急性低氧对肺动脉,肾动脉及肠系膜动脉平滑肌张力的影响

对离休大鼠肺外、肾及肠系膜动脉血管环进行体外灌流,观察,急性低氧对平滑肌张力的影响。急性低氧（灌流液ＰＯ＿２４±０．７ｋＰａ）１０—１５ｍｉｎ对肺外和肠系膜动脉环静息张力无明显影响;用苯肾上腺素（１０￣（－６）ｍｏｌ／Ｌ）或ＫＣｌ（３０ｍｍｏｌ／Ｌ）预激肺动脉后给予低氧亦不能明显改变预激肌张力。急性低氧对肾动脉环的肌张力影响较显著,低氧引起一随时间变化的收缩峰,复氧（通９５％Ｏ＿２＋５％ＣＯ＿２混合气体）后肌张力又呈先升高后下降的变化;苯肾上腺素或ＫＣｌ预激肾功脉环后给予急性低氧,张力增加较明显,５—１０ｍｉｎ后张力下降至较预激稳定值低,复氧后张力回复。用无钙灌流液灌流肾动脉标本可取消低氧对静息张力及ＫＣｌ预激后张力的影响。α受体拮抗剂酚妥拉明１×１０￣（－６）—５０×１０￣（－６）ｍｏｌ／Ｌ或钙拮抗剂维拉帕米１×１０￣（－６）—５×１０￣（－６）ｍｏｌ／Ｌ不能取消低氧对肾动脉的作用,但前者能抑制复氧肌张力增加。结果显示急性低氧对离体肾动脉平滑肌有直接作用。     

大鼠小肠肠系膜微血管血流随温度变化的光学检测

利用CCD显微成像技术和激光散斑技术,对局部加热（41℃-54℃,30min）下大鼠小肠肠系膜微血管的管径（直径约15μm-50μm)和血流速率的变化进行实时,在体监测,并由二者计算血流量的变化。结果表明：41℃,43℃,45℃,46℃各温度点30min的加热过程中,血流速度变化平缓,血管管径和血流量明显增加,最终均逐渐趋趋于恒定。49℃时,血流速率仅在前12min内增加,30min时已降至低于初始值,血管管径及血流量在14min时达最大后开始减小,加热停止时仍旧高于初始值。温度高于49℃时（51℃,54℃）血流速率,管径,血流量呈现先升高后下降的变化趋势,在30min时,三者均低于初始值,由此可知,加热时间为30min,大鼠肠系膜微血管的临界温度为49℃;在相同的时间条件下,热损伤速率随温度升高而增加。     

大鼠肠系膜动脉的立式包埋及内皮损伤的评估方法

目的建立一种新的小血管立式包埋方法,并通过对内皮损伤的定量分析来评估血管的功能。方法 (1)肠系膜动脉的分离:首先游离大肠小肠部分至体外,暴露出肠系膜动脉,随后用剪刀游离出带有少量组织的肠系膜动脉,最后在镜下剔除黏连组织;(2)肠系膜动脉的立式包埋;(3) HE染色、免疫荧光染色观察肠系膜动脉的结构和内皮损伤程度。结果大鼠肠系膜动脉立式包埋及血管内皮评估方法,能够快速、有效地得到良好形态的大鼠肠系膜动脉切片,并给出小血管病变的病理学研究方法。结论本方法能够降低病理切片的制作难度,为血管病变的研究提供了可借鉴的研究方法,可以进一步推广至其它动物或临床病人的小血管研究。     

孤立性肠系膜上动脉夹层介入血管腔内治疗的初步体会

目的:评价介入血管腔内治疗孤立性肠系膜上动脉夹层(ISMAD)的安全性和疗效.方法:5例患者均通过腹部CT及血管造影明确诊断ISMAD,本组病例确诊后行介入血管腔内治疗,术后继予抗凝抗血小板治疗,并术后1、3、6个月进行CTA或血管造影随访.结果:5例患者手术成功率100％,其中支架联合弹簧圈栓塞2例,双支架重叠技术3例,无并发症发生.全部患者术后3周内症状逐渐消失;术后3～6个月时肠系膜上动脉CTA及血管造影显示动脉瘤腔不显影,支架腔内血流通畅;随访3～12个月(平均7.8个月)夹层动脉瘤无复发.结论:介入血管腔内治疗是治疗ISMAD的安全有效的方法.     

