心脑血管病患者微血栓与D－2聚体、血小板聚集的相互关系

观察２０例急性脑梗塞，３０例冠心病在微循环中微血栓的变化，同时检测血小板聚集率、Ｄ－２聚体。结果表明微血栓阳性组血小板聚集率、Ｄ－２聚体均高于微血栓阴性组。治疗后二组血小板聚集、Ｄ－２聚体明显减少。提示微血栓、Ｄ－２聚体及血小板聚集率可作为评定冠心病、脑梗塞病情变化的一种指标     

成年大鼠肠系膜血管中CGRP免疫反应神经纤维的密度分布

用免疫组织化学ＡＢＣ法结合葡萄糖氧化酶ＤＡＢ－硫酸镍铵显色及交点计数法测量纤维密度的定量技术，研究了ＣＧＲＰ免疫反应神经纤维（ＣＧＲＰ－ＩＲＦ）在成年大鼠肠系膜上动脉和静脉中的密度分布规律。结果发现，成年大鼠肠系膜上动脉（ＳＭＡ）和静脉（ＳＭＶ）及其各级分支血管上含有较密集的呈网络状走行的ＣＧＲＰ－ＩＲＦ。ＳＭＡ中ＣＧＲＰ－ＩＲＦ的密度不随分支级别的增加而变化；而ＳＭＶ中ＣＧＲＰ－ＩＲＦ的密度随分支级别的增加呈指数曲线减少。此两种伴行血管之间ＣＧＲＰ－ＩＲＦ的密度在较细的血管分支中基本一致，而在较粗的血管分支中ＳＭＶ中ＣＧＲＰ－ＩＲＦ的密度大于ＳＭＡ中。     

心脑血管病患者微血栓与D－2聚体、血小板聚集的相互关系

观察２０例急性脑梗塞，３０例冠心病在微循环中微血栓的变化，同时检测血小板聚集率、Ｄ－２聚体。结果表明微血栓阳性组血小板聚集率、Ｄ－２聚体均高于微血栓阴性组。治疗后二组血小板聚集、Ｄ－２聚体明显减少。提示微血栓、Ｄ－２聚体及血小板聚集率可作为评定冠心病、脑梗塞病情变化的一种指标     

大鼠肠系膜上动脉和静脉各级分支中NPY免疫反应神经纤维密度的相…

用免疫组织化学ＡＢＣ法结合葡萄糖氧化酶－ＤＡＢ－硫酸镍铵（ＧＤＮ）增强显色技术，对大鼠肠系膜上动脉和静脉及其分支中ＮＰＹ免疫反应神经纤维的形态和分布进行了研究，并用交点计数法统计了其密度。结果发现，ＮＰＹ免疫反应神经纤维的密度随肠系膜上动脉和静脉分支级别的增加而增加；肠系膜上动脉和静脉中相应分支级别上的ＮＰＹ免疫反应神经纤维的密度没有显著差异。     

四肢动脉内血栓形成的动脉内溶栓治疗

目的 :探讨四肢动脉内血栓形成的动脉内溶栓治疗价值。方法 :2 8例四肢动脉内血栓形成者 ,按治疗方式分三组 :16例行单纯动脉内导管溶栓 (A组 ) ;7例急性血栓者行单纯超声溶栓 (B组 ) ;5例慢性血栓者行超声溶栓结合动脉内导管溶栓 (C组 )。结果 :2 8例肢体动脉阻塞均溶栓成功 ,无 1例产生并发症。A、B、C三组的平均溶栓时间分别为 6.4± 5 .9h、0 .9± 0 .3h和 8.4± 4.5h ,A组的溶栓时间明显长于B、C组 (P <0 .0 5 )。对于慢性血栓形成者 ,超声溶栓结合导管溶栓的疗效较单纯动脉内导管溶栓或单纯超声溶栓者好。超声溶栓还能加快溶栓进程。结论 :动脉内溶栓治疗是四肢动脉内血栓形成的安全有效的治疗方法     

