内皮素对失血性休克鼠脑微循环的影响及尼莫地平、川芎嗪的治疗作用

利用大鼠颅骨开窗观察脑软膜微循环的方法研究了内皮素（ＥＴ－１）从１０－７～１０－１０Ｍ对脑软膜微循环的影响以及失血性休克时脑软膜对ＥＴ－１的反应性。并用１０－７Ｍ造成失血性休克后脑血管痉挛的模型，观察尼莫地平、川芎嗪、６５４－２内对皮素引起血管痉挛的治疗作用。结果显示：１０－９、１０－８、１０－７Ｍ三种浓度ＥＴ－１可使脑软膜小动脉、细动脉强烈收缩，收缩率分别为２７．７％、１６．８％、７８．５％，其收缩强度与ＥＴ－１的浓度有关。对静脉的作用不明显。１０－１０ＭＥＴ－１可使细动脉轻度扩张。出血性休克时，脑软膜血流明显减慢，小动脉、细动脉管径对ＥＴ－１的收缩作用更敏感，脑组织血流明显减少。尼莫地平具有较好的拮抗ＥＬ－１引起脑软膜动脉的收缩和改善局部微循环的作用。川芎嗪也能拮抗ＥＴ－１引起脑软膜动脉的收缩，但作用较尼莫地平弱。６５４－２不能缓解ＥＴ－１对脑软膜动脉的收缩作用。     

脑康复冲剂对大鼠软脑膜微循环作用的实验研究

目的：脑康复冲剂临床用于治疗脑血栓血瘀证患者，本实验观察其对在大鼠实验性软脑膜微循环障碍的影响。方法：大鼠预防性给药，用高分子右旋糖酐水溶液静脉注射形成大鼠软脑膜的微循环障碍，观察脑康复冲剂对大鼠微循环的影响。结果：用高分子右旋糖酐造模后，大鼠软脑膜的微循环发生障碍，表现为血液流速减慢、血细胞聚集等，脑康复冲剂组血流速度开始减慢的时间明显比生理盐水对照组延长，且分级数也明显优于生理盐水组，对高分子右旋糖酐造成的血液流态障碍，脑康复组明显好于生理盐水组（P＜0．05），毛细血管网交叉点数开始减少的时间也比生理盐水对照组延长，差异显著（P＜0．01）。结论：脑康复冲剂使大鼠血流速度和血液流态得到改善，具有预防和改善动物脑微循环障碍的作用。     

电刺激中缝背核对家兔脑皮质微血流的影响

目的应用氢清除法测定局部脑组织血流（ｒＣＢＦ）及观测软脑膜血管微循环,探讨电刺激兔中缝背核（ＤＲＮ）对脑皮质微血流的影响及其机理。方法选用健康家兔３３只、随机分为四组。单纯刺激组（ｎ＝１５）．单纯刺激ＤＲＮ后,连续观察３０ｍｉｎ内局部脑组织血流（ｒＣＢＦ,ｎ＝１０）或软脑膜血管微循环的变化（ｎ＝５）。尼莫地平组（ｎ＝６）,在电刺激ＤＲＮ之前先静注尼莫地平（５μｇ／ｋｇ）。切断颈交感神经组（ｎ＝６）。切断两侧预交感神经后、再刺激 ＤＲＮ,破坏兰斑核组（ＬＣ, ｎ＝６）,破坏同侧兰斑核后再刺激ＤＲＮ,分别观察ｒＣＢＦ的变化。结果电刺激ＤＲＮ后脑皮质ｒＣＢＦ减少４４．２％（Ｐ＜０．０１）,软脑膜微动脉管径缩小,血流速度减慢,血流量减少,作用持续 １５ｍｉｎ。而尼莫地平可取消其作用。切断颈交感神经或破坏ＬＣ后再刺激ＤＲＮ,ｒＣＢＦ分别减少１５．８％和１６．６％（Ｐ＜０．０５）。ｒＣＢＦ降低幅度均小于正常动物。电刺激ＤＲＮ对半球脑血流动力学无显著影响。结论电刺激中缝背核可致兔脑皮质微动脉收缩,局部组织血流减少、其途径有二;一是中枢性５－ＨＴ能神经元兴奋引起的直接缩血管作用;二是通过激活中枢和外周去甲肾上腺素能神经系统引起     