孤立性肠系膜上动脉夹层介入血管腔内治疗的初步体会

目的:评价介入血管腔内治疗孤立性肠系膜上动脉夹层(ISMAD)的安全性和疗效。方法:5例患者均通过腹部CT及血管造影明确诊断ISMAD,本组病例确诊后行介入血管腔内治疗,术后继予抗凝抗血小板治疗,并术后1、3、6个月进行CTA或血管造影随访。结果:5例患者手术成功率100%,其中支架联合弹簧圈栓塞2例,双支架重叠技术3例,无并发症发生。全部患者术后3周内症状逐渐消失;术后3～6个月时肠系膜上动脉CTA及血管造影显示动脉瘤腔不显影,支架腔内血流通畅;随访3～12个月(平均7.8个月)夹层动脉瘤无复发。结论:介入血管腔内治疗是治疗ISMAD的安全有效的方法。     

家兔肠系膜上动脉闭塞性休克前后的血清比较蛋白质组学初步研究

目的：探讨家兔肠系膜上动脉闭塞性（SMAO）休克前后血清蛋白质组学变化及其在SMAO休克发生中的作用。方法：应用家兔肠系膜上动脉夹闭法复制家兔SMAO休克模型,在此基础上通过双向电泳分离家兔SMAO休克前后血清中的蛋白,找出凝胶上的差异蛋白点,用基质辅助激光解吸/电离串联飞行时间质谱技术进行鉴定,并通过生物信息学对差异蛋白的功能进行分析。结果：在家兔SMAO休克前后血清双向电泳图谱中发现19个差异蛋白点,其中11个蛋白质点在SMAO休克后血清中表达明显上调;8个蛋白质点在SMAO休克后血清中表达明显下调。从中选取4个差异最明显的点经基质辅助激光解吸/电离串联飞行和数据库搜索共鉴定出符合条件的2个差异蛋白点,为对氧磷酶和触珠蛋白,均在SMAO休克后血清中含量增高。结论：家兔SMAO休克前后血清蛋白质组会发生明显变化,对氧磷酶和触珠蛋白可能参与了SMAO休克后机体的代偿调节。     

炎症介质对离体大鼠肠系膜动脉降钙素基因相关肽释放的影响

本工作目的是在离体大鼠肠系膜动脉床灌流模型上,观察几种常见炎症介质：前列腺素Ｅ２（ＰＧＥ２）、缓激肽（ＢＫ）、组胺（ＨＩＳ）、血小板活化因子（ＰＡＦ）及５－羟色胺（５－ＨＴ）对血管周围感觉神经介质ＣＧＲＰ释放的直接影响。结果显示：ＰＧＥ２（１－１００μｍｏｌ／Ｌ）和ＢＫ（５－１０μｍｏｌ／Ｌ）能引起大鼠肠系膜动脉床时间和浓度依赖性地释放ＣＧＲＰ。ＨＩＳ,ＰＡＦ和５－ＨＴ则未见明显作用。结果提示,ＰＧＥ２与ＢＫ可能是引起血管周围感觉神经兴奋和ＣＧＲＰ释放的主要炎症介质。     