低分子右旋糖杆与中药“升脉”在透析过程中出现低血压的特殊应用

慢性肾功能衰竭 (ＣＲＦ)在维持性血液透析 (ＨＤ)中 ,随着ＨＤ时间的延长 ,在ＨＤ过程中发生低血压 ,已成为透析室常见的问题之一 ,也是ＨＤ中较危险的问题之一 ,处理不当 ,可以继发心绞痛、心肌梗死、脑梗死、肠系膜动脉血栓等严重并发症。因此 ,为了确保ＨＤ的正常进行 ,保持适当的血压水平是不可缺少的。有些患者还表现为经常性低血压 ,这些患者不仅在ＨＤ时 ,而且在非ＨＤ时也呈现低血压〔收缩压为 13.3ｋＰａ(10 0ｍｍＨｇ)以下 ,除外心功能衰竭等引起的低血压〕。这些患者就更应该引起医务人员的注意 ,以避免严重并发症的发生。北京…     

急性心肌梗塞的溶栓治疗及微循环观察

观察尿激酶溶栓治疗急性心肌梗塞（AMI）的疗效及微循环中做血栓的变化。按WHO规定的AMI诊断标准选择病例．按1992年全国统一的溶栓方案治疗，观察溶栓前后球结膜微循环改变。对微循环中有微血栓记录溶栓前后的微血栓数量，并与溶栓结果对比分析。其中16例AMI溶栓治疗后再通者13例，再通率81．25％。溶栓前微循环中有微血栓者11例，溶栓后仅有3例。微血栓出现率由溶栓前的68．75％下降至溶栓后18．75％，统计学处理差异非常显著（p＜0．001）。13例再通者无一例再出现微血栓。可见尿激酶溶栓治疗急性心肌梗塞效果肯定，对消溶微血栓有显著作用。可把微血栓作为尿激酶治疗AMI后冠脉再通的一项辅助指标。     

急性心肌梗塞的溶栓治疗及微循环观察

观察尿激酶溶栓治疗急性心肌梗塞（ＡＭＩ）的疗效及微循环中微血栓的变化。胺ＷＨＯ规定的ＡＭＩ诊断标准选择病例，按１９９２年全国统一的溶栓方案治疗，观察溶栓前后球结膜循环改变。对微循环中有微血栓记录溶栓前后的微血栓数量，并与溶栓结果对比分析。其中１６例ＡＭＩ溶栓治疗后再通者１３例，再通率８１．２５％。溶栓前微循环中有微血栓者１１例，溶栓后仅有３例。微血栓出现率由溶栓前的６８．７５％下降至溶栓后１８．７     

山莨菪碱对蛛网膜下腔出血后基底动脉产生EDRF的作用及抗…

用山莨菪碱（６５４－２）防治蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛，观察６５４－２对基底动脉中ＥＤＲＦ，ＭＤＡ，ＳＯＤ，ｃＧＭＰ，Ｃａ＾２＋，Ｎａ＾２＋的影响。结果表明，应用６５４－２后降低了基底动脉中ＭＤＡ产生及Ｃａ＾２＋Ｎａ＾＋的含量，与ＳＡＨ组比，ＥＤＲＦ释放增加，ＳＯＤ活性及ｃＧＭＰ水平提高，基底动脉内皮细胞受到保护，基底动脉收缩幅度减小。提示，６５４－２可通过保护内皮细胞，减轻氧自由基损伤     

山莨菪碱对蛛网膜下腔出血后基底动脉产生EDRF的作用及抗痉挛机制研究

用山莨菪碱（６５４－２）防治蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛，观察６５４－２对基底动脉中ＥＤＲＦ，ＭＤＡ，ＳＯＤ，ｃＧＭＰ，Ｃａ￣（２＋），Ｎａ￣＋的影响。结果表明，应用６５４－２后降低了基底动脉中ＭＤＡ产生及Ｃａ￣（２＋）Ｎａ￣＋的含量，与ＳＡＨ组比，ＥＤＲＦ释放增加，ＳＯＤ活性及ｃＧＭＰ水平提高，基底动脉内皮细胞受到保护，基底动脉收缩幅度减小。提示，６５４－２可通过保护内皮细胞，减轻氧自由基损伤，拮抗Ｃａ￣（２＋）Ｎａ￣＋在细胞内的蓄积，从而促进内皮细胞ＥＤＲＦ释放，引起血管舒张，明显减轻ＳＡＨ后的脑血管痉挛。     

Blood-brain barrier permeability to manganese and to Gd-DOTA in a rat model of transient cerebral ischaemia