卒中型高血压大鼠心肌线粒体Ca~（2＋），Mg~（2＋）—ATPase及膜流动

本文比较了卒中型自发往高血压鼠（ＳＨＲｓｐ）和京都Ｗｉｓｔａｒ正常血压鼠（ＷＫＹ）心肌线粒体Ｃａ￣（２＋），Ｍｇ￣（２＋）－ＡＴＰａｓｅ活力及膜流动性。用定磷法测得ＷＫＹ和ＳＨＲｓｐ的Ｃａ￣（２＋），Ｍｇ￣（２＋）－ＡＴＰａｓｅ活力（２５℃）分别为０．２８７±０．０１６及０．２１８±０．０１７μｍｏｌ／（ｍｉｎ．ｍｇ）（－ｘ±Ｓｘ）。ＳＨＲｓｐ心肌线粒体Ｃａ￣（２＋），Ｍｇ￣（２＋）－ＡＴＰａｓｅ活力降低２４．７％，两组比较有显著差异（Ｐ＜０．０１，ｎ＝９）．以ＤＰＨ标记心肌线粒体膜，测得ＷＫＹ和ＳＨＲｓｐ的荧光偏振值分别为０．１８７±０．００３及０．１８１±０．００３（Ｐ＞０．０５，ｎ＝６）。     

大剂量激素对脑创伤家兔脑微循环及血液流变性的影响

为探讨大剂量激素对脑创伤后脑微循环及血液流变性的影响，将２４只家兔随机等分为３组：标准对照组、损伤对照组和地塞米松治疗组。分别在伤前０．５ｈ、伤后０．５ｈ、１ｈ、２ｈ、３ｈ测量软脑膜微动脉管径和血流速度的变化及伤后３ｈ血液流变学指标。结果表明：大剂量激素在伤后０．５ｈ就能明显地扩张损伤处软脑膜的微动脉并使血流速度明显加快。伤后３ｈ能明显降低血沉、全血粘度、红细胞压积及纤维蛋白原含量，并明显增强红细胞的变形能力，降低其聚集性。这些结果表明大剂量激素能明显改善脑创伤后家兔的脑微循环及血液流变性     

静脉注射牛磺酸和内毒素后家兔血清Fe2+、Zn2+、Cu2+含量变化

实验将１６只新西兰兔随机分为４组,由耳缘静脉注射被试物：１－ＮＳ（０－９％ＮａＣｌ１ｍＬｋｇ）;２－Ｔａｕ（３ｍｍｏｌｋｇ）;３－ＥＴ（１００ＥＵｋｇ）;４．ＥＴ（１００ＥＵｋｇ）＋Ｔａｕ（３ｍｍｏｌｋｇ）。在注射后４ｈ从颈动脉取血,离心取血清,用原子分光光度法检测血清Ｆｅ２＋、Ｚｎ２＋、Ｃｕ２＋含量结果见表１：表１　４组家兔血清Ｆｅ２＋、Ｚｎ２＋、Ｃｕ２＋含量（ｍｇＬ,珋ｘ±ｓ,ｎ＝４）ＧｒｏｕｐＦｅ２＋Ｚｎ２＋Ｃｕ２＋ＮＳ３－６１±０－７７１－２２±０－５５０－５７±０－１７Ｔａ…     