树鼩(Tupaia belangeri chinensis)的脑底动脉环

用25只树鼩,从升主动脉灌注带色的橡胶乳液,在解剖显微镜下进行解剖观察,用目测微尺进行测量。大多数树鼩(22只)有完整的脑底动脉环。由左、右大脑前动脉向内侧各发一前交通动脉组成大脑前总动脉。前交通动脉口径为大脑前动脉的75～85％。后交通动脉口径与大脑后动脉相近,连于颈内动脉与大脑后动脉(基底动脉的分支)之间。测量了组成脑底动脉环有关动脉的口径。由于后交通动脉足够粗大,只有中断左、右颈总动脉和左、右椎动脉,才能造成全脑缺血。     

触珠蛋白在家兔肠系膜上动脉闭塞性休克前后血清差异表达的研究

目的:探讨家兔肠系膜上动脉闭塞性(SMAO)休克前后血清蛋白质组学变化及触珠蛋白的差异表达情况。方法:应用家兔肠系膜上动脉夹闭法复制家兔SMAO休克模型,在此基础上通过双向电泳-质谱-生物信息学方法分析鉴定SMAO休克前后血清中的差异蛋白,并应用Western blot和Elisa对血清触珠蛋白在SMAO休克前后血清中的差异表达情况进行验证。结果:在家兔SMAO休克前后血清双向电泳图谱中发现19个差异蛋白点,其中11个蛋白质点只见于SMAO休克后血清双向电泳图中;8个蛋白质点明显见于SMAO休克前的血清双向电泳图中。鉴定并验证了触珠蛋白在SMAO休克后血清中含量增高。结论:家兔SMAO休克后血清触珠蛋白含量增高,可能参与了SMAO休克后机体的代偿调节。     

共聚焦显微镜不同倍数物镜下肠系膜动脉三级分支张力和Ca~(2+)信号同步变化的比较

本文旨在建立优化的观察肠系膜动脉三级分支(sMA,直径100~300μm)血管张力和血管平滑肌细胞(vascular smooth muscle cells,VSMCs)内Ca~(2+)信号的同步变化的实验方法。分别采用DMT 360CW激光共聚焦微血管张力测定系统和Nikon C2激光共聚焦显微镜,同时记录Ca~(2+)通道激动剂KCl、内皮素-1(endothelin-1,ET-1)以及Ca~(2+)通道抑制剂钆离子(Gd3+)诱导的去内皮sMA血管张力和VSMCs内Ca~(2+)信号的变化,并对共聚焦显微镜不同物镜(10×、20×、40×)下记录到的Ca~(2+)信号荧光值变化量进行对比分析,探索最佳的实验条件。结果显示,KCl可引起sMA显著收缩,20×、40×物镜下VSMCs内Ca~(2+)信号会同步增强,相比40×物镜,20×物镜下Ca~(2+)信号变化量更大,荧光值更稳定,而10×物镜下VSMCs内Ca~(2+)信号变化不明显;不同浓度的ET-1能够引起sMA浓度依赖性收缩,同样20×物镜下VSMCs内Ca~(2+)信号也呈浓度依赖性同步增强;ET-1预收缩sMA后加入Gd3+显著降低ET-1诱导的血管收缩效应,相应地20×物镜下VSMCs内Ca~(2+)信号也显著降低。以上结果表明,Ca~(2+)通道激动剂或抑制剂引起血管收缩或舒张的同时,VSMCs内Ca~(2+)信号会发生相应的变化,提示本实验方法可同步记录两者的变化,而且共聚焦显微镜20×物镜为最佳的实验条件。与分别应用血管张力检测技术测定血管张力变化和动态细胞荧光成像技术测定VSMCs内Ca~(2+)信号变化的方法相比,同步检测张力和Ca~(2+)信号的变化更简单实用,有效避免了不必要的实验误差。     

Intracellular renin increases the inward calcium current in smooth muscle cells of mesenteric artery of SHR. Implications for hypertension and vascular remodeling

