血压对自发性高血压大鼠脑出血后血肿周围水肿的影响

目的 探讨自发性高血压大鼠(spontaneous hypertensive rat,sHR)脑出血后血肿与血肿周围水肿变化以及血压与血肿周围水肿的相关性.方法 24只6月龄雄性SHR,随机分为脑出血1、3、5和7d组(每组6只).尾袖法测定血压,Ⅳ型胶原酶注入尾壳核建立脑出血模型,磁共振T2加权成像观察血肿、血肿周围水肿.结果 模型制作后1d时的血压较模型制作前显著降低,3d起血压逐渐升高.平行轮廓检验显示,血压变化率与血肿周围水肿体积变化率之间的总体轮廓相互平行(F=2.820,P =0.063),重合轮廓检验显示,两者总体轮廓不重合(F=10.961,P=0.000),即血肿周围水肿体积变化率与血压变化率趋势一致.收缩压变化率与血肿周围水肿体积变化率(r=0.527,P=0.024)和血肿体积变化率(r=0.755,P=0.000)均呈显著正相关.结论 SHR脑出血当天脑水肿即出现并迅速扩大,3d时达峰值,此后逐渐消退.脑出血后1d时血压显著下降,3d起开始逐渐升高,直至7d.血压与血肿周围水肿体积的变化趋势相互平行,收缩压变化率与血肿周围水肿体积变化率呈正相关.     

Detailed Disease Processes of Cerebral Pericytes and Astrocytes in Stroke-Prone SHR

We examined ultrastructurally cerebral pericytes and astrocytes in 20 normotensive Wistar Kyoto rats and 60 asymptomatic stroke-prone spontaneously hypertensive rats, which were sequentially killed at 4–52 weeks of age. Another 30 SHRSP were killed soon after they showed symptoms of stroke. We found two kinds of pericytes around the capillaries; granular pericytes and filamentous pericytes. Granular pericytes possibly serve as scavenger cells in the central nervous system and became active and grew in size with time. In contrast, filamentous pericytes degenerated during the development of hypertension. Degeneration of the filamentous pericytes was involved in an increase of endothelial permeability. Increased permeability caused focal and then circumferential swelling of the astrocytes around the capillaries. Swelling of the astrocytes seemed to accelerate the production of attachment plaques. Following this increase in the number of attachment plaques, numerous astrocytic filaments were produced within the cytoplasm. As a result, fibrous astrocytes were fully developed. Adjacent to the fibrous astrocytes we detected opening of the interendothelial junctions as well as dead neurons. From these observations we propose that astrocytes perform the main function in trophic interactions among cerebral endothelial cells, astrocytes, and neurons and that dysfunction of astrocytes disturbs the neural environment, resulting in neuronal death.     

“血不利则为水”理论论治心力衰竭研究

心力衰竭是临床常见难治疾病,是众多心血管疾病常见的直接死亡原因之一,其病因病机与气、血、水关系密切,其发展规律多在本“虚”的基础上产生了“瘀”“水”等病理产物,而“瘀”“水”又可互生,相因为病。张仲景在《金匮要略·水气病篇》中提出的“血不利则为水”这一论点,阐述了血水相因为病的内在联系,与心力衰竭的病机相吻合,同时也为活血利水法的实施提供了理论依据。本文结合心力衰竭的临床表现和病因病机,讨论分析“血不利则为水”的内涵及其在心力衰竭治疗中的应用和机理,认为在心力衰竭的治疗上当兼顾本虚和标实,在益气补虚的基础上灵活运用活血利水法,三者并用,各有侧重,为心力衰竭的临床治疗和实验研究提供理论依据和新的思路。     

脑出血后脑水肿的磁共振波谱成像及相关因素的分析

目的观察脑出血后迟发反常性脑水肿的磁共振波谱特点,并对其发生相关因素进行分析。方法对12例脑出血后第7天及14天脑水肿患者分别进行磁共振波谱成像（MRS）检查,观察血肿周围迟发水肿组织的MRS谱线特点,与脑出血后一周水肿的谱线的进行对照研究,定量分析相关代谢物的峰值的变化。结果9例患者获得满意谱线,血肿周围的14d水肿区NAA／Cr较7d血肿周围水肿区域明显降低（15．7％±9．2％）（P〈0．01）。在第14天谱线中,7例检测出的乳酸峰,8例患者检测出甘露醇峰。结论脑出血水肿区MRS的NAA／Cr降低及乳酸峰出现,说明水肿区神经元的受损及缺血,迟发反常水肿区的甘露醇峰的存在,对迟发反常水肿起到重要作用,提示局部的血一脑脊液屏障的破坏。     

低分子右旋糖酐联合呋塞米治疗肾病综合征水肿的疗效观察

目的观察低分子右旋糖酐联合呋塞米对原发性。肾病综合征患儿的利尿作用。方法采取自身对照方法,对2008年1月至2008年12月在中山大学附属第一医院就诊的74例原发性肾病综合征患儿先后给予生理盐水联合呋塞米、低分子右旋糖酐联合呋塞米进行利尿治疗,观察比较两种利尿方法的效果。结果患儿使用低分子右旋糖酐联合呋塞米时的24h尿量、尿钠和尿钾多于生理盐水联合呋塞米时,24h尿量尤为显著（P〈0．05）;在静脉滴注低分子右旋糖酐联合呋塞米的过程中有12例患儿出现血压升高,其中7例出现高血压,所有血压升高者在停药后血压均可自行恢复正常,有1例患儿出现过敏反应。结论低分子右旋糖酐联合呋塞米能快速、有效地治疗肾病综合征患儿水肿,但需注意监测血压变化和防治过敏反应。     

实验性大鼠脑出血后白细胞介素2和8表达的变化

目的观察实验性大鼠脑出血后白细胞介素2和白细胞介素8的表达及其与脑出血后脑含水量变化的关系。方法通过采用未抗凝新鲜自体股动脉血注入大鼠尾状核建立脑出血动物模型,用放射免疫法测定脑出血后6 h1、2 h、24 h、3天6、天和10天等时间点白细胞介素2和白细胞介素8的表达,用干重—湿重法测定脑出血后脑含水量的变化,并与白细胞介素2和白细胞介素8进行相关分析。结果与对照组比较,血肿周围组织中白细胞介素2水平在脑出血后6 h和1天显著降低(P<0.01),3天时轻度降低(P>0.05),6天时达高峰(P<0.01),10天时接近正常(P>0.05)。白细胞介素8水平在脑出血后1天和3天时显著升高(P<0.05),6天时降至正常(P>0.05)。血肿周围组织含水量在脑出血后6 h轻度增加(P>0.05),1天时增加显著(P<0.01),3天时达高峰(P<0.01),10天时基本恢复正常。白细胞介素8的变化与脑含水量的变化趋势一致(R2=0.861)。结论白细胞介素2有利于抑制脑水肿的形成;白细胞介素8可能参与实验性脑出血后血肿周围水肿的发生、发展。