重组白介素—1受体拮抗剂对实验性肝损伤保护作用 …

白介素－１（ＩＬ－１）是重要的炎症因子之一，在肝损伤中起着重要的作用。为研究重组ＩＬ－１受体拮抗剂ｒＩＬ－１ｒａ）对四氯化碳（ＣＣＩ４）诱导的肝损伤的保护作用，将２４只Ｗｉｓｔａｒ大鼠随机分为５组：即正常对照组（ｎ＝５），造模组（ｍ＝５），ｒＩＬ－１ｒａ高剂量（０．５ｍｇ／１００ｇ）组（ｎ＝５），中剂量（０．２ｍｇ／１００ｇ）组（ｎ＝５）和低剂量（０．１ｍｇ／１００ｇ）组（ｎ＝４）。检测处理６周末     

大鼠体与其足体积,足表面积相关曲线的研究

本文根据理论分析和实验数据得出大鼠体重Ｗ与其足体积Ｖ、足表面积Ｓ的相关曲线分别为：Ｖ＝－０．３７７８＋０．００７７７８Ｗ和Ｓ＝－３．０５４＋０．２９６５Ｗ２／３，实测值与理论值最大相对误差分别小于５．７％和４．４％，比表面积约为３５．４ｃｍ２／ｋｇ体重。因此可根据稳定易测的大鼠体重分别方便地计算其足体积和足表面积，借以求出给药剂量     

用逐步回归探讨影响鼻咽癌转移的主要因素

目的：探讨与非角化性鼻咽癌（ｎａｓｏｐｈａｒｙｎｇｅａｌｃａｒｃｉｎｏｍａ，ＮＰＣ）转移有关的主要因素。方法：采用逐步回归的方法，对８３例非角化性ＮＰＣ１５项可能与转移有关的因素进行筛选。结果：在不同的Ｆ值水平下筛选出与ＮＰＣ转移发生最相关的因素，它们是癌内血管密度，血管壁上层粘蛋白（ＬＮ）表达异常，癌巢内淋巴细胞（ＬＣ）浸润量，癌细胞间变程度与患者年龄。这５个因素包括在逐步回归方程中（Ｙ＝１．４７６８－０．０９５７Ｘ１＋２．６６５Ｘ３＋０．００３１Ｘ９－０．２９４８Ｘ１３－０．３１０Ｘ１５，ＭＲ＝０．７０７４ｓｘ＝０．６４８９Ｆ＝１５．４２４７Ｐ＜０．０１），进而用方程进行回顾性推断８３例ＮＰＣ转移率为７３．４９％，明显高于临床记录发现的转移率（５９．０４％）。结论：逐步回归方程的建立为临床正确判断ＮＰＣ转移，以确定治疗提供有价值的参考依据     

外源蜕皮激素和保幼激素类似物对长角血蜱生殖的影响

在长角血蜱雌虫生殖发育的不同时期：刚蜕出（ＭＤ）、刚饱血（ＥＤ）和饱血后２ｄ（２－ＰＥ）局部施用２０－羟基蜕皮酮（２０－Ｅ）和／或法尼醇。结果表明：法尼醇处理ＭＤ组，延缓产卵，抑制卵巢对卵黄蛋白（Ｖｎ）的摄取，降低平均产卵力，且与剂量呈线性相关：ｙ＝５３．１１－０．０８ｘ，高剂量（大于５０μｇ／蜱）引起高死亡率（５０．０－１００．０％不等）；法尼醇处理ＥＤ组，抑制卵巢对Ｖｎ的摄取，降低平均产卵力，高剂量（５００μｇ／蜱）引起高死亡率（８６．７％），低剂量延缓产卵，而高剂量无影响；法尼醇处理２－ＰＥ组，缩短产卵前期，且与剂量呈线性关系：ｙ＝８．５２－０．０１５８ｘ，１－１００μｇ／蜱剂量增加平均产卵力和提高卵巢对Ｖｎ摄取，５００μｇ／蜱剂量严重抑制产卵力；２０－Ｅ处理２－ＰＥ织，延长产卵前期，降低平均产卵力，但利于卵巢对Ｖｎ摄取；法尼醇和２０－Ｅ共同处理２－ＰＥ组，有利于卵巢对Ｖｎ摄取，不同剂量法尼醇和１０μｇ／蜱的２０－Ｅ组合，缩短产卵前期，与２０μｇ／蜱的２０－Ｅ组合，延缓产卵，两种激素一定的组合，提高平均产卵力，各种处理都不影响产卵历期。     