Loss of integrity of the blood-brain barrier (BBB) and brain swelling is a potentially lethal complication of reperfusion in human stroke. To assess the time course of BBB modifications, we performed angiography, diffusion-weighted imaging, T1-weighted (T1 W) imaging and T1 mapping, and monitored acute changes after middle cerebral artery occlusion and recanalization in rats (n = 27). The animals were grouped according to the duration of occlusion: 30 min (group A, n = 8), 1 h 30 min (group B, n = 9), and 2 h 30 min (group C, n = 10). For 17 animals (four in group A, six in group B, and seven in group C), MnCl2 and dimeglumine gadoterate (Gd-DOTA) were injected at 13 min and 34 min after recanalization, respectively. The 10 remaining animals (control groups) underwent the same acquisition protocols, but no contrast agents were injected. Cell damage was determined 1 h after recanalization on haematoxylin and eosin-stained sections. Our results indicate that in the middle cerebral artery occlusion model in the rat, changes in BBB permeability assessed by contrast agent extravasation occur within the first hour of reperfusion, even after an occlusion period not exceeding 30 min. No differences between BBB permeability to Gd-DOTA and Mn2+ were detected in our experimental conditions. The reduction in apparent diffusion coefficient during occlusion appears to be a good predictor of BBB modifications after reperfusion in this model.     

盐酸戊乙奎醚对高黏血症大鼠微循环和血液流变性的影响

目的 观察盐酸戊乙奎醚（Penehyclidine Hydrochloride，PHC）对大鼠肠系膜微循环及血液流变性的影响。方法 健康成年SD大鼠舌静脉给予10％的高分子右旋糖酐（high molecular dextran，HMD）3．5nl／kg制造高血黏症动物模型，镜下活体观察大鼠肠系膜微循环微血流流态变化，造模成功后给予PHC0．023、0．07、0．2mg/kg，山莨菪碱（anisodamine，Ani）2mg／kg，生理盐水2ml／kg，继续观察微血流流态变化。给药后40min取血做血液流变性检测及血栓烷素A3（thromboxan A2，TXA2）与前列环素（prostaglandln I2，PGI2）含量测定。结果 模型组与正常对照组比较，血流明显变缓，血流态为粒摆流或近停滞状态，全血黏度、血浆黏度、红细胞比容、红细胞电泳时间、血沉方程K值、TXA2及TXA3／PGI2均有极显著性差异（P〈0．01）；PHC0．2ms／kg组能明显改善血浆黏度，在PHC0．023、0．07、0．2mg／kg及Ani 2mg／kg组除血浆黏度外均得到明显改善，与模型组比较P〈0．05。结论 PHC可改善HMD引起的急性微循环障碍及血液流变性异常。     

Atropine and hexamethonium-sensitive,Ca/K-modulated,reversible swelling of mast cells in rat mesentery,due to feeding or exposure to carbachol

Transitory swelling of mesenteric mast cells was observed when 24 h-fasted rats were given access to food. Atropine, an anti-muscarinic drug given (1 mg/kg, i.p.) 60 min prior to feeding, prevented this response; carbachol, a cholinomimetic drug caused it to occur when given (2 g/kg, i.v., 10 min) to fasted rats. Mast cells in the mesentery excised from fasted rats, presented swellingin vitro within 1 min following exposure to 10^–7 M carbachol. This response was inhibited by atropine (10^–8 M) or hexamethonium (10^–8 M), indicating that stimulation of a parasympathetic nerve pathway, reported to exist in rat mesentery, could induce mast cell swelling. Exposure to a Ca²⁺ free medium also led to rapid swelling of mast cells in the mesentery excised from fasted rats. This result, as well as inhibition of the mast cell response to carbachol caused by increasing the Ca²⁺ (but not by increasing the Mg²⁺) content of the incubation medium, suggests that swelling was caused by a sudden decrease of Ca at mast cell membrane sites controlling ion/water fluxes. Mast cells swollen by feeding, carbachol, or Calack, reverted to their original condition within 20 min when incubated in balanced salt buffer. Such reversal did not occur in a KCl-enriched medium. An equivalent (in terms of ionic, strength), increase in NaCl, did not reproduce this effect, indicating that mast cells have K⁺-dependent means of compensating for endogenously or drug-induced volume changes. Swelling caused by cholinergic stimulation of mast cells was not accompanied by granule exocytosis. The, implication of these findings, as well as of the kininogen decrease previously reported to occur in carbachol-treated rat bloodin vivo orin vitro, is discussed in terms of putative mast cell-controlled, localized homeostasis in the rat mesentery.     