The influence of intracellular renin on the inward calcium current in isolated smooth muscle cells from SHR mesenteric arteries was investigated. Measurements of calcium current were performed using the whole cell configuration of pCLAMP. The results indicated that: 1) renin (100 nM) dialyzed into smooth muscle cells, increased the inward calcium current; 2) verapamil (10–9 M) administered to the bath inhibited the effect of renin on the inward calcium current; 3) concurrently with the increase of calcium current a depolarization of 6.8 +/− 2.1 mV (n = 16)(P < 0.05) was found in cells dialyzed with renin; 4) intracellular dialysis of renin (100 nM) into smooth muscle cells isolated from mesenteric arteries of normal Wystar Kyoto rats showed no significant change on calcium current; 5) aliskiren (10–9 M) dialyzed into the cell together with renin (100 nM) abolished the effect of the enzyme on the calcium current in SHR; 6) Ang II (100 nM) dialyzed into the smooth muscle cell from mesenteric artery of SHR in absence of renin, decreased the calcium current-an effect greatly reduced by valsartan (10–9 M) added to the cytosol; 7) administration of renin (100 nM) plus angiotensinogen (100 nM) into the cytosol of muscles cells from SHR rats reduced the inward calcium current; 8) extracellular administration of Ang II (100 nM) increased the inward calcium current in mesenteric arteries of SHR. Conclusions: intracellular renin in vascular resistance vessels from SHR due to internalization or expression, contributes to the regulation of vascular tone and control of peripheral resistance-an effect independently of Ang II. Implications for hypertension and vascular remodeling are discussed.     

消痰化瘀利窍方对慢性间歇性低氧大鼠肠系膜动脉损伤的改善作用

目的:观察消痰化瘀利窍方对慢性间歇性低氧(CIH)大鼠肠系膜动脉功能损伤的作用,并探讨其可能机制。方法:48只雄性SD大鼠随机分为4组(n=12),常氧对照组(Normoxia)、慢性间歇性低氧组(CIH)、慢性间歇性低氧中药干预组(Formula+CIH)、中药对照组(Formula)。CIH与Formula+CIH组置于间歇性低氧装置,通过充入氮气、氧气使O2含量在9%至21%间循环,每循环3min;Normoxia和Formula组则充入空气。其中,Formula+CIH与Formula组于每日造模前中药水煎液灌胃(24g/kg),而CIH组与Normoxia组给予等量生理盐水。造模结束后,应用HE染色观察各组大鼠肠系膜动脉的组织病理学改变,通过微血管环技术观察ACh、L-Arg诱导的肠系膜动脉舒张反应,通过ELISA技术检测大鼠造模前及造模21d血清一氧化氮(NO)的含量并应用Westernblot技术测定肠系膜动脉eNOS和p-eNOS的蛋白水平。结果:与Normoxia组相比,CIH组大鼠肠系膜动脉内皮明显损伤、中膜增厚,ACh、L-Arg诱导的肠系膜动脉舒张反应明显减弱,血清中NO水平及肠系膜动脉p-eNOS/eNOS比值显著降低。消痰化瘀利窍方干预能够减轻大鼠肠系膜动脉的内膜与中膜病理损伤,改善肠系膜动脉舒张功能,提高血清NO含量及肠系膜动脉eNOS磷酸化水平。而单纯给予消痰化瘀利窍方大鼠与Normoxia组相比各指标均未发现显著变化。结论:消痰化瘀利窍方可以减轻慢性间歇性低氧引起的大鼠肠系膜动脉功能损伤,其机制与提高NO的生物利用度有关。     

Seasonal changes in the Modulus of Elasticity of living branches of three coniferous species

The seasonal changes in the Modulus of Elasticity (E) of living branches ofCryptomeria japonica, Chamaecyparis obtusa andLarix leptolepis were investigated over a period of 1 year by means of a quick and non-destructive method previously introduced by the authors. Two sample trees were used for each species and 12 branches were selected from each tree. Readings of the experiments began in summer 1992 and were successively conducted in autumn 1992, winter 1993, spring 1993 and finally in summer 1993. Our investigations revealed that meanE values increased in cold seasons and decreased in warm or hot seasons. Mean values ofE estimated in summer (1993) were relatively close to those estimated in summer 1992 indicating that any changes that occurred were the direct result of the environmental factors prevailing in the intervening seasons. Extremely high meanE values were measured when the branches were in a frozen state in winter; 69.4%, 29.9% and 24.6% higher than the previous summer for branches ofCryptomeria japonica, Chamaecyparis obtusa andLarix leptolepis, respectively. This sharp increase over the initialE values measured in summer 1992 was quite likely due to the freezing effect of rime on the branches.     