刺激中缝背核观察尼莫地平及颈交感神经对家兔脑皮质微血流的影响

目的 :探讨电刺激兔中缝背核 (DRN)对家兔脑皮质微血流的影响及其机理。方法 :应用氢清除法测定局部脑组织血流 (rCBF)及观测软脑膜血管微循环。结果 :电刺激DRN后脑皮质rCBF减少 44 .2 % (P<0 .0 1) ,软脑膜微动脉管径缩小 ,血流速度减慢 ,而尼莫地平可取消其作用。切断颈交感神经后再刺激DRN ,rCBF减少 15 .8% (P <0 .0 5 )。结论 :电刺激DRN可导致脑皮质微动脉收缩 ,局部血流减少。尼莫地平可解除脑皮质微血管痉挛。切断颈交感神经有降低rCBF的作用。     

聪灵胶囊对小鼠软脑膜微循环障碍的改善作用

目的 观察聪灵胶囊对小鼠软脑膜微循环障碍的改善作用。方法 将60只小鼠随机分为聪灵胶囊大、中、小剂量组、阳性对照组和正常对照组，分别于灌胃给药10d后，开颅窗观察小鼠软脑膜微循环，然后在软脑膜局部滴加去甲肾上腺素复制微循环障碍模型，观察微循环障碍时小鼠软脑膜微循环。结果 聪灵胶囊各剂量组均可改善去甲肾上腺素所致的小鼠软脑膜局部微循环障碍．使微动脉扩张，血流增快，每视野交织网点数增多，对血流流态也有一定的改善作用，使血色变红。9min后聪灵胶囊各剂量组软脑膜局部微循环障碍基本恢复，而空白对照组恢复不明显。结论 聪灵胶囊能改善小鼠软脑膜微循环。     

Collateral blood flow in different cerebrovascular hierarchy provides endogenous protection in cerebral ischemia

Collateral blood flow as vascular adaptions to focal cerebral ischemia is well recognized. However, few studies directly investigate the dynamics of collateral vessel recruitment in vivo and little is known about the effect of collateral blood flow in different cerebrovascular hierarchy on the neuropathology after focal ischemic stroke. Here, we report that collateral blood flow is critically involved in blood vessel compensations following regional ischemia. We occluded a pial arteriole using femtosecond laser ablating under the intact thinned skull and documented the changes of collateral flow around the surface communication network and between the surface communication network and subsurface microcirculation network using in vivo two photon microscopy imaging. Occlusion of the pial arteriole apparently increased the diameter and collateral blood flow of its leptomeningeal anastomoses, which significantly reduced the cortical infarction size. This result suggests that the collateral flow via surface communicating network connected with leptomeningeal anastomoses could greatly impact on the extent of infarction. We then further occluded the target pial arteriole and all of its leptomeningeal anastomoses. Notably, this type of occlusion led to reversals of blood flow in the penetrating arterioles mainly proximal to the occluded pial arteriole in a direction from the subsurface microcirculation network to surface arterioles. Interesting, the cell death in the area of ischemic penumbra was accelerated when we performed occlusion to cease the reversed blood flow in those penetrating arterioles, suggesting that the collateral blood flow from subsurface microcirculation network exerts protective roles in delaying cell death in the ischemic penumbra. In conclusion, we provide the first experimental evidence that collateral blood vessels at different cerebrovascular hierarchy are endogenously compensatory mechanisms in brain ischemia.     