应用光-化学法血栓生成模型研究急慢性疗法下阿司匹林的抗血栓作用

采用光—化学法在大鼠肠系膜微静脉建立活体血栓生成模型，研究了在急性（一次用药）与慢性（每日给药，一周）条件下阿司匹林的抗血栓作用。慢性阿司匹林用药组与生理盐水对照组相比，可以明显减缓血栓生长速度，延长血栓栓塞时间，表明阿司匹林对血栓形成有一定的抑制作用。而急性用药组的抗栓作用并不明显     

A novel lysophosphatidic acid analog, LXR-1035, inhibits leukocyte-endothelium interaction via inhibition of cell adhesion molecules

A novel synthetic phosphorothioate analog of oleoyl lysophosphatidic acid LXR-1035 was studied for its ability to modulate leukocyte-endothelial cell interactions using intravital microscopy of the rat mesentery. Superfusion of the rat mesentery with 50 microM L-NAME elicited a significant, time-dependent increase in leukocyte rolling, adherence, and transmigration compared to control rats superfused with Krebs-Henseleit solution. However, superfusion of the rat mesentery with 300 nM LXR-1035 consistently attenuated 65-87% of the L-NAME-induced leukocyte rolling, adherence, and transmigration, without altering systemic blood pressure or mesenteric venular shear rate. Similar results were also obtained in rats subjected to 90 min of hemorrhage followed by 90 min of reperfusion. Resuscitation from hemorrhage increased significantly the number of rolling, adherent, and transmigrated leukocytes in the rat mesenteric microcirculation. However, superfusion of the rat mesentery with LXR-1035 markedly attenuated the leukocyte-endothelium interaction occurring after hemorrhage and reinfusion by 75+/-12%. Immunohistochemical localization of P-selectin expression on mesenteric venular endothelium was significantly increased after exposure to L-NAME and after hemorrhage-reinfusion, which was significantly attenuated by LXR-1035 (P<0.05). In addition, treatment of isolated rat neutrophils with 300 nM LXR-1035 significantly attenuated leukotriene B4-induced up-regulation of CD18 (P<0.05). Our data clearly demonstrate that LXR-1035 can potently inhibit the recruitment of leukocytes in the mesenteric rat microvasculature by attenuating cell-surface expression of adhesion molecules.     

Effect of rat CINC/gro, a member of the interleukin-8 family, on leukocytes in microcirculation of the rat mesentery.

Rat cytokine-induced neutrophil chemoattractant (CINC) is a member of the IL-8 family, and its human counterpart is gro/MGSA but not IL-8. We ascertained that chemically synthesized CINC was comparable to native CINC/gro with regard to chemotactic activity for rat neutrophils and studied the effect of synthesized CINC/gro on circulating leukocytes in microvascular vessels of rat mesentery. Exposure of rat mesentery to 10(-8)M authentic CINC/gro induced neutrophil adherence to and extravasation from postcapillary venules (PCVs) but not from capillaries or arterioles. CINC/gro concentrations as low as 10(-10) M were effective in causing neutrophil adherence. Neutrophils adhered to thin PCVs (mean diameter, approximately 25 microns) after exposure to CINC/gro for 15 min. The mean diameters of the PCV with adherence of neutrophils after exposure to CINC/gro for 30 and 60 min were 37 and 43 microns, respectively. The diameters of PCV with extravasation of neutrophils also increased in a time-dependent manner. The starting position of adherence of neutrophils was approximately 25-50 microns away from the upper junction of two vessels and remained virtually unchanged during exposure to CINC/gro for 60 min. However, the distance from the start to the end of neutrophil adherence increased in a time-dependent manner. The effect of CINC/gro on adherence and extravasation of leukocytes was neutrophil specific since other leukocytes such as lymphocytes and monocytes were not identified among the adherent and extravasated leukocytes.     

Treatment with rIFN-gamma has no effect on cardiac allograft rejection.

The effect of recombinant rat interferon-gamma (rRIFN-gamma) on allograft rejection was studied in two rat heart transplantation models. Recipients were treated with rRIFN-gamma by intraperitoneal or intravenous injection, either by bolus or continuous infusion. Treatment was started after transplantation and continued during a period ranging from 4 to 10 days; dosages varied from 2.5 x 10(2) U/kg/day to 3 x 10(6) U/kg/day. Controls were infused with PBS. Treatment with rRIFN-gamma had no effect on allograft survival, irrespective of the route of administration, the dosage used or the duration of treatment. Higher dosages of rRIFN-gamma induced serious morbidity and mortality. In conclusion, systemic treatment of cardiac allograft recipients with rRIFN-gamma has no effect on graft rejection and is associated with serious toxicity and mortality when high dosages are used.     

