急性期血压升高,并有自发性下降趋势.卒中类型及高血压史与血压呈正相关,心脏病史及年龄与血压呈负相关.     

缺血性卒中血压控制新展望——2011 AHA/ASA缺血性卒中及短暂性缺血性发作预防指南

2010年12月在STROKE官方网站上率先公布了《2011版AHA/ASA缺血性卒中及短暂性缺血性发作（TIA）预防指南》（后简称《指南》）[1],与2006版（2）及2006版之后的部分更新相比,该新版指南在针对血压控制方面,     

卒中急性期血压管理的研究现状

高血压为卒中的独立危险因素,适当降低血压是卒中一级和二级预防的重要组成部分[1].血压升高是卒中急性期的常见并发症,与预后不良相关.由于缺乏确切的临床试验证据,卒中急性期血压水平与临床预后的相关性及血压控制原则目前仍未达成一致意见[2].国际高血压协会对此提出了3个尚待解决的问题[3]:急性缺血性卒中患者血压升高时是否需要降压治疗;无高血压者是否应在不增加出血风险的前提下行升压治疗以改善缺血区的血流灌注?原发性脑出血急性期的患者是否需要降压治疗?长期降压治疗的患者,急性卒中后应继续使用还是停用降压药物?我们综述卒中急性期血压变化及血压管理的研究,并总结目前卒中急性期的血压治疗指南.     

Development of the projection from the nucleus of the brachium of the inferior colliculus to the superior colliculus in the ferret

Neurons in the deeper layers of the superior colliculus (SC) have spatially tuned receptive fields that are arranged to form a map of auditory space. The spatial tuning of these neurons emerges gradually in an experience-dependent manner after the onset of hearing, but the relative contributions of peripheral and central factors in this process of maturation are unknown. We have studied the postnatal development of the projection to the ferret SC from the nucleus of the brachium of the inferior colliculus (nBIC), its main source of auditory input, to determine whether the emergence of auditory map topography can be attributed to anatomical rewiring of this projection. The pattern of retrograde labeling produced by injections of fluorescent microspheres in the SC on postnatal day (P) 0 and just after the age of hearing onset (P29), showed that the nBIC-SC projection is topographically organized in the rostrocaudal axis, along which sound azimuth is represented, from birth. Injections of biotinylated dextran amine-fluorescein into the nBIC at different ages (P30, 60, and 90) labeled axons with numerous terminals and en passant boutons throughout the deeper layers of the SC. This labeling covered the entire mediolateral extent of the SC, but, in keeping with the pattern of retrograde labeling following microsphere injections in the SC, was more restricted rostrocaudally. No systematic changes were observed with age. The stability of the nBIC-SC projection over this period suggests that developmental changes in auditory spatial tuning involve other processes, rather than a gross refinement of the projection from the nBIC.     

Mechanisms of the suppression of the nociceptive reflex of the opening of the mouth during stimulation of the structures of the limbic brain

The comparative effectiveness of the inhibitory influence of tetanic stimulation of hypothalamus, amygdala and limbic cortex on EMG-response of m. digastricus evoked by electrical stimulation of tooth pulp nociceptive afferents was studied in cats anesthetized with a mixture of chloralose and nembutal. It was found that inhibition of the EMG-component of the jaw-opening reflex is most pronounced in case of stimulation of medial and lateral region of the hypothalamus, the inhibitory effect of central and medial nuclei of the amygdala is less pronounced and the effect of the limbic cortex is the weakest. It was shown that the mechanism of the antinociceptive effect of tetanic stimulation of the hypothalamus is not related to the concomitant increase of the blood pressure. After stabilization of the blood pressure the suppressive effect of the hypothalamus remains without changes, that points out to a direct, primary, not baro-afferent mechanism of the inhibition of the activity of nociceptive neurons of the trigeminal sensory nuclei. Noradrenaline, injected intravenously, induced a large increase of the blood pressure accompanied by a pronounced inhibition of the pain reflex. Angiotensin causes the same degree of blood pressure elevation without changes in the amplitude of the EMG-response of the pain reflex. Hypothalamic and noradrenergic mechanisms for control of pain sensitivity are discussed.     

The organization of the connections between the cortex and the claustrum in the monkey

The distribution of labelled cells and of extracellular granules in the claustrum has been studied after injections of horseradish peroxidase in several areas of the neocortex. The frontal and parietal lobes are related to the anterior and posterior halves respectively of the claustrum, and the occipital and temporal cortex to the posterior and inferior margins. Parts of the claustrum related to areas of the cortex in the frontal lobe overlap considerably in the antero-posterior dimension with parts related to widely separated but interconnected areas of the parieto-temporal cortex. Areas of cortex within one lobe which are interconnected are related to parts of the claustrum which overlap in the dorsoventral dimension.     

Experimental study of the projections of the nucleus of the tractus solitarius and the area postrema in the cat

Projections from the area postrema and adjacent parts of the medial solitary nucleus are demonstrated with the Nauta method following lesions limited exclusively to these structures. Experiments are controlled with lesions involving adjacent bulbar regions, cerebellum, and spinal cord. Ascending pathways in the dorsal and lateral columns of the spinal cord project ipsilaterally to the area postrema and bilaterally to a para-alar nucleus in the ventral periphery of the nucleus gracilis. Neurons in the area postrema project mainly inspilaterally to the dorsal and medial regions of the medial solitary nucleus. Neurons in the posterior half of the medical solitary nucleus project ipsilaterally to the lateral solitary nucleus, dorsal vagal nucleus, ambigus, retrofacial nucleus, and dorsal and lateral bulbar reticular formation. Projections to nuclei intercalatus and prepositus hypoglossi, bilaterally, and to the ipsilateral dorsal tegmental nucleus by way of the dorsal longitudinal fasciculus are also shown. No direct projections to the diencephalon are demonstrated. Control lesions in the dorsal column nuclei reveal projections to the contralateral inferior olive and thalamic reticular and ventrobasal nuclei, but not to the projection sites of the solitary nucleus. Evidence is given to support the hypothesis that ascening visceral pathways are interruped in the bulbar reticular formation and dorsal tegmental nucleus before reaching the diencephalon. Correlations are suggested with functional aspects of the central autonomic and reticular activating systems.