阻断颈淋巴加重实验性蛛网膜下腔出血软脑膜脑微循环异常

目的探讨脑淋巴引流阻滞对蛛网膜下腔出血（SAH）后软脑膜微循环的影响。方法选用成年健康Wistar大鼠,随机分为正常对照组（A组）、SAH组（B组）、颈淋巴阻断＋SAH组（CLB＋SAH组,C组）。采用枕大池二次注血法建立SAH模型。监测动脉血压和血气,在体观察脑膜微循环血流及管径变化。结果各组动物生理指标相对恒定。B、C微动脉、微静脉明显痉挛,而C组更为严重;A组软脑膜微循环血供丰富,血流快速无凝集。B、C组微循环血流多呈泥沙样流动,甚至可见血流郁滞、摆动,以C组更为显著。结论脑淋巴引流途径在SAH后脑微循环障碍和脑损伤中可能起重要作用。     

ATP release and hydrolysis contribute to rat pial arteriolar dilatation elicited by neuronal activation

Owing to their intimate anatomical relationship with cerebral arterioles, astrocytes have been postulated as signal transducers, transferring information from activated neurones to the cerebral microcirculation. These forwarded signals may involve the release of vasoactive factors from the end-feet of astrocytes. This mechanism is termed 'neurovascular coupling' and its anatomical components (i.e. neurone, astrocyte and vascular cells) are termed the 'neurovascular unit'. The process of neurovascular coupling often involves upstream dilatation. This is necessary during periods of increased metabolic demand, in order to permit more blood to reach dilated downstream vessels, thereby improving nutrient supply to the activated neurones. Without it, that downstream dilatation might be ineffective, placing neurones at risk, especially during episodes of intense neuronal activity, such as seizure. In the brain, pial arterioles represent important 'upstream' vascular segments. The pial arterioles overlie a thick layer of astrocytic processes, termed the glia limitans. This essentially isolates pial arterioles, anatomically, from the neurones below. Vasodilating signals that originate in the neurones therefore reach the pial arterioles via indirect pathways, primarily involving astrocytes and the glia limitans. Here we discuss a process whereby purinergic mechanisms play a key and neuronal activity-dependent role in astrocyte to astrocyte communication, as well as in glia limitans to pial arteriolar signals leading to vasodilatation.     

针刺对家兔脑软膜微血管管径及血流速度的影响

本文用电针足三里、曲池、人中和内关穴，观察家兔软脑膜微动脉和微静脉管径及血流速度的变化。结果刺激足三里引起激动脉扩张，血流速度加快，作用明显；电针曲池亦引起微动脉扩张，血流速度加快，但作用较弱；电针人中，内关引起微动脉收缩，血流速度减慢，微静脉反应均较弱。     

微循环荧光造影的安全性及其控制

用围堤式颅窗软脑膜微循环观察方法探讨了微循环荧光造影的安全性。发现：５０Ｗ超高压汞灯的激发光（波长峰值４９０ｎｍ）照射９０ｍｉｎ对血管内皮和平滑肌均有损伤作用。可使微动脉对乙酰胆碱和硝普钠的扩张反应减弱（血管内径变化分别由３７．５％±７．９％降至２３．８％±１１．９％，由４１．１％±２０．８％降至３６．７％±１１．１％，（Ｐ＜０．０５）。单独注射荧光素钠对血管反应性无影响。在激发光持续照射下注射５％荧光素钠０．２ｍｌ进行微循环荧光造影６次（１次／１５ｍｉｎ），血管明显损伤，微动脉对乙酰胆碱和硝普钠的扩张反应分别由４３．５％±１６．９％降至２２．０％±１３．３％，５５．４％±１７．９％降至２５．１％±１４．０％，Ｐ＜０．０５，且伴有严重的血栓形成。认为：控制激发光照射时间以及荧光素钠的浓度和剂量，可以防止上述损伤的发生。     

Antagonism by (D-Pro2, D-Trp7,9)-substance P of the cerebrovascular dilatation induced by substance P