Disruption of the rat mesenteric arterial bed endothelial function by air perfusion

The impact of air perfusion on the endothelial function of the rat mesenteric arterial bed (MAB; perfused with Krebs' bicarbonate plus indomethacin) was compared to that of the NO synthase inhibitor, N^ω-nitro-L-arginine methyl ester (L-NAME). Air shifted the dose-response curve for the alpha-adrenoceptor agonist, norepinephrine (NE) to the left (ED_50%: 2.9 ± 0.7 to 0.9 ± 0.7 μg, P < 0.05); maximal vasoconstriction did not change. L-NAME produced a similar increase in midrange sensitivity (ED_50% 1.4 ± 0.7 μg, P < 0.05) and a 20% increase in maximum (152 ± 6 to 183 ± 7 mmHg, P < 0.05). Electromechanical stimulation with potassium chloride (KCL) was not modified by reserpine. Neither air nor L-NAME modified midrange sensitivity to KCL. L-NAME produced a 17% increase in maximum (91 ± 4 to 107 ± 5 mmHg, P < 0.05); reserpine abolished the latter effect. Air and L-NAME diminished endothelium-dependent vasodilation elicited by carbachol. Air did not modify endothelium-dependent vasodilation elicited by sodium nitroprusside; this response was potentiated by L-NAME. In summary, air and L-NAME produced similar effects on receptor-dependent activation of the endothelial L-arginine nitric oxide (NO) pathway. Potentiation by L-NAME of the maximal electromechanical response suggests the existence of a tone-dependent NO system. Abolition of the latter response by reserpine suggests that this system is of sympathetic origin.     

The stomach and/or upper duodenum contain sites of action that control meal size and intermeal interval length by exogenous rat gastrin releasing peptide

The site(s) of action that control the reduction of food intake in response to the amphibian skin peptide bombesin (Bn) has been determined to be the area supplied by the celiac artery (CA), i.e., the stomach and the upper duodenum. Here, we investigated the gastrointestinal site(s) of action which controls meal size (MS) (normal rat chow) and intermeal interval length (IMI) by the mammalian homologues of Bn gastrin releasing peptides (GRP-10, GRP-27 and GRP-29, 0.01, 0.05, 0.1, 0.2 and 0.5 nmol/kg) infused in the CA, the cranial mesenteric artery (CMA, supplying the small and large intestine), the femoral artery (FA, control) and the portal vein (PV, draining the gastrointestinal tract, control) in freely fed rats immediately prior to the onset of the dark cycle. We found that (1) GRP-29 (0.05, 0.1, 0.2 and 0.5 nmol/kg) and GRP-27 (0.2 and 0.5 nmol/kg) in the CA and GRP-29 (0.5 nmol/kg) in the CMA reduced the MS relative to saline, (2) GRP-29 (0.1, 0.2 and 0.5 nmol/kg) and GRP-27 (0.2 and 0.5 nmol/kg) in the CA prolonged the IMI, (3) GRP-29 (0.1, 0.2 and 0.5 nmol/kg) in the CA and GRP-29 (0.5 nmol/kg) in the CMA increased the satiety ratio (SR, IMI/MS – the amount of food consumed per a given unit of time) and (4) neither peptide nor route showed any effect on the second MS. These results support an upper gastrointestinal site of action for MS and IMI length by GRP-27 and GRP-29, which is most likely the stomach and/or the duodenum.