川芎嗪对家兔肠系膜细动脉血管血管运动的抑制作用

在全身动脉血压控制下应用显微录像静画步进和二点光电法同步测定了川芎嗪对话体家兔肠系膜细动脉的内径、血流速度和血管运动的影响及其相互间的关系。结果发现川芎嗪有浓度依赖性的降压作用。给药后３０ｓ血压开始下降并持续１ｍｉｎ。８ｍｇ／ｋｇ比４ｍｇ／ｋｇ给药组降压作用大，２ｍｇ／ｋｇ组效果不明显。伴随血压下降８ｍｇ／ｋｇ给药组细动脉血流速度减慢，但内径无变化，４ｍｇ／ｋｇ和２ｍｇ／ｋｇ组效果不明显。又在活体显微镜下在３０～５０μｍ细动脉水平直接证明了川芎嗪有抑制局部投予去甲肾上腺素引起的血管运动的作用。并发现１６ｍｇ／ｋｇ比８ｍｇ／ｋｇ给药组抑制作用时间长。即使全身血压不变，细动脉血流也随血管运动周期变化，细动脉舒张血流量增加。将给去甲肾上腺素前与给川芎嗪后的内径对比变化不明显。提示ＴＭＰ的作用本质是抑制去甲肾上腺素引起的血管运动而不是扩张血管。     

Frequency of climbing behavior as a predictor of altered motor activity in rat forced swimming test

Previous work has shown that the frequency of climbing behavior in rats submitted to the forced swimming test (FST) correlated to the section's crosses in the open field test, which suggest it might be taken as a predictor of motor activity in rat FST. To investigate this proposal, the frequency, duration, as well as the ratio duration/frequency for each behavior expressed in the FST (immobility, swimming and climbing) were compared in animals treated with a motor stimulant, caffeine (CAF), and the antidepressant, clomipramine (CLM). Male Wistar rats were submitted to 15min of forced swimming (pre-test) and 24h later received saline (SAL, 1ml/kg, i.p.) or CAF (6.5mg/kg, i.p.) 30min prior a 5-min session (test) of FST. To validate experimental procedures, an additional group of rats received three injections of SAL (1ml/kg, i.p.) or clomipramine (CLM, 10mg/kg, i.p.) between the pre-test and test sessions. The results of the present study showed that both drugs, CLM and CAF, significantly reduced the duration of immobility and significantly increased the duration of swimming. In addition, CAF significantly decreased the ratio of immobility, and CLM significantly increased the ratio of swimming and climbing. Moreover, CLM significantly increased the duration of climbing but only CAF increased the frequency of climbing. Thus, it seems that the frequency of climbing could be a predictor of altered motor activity scored directly in the FST. Further, we believe that this parameter could be useful for fast and reliable discrimination between antidepressant drugs and stimulants of motor activity.     

Acute exposure of uranyl nitrate causes lipid peroxidation and histopathological damage in brain and bone of Wistar rat.

Although the kidneys are the main target organs for uranium (U) toxicity, recent studies have shown that U can cross the blood-brain barrier to accumulate in the brain. Uranyl nitrate (U-238)induced oxidative damage was investigated in brain and bone of Wistar rats after intraperitoneal injection of uranyl nitrate at acute doses either nephrotoxic (576 microg of U/kg body weight) or subnephrotoxic (144 microg U/kg body weight). The health effects of U administration at 576 microg of U/kg body weight were seen in terms of decrease in food intake and no gain in body weight compared to respective controls. These alterations were correlated with increased lipid peroxidation as measured by thiobarbituric acid reactive substances in rat brain and bone. However, at lower dosage of U (144 microg U/kg body weight), no significant lipid peroxidation was observed in brain and bone. Histological examination of U-treated (576 microg of U/kg body weight) rat brain tissues showed marked and diffuse cystic degeneration and a similar pattern in histological alterations was observed in kidneys in treated animals; whereas no significant histological change was observed in rat brains and kidney treated with a lower dose of U (144 microg U/kg body weight). It is concluded that administration of U at an acute nephrotoxic dose caused oxidative stress in brain and bone manifested as lipid peroxidation and histopathological damage.