The effects of (D-Pro2, D-Trp7,9)-substance P, a structural analogue of substance P, were examined in two models on cerebrovascular responses to substance P(SP) in cats; in vitro using segments of the middle cerebral artery and in situ by microapplication of the peptides close to pial arterioles. (D-Pro2, D-Trp7,9)-SP in concentrations up to 6.6 x 10(-6) M was without significant effect upon isolated middle cerebral arteries under normal conditions and in arteries contracted with prostaglandin F2 alpha. SP caused concentration-dependent relaxations of middle cerebral arteries contracted by prostaglandin F2 alpha (mean +/- SE; EC50: 2.0 +/- 1.6 x 10(-9) M). The presence of (D-Pro2, D-Trp7,9)-SP shifted the concentration-response curve of SP towards higher concentrations without significantly effecting the maximum response of the arteries to SP. A relaxation by 24.2 +/- 4.0% (n = 6) was obtained in prostaglandin F2 alpha contracted arteries by increasing the potassium concentration with 2 mM in the buffer solution. This response to potassium was unaltered in the presence of 6.6 x 10(-6)M of (D-Pro2, D-Trp7,9)-SP (25.0 +/- 7.1%, n = 5). Perivascular microapplication of SP around individual pial arterioles in situ effected dose-dependent increases in vascular calibre (mean response 14.5 +/- 2% with SP, 10(-7)M). The concomitant perivascular administration of (D-Pro2, D-Trp7,9)-SP (6.6 x 10(-6)M), which alone did not alter the arteriolar calibre, attenuated significantly the cerebrovascular response to SP (mean response 1.5 +/- 3.2%). On the basis of the agonist-antagonist relation found, these observations point to the possibility of a specific SP receptor site in cerebral arteries and arterioles.     

Oxygen-dependent mechanisms in cerebral autoregulation

Autoregulatory adjustments in the caliber of cerebral arterioles were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation. Increased venous pressure caused slight, but consistent, arteriolar dilation, at normal and at reduced arterial blood pressure and irrespective of whether or not intracranial pressure was kept constant or allowed to increase. Arterial hypotension caused arteriolar dilation which was inhibited partially by perfusion of the space under the cranial window with artificial CSF equilibrated with high concentrations of oxygen. This vasodilation was inhibited to a greater extent by perfusion of the space under the cranial window with fluorocarbon FC-80, equilibrated with high concentrations of oxygen. CSF or fluorocarbon equilibrated with nitrogen did not influence the vasodilation in response to arterial hypotension. The response to increased venous pressure was converted to vasoconstriction when fluorocarbon equilibrated with high concentrations of oxygen was flowing under the cranial window. The vasodilation in response to arterial hypotension was inhibited by topical application of adenosine deaminase. The results show that both metabolic and myogenic mechanisms play a role in cerebral arteriolar autoregulation. Under normal conditions, the metabolic mechanisms predominate. The presence of the myogenic mechanisms may be unmasked by preventing the operation of the metabolic mechanisms. The major metabolic mechanism seems to be dependent on changes in PO₂ within the brain with secondary release of adenosine.     

头风愈滴丸对小鼠软脑膜微循环障碍的改善作用

目的观察头风愈滴丸对小鼠软脑膜微循环障碍的改善作用。方法颅窗法观察正常小鼠软脑膜微循环，然后经小鼠尾静脉注射10％高分子右旋糖酐0．1ml／10g复制软脑膜微循环障碍模型，观察头风愈滴丸对小鼠软脑膜微动脉、微静脉管径的变化以及每视野毛细血管交叉网点数目的变化。结果头风愈滴丸各剂量组能明显的增加微动脉管径及毛细血管网交叉点数目，且微静脉管径也有一定的增加，并呈一定的量效关系。结论头风愈滴丸能明显改善小鼠软脑膜微循环障碍，该作用可能是其防治偏头痛发生的机制之一。