实验性急性胰腺炎早期胰组织氧供及微循环

于家兔急性出血性胰腺炎早期阶段研究了胰组织氧供及胰腺微循环的变化。实验证明急性胰腺炎后１０ｍｉｎ即可见到胰组织氧分压下降（５．５７±１．０２ｋＰａ）及胰腺微循环血流减少（１１．８６％±４．９１％），至２ｈ末仍明显降低（６．０２±１．７ｋＰａ／９．１４％±５．８７％），与发病前（９．１１±１．３４ｋＰａ／２１．７１％±１１．４０％）有明显差别。诱发急性胰腺炎后１及２ｈ均见血清α－淀粉酶（１２２７．５７±７８８．２７及１６９８．２９±６８１．０３Ｕ／Ｌ）较急性胰腺炎前（５２６．８６±１５６．３４Ｕ／Ｌ）明显增高。病理检查证明疾病模型符合急性出血性胰腺炎变化。由此认为研究胰组织氧供较单纯研究血液循环（包括微循环）更重要，设法改善胰组织氧供是进行实验与临床治疗的必要措施。     

兔急性脑缺氧时脑及脑脊液内腺嘌呤核苷含量的变化

本文报告了由低张性低氧血症所致兔急笥脑缺氧时脑组织内腺苷、次黄嘌呤核苷及次黄嘌呤水平分别从正常对照的５３．３±２．９、１１５．６±１１．８及１８６．５±１０．３增至８１６．４±５９．０、１０４９．７±３７．５及７０４．４±５５．３μＭ／ｇ（Ｘ±ＳＤ），各组间Ｐ值均＜０．０１至０．０５。同步测定的脑脊液中三种腺嘌呤核苷水平分别从正常对照的１．６±０．８、５．１±１．０及１３３．９±５０．８增至７．０     

骶前区静脉丛的解剖学特点及临床意义

目的：研究骶前区静脉丛（Ｖｅｎｏｕｓ ｐｌｅｘｕｓ ｏｆ ｐｒｅｓａｃｒａｌ ｒｅｇｉｏｎ ，ＶＰＰＳＲ） 的解剖学特点，为骶前区静脉破裂大出血的防治提供解剖学基础。方法：在３４ 具成人尸体上，分虽观测ＶＰＰＳＲ 的组成、管壁、瓣膜、长度及直径。结果：ＶＰＰＳＲ 管壁薄、缺少静脉瓣，呈网状。ＶＰＰＳＲ Ｓ１～５ 横干的长度和直径（ Ｆ 检验） 均有显著差异，Ｐ＜ ０ ．０５ 。其长度平均（ 珋ｘ ±ｓ） ：Ｓ１ 为３ ．２ ±１ ．５ ｃｍ ，Ｓ２ 为４ ．４ ±１ ．０ ｃｍ ，Ｓ３ 为３ ．５ ±１ ．１ ｃｍ ，Ｓ４ 为２ ．３ ±０ ．９ ｃｍ ，Ｓ５ 为１ ．０ ±０ ．３ ｃｍ ；其直径平均（珋ｘ ±ｓ） ：Ｓ１ 为１ ．２ ±０ ．７ ｍ ｍ ，Ｓ２ 为２ ．５ ±１ ．５ ｍ ｍ ，Ｓ３ 为２ ．５ ±１ ．５ ｍ ｍ ，Ｓ４为１ ．７ ±１ ．５ ｍ ｍ ，Ｓ５ 为０ ．９ ±０ ．６ ｍ ｍ 。Ｓ４ 椎体前穿通支静脉口径２ ～４ ｍ ｍ 占８ ．８ ％ ，０ ．１ ～１ ．９ ｍ ｍ 占９１ ．２ ％ 。结论：ＶＰＰＳＲ 解剖变异多、血管壁薄、缺少静脉瓣是引起ＶＰＰＳＲ 损伤大出血甚至死亡的解剖学基础。     

股骨中段骨膜瓣移植的解剖及其临床应用

在４５侧经动脉内灌注红色乳胶的成人下肢标本上，解剖观测了股中间肌近端血管及其骨膜支的来源，分支分布。结果表明：近端的股动脉来自旋股外侧动脉占５７．５％；来自股深动脉占２８．９％；来自股动脉占１３．１％。肌动脉干长１５．８±０．７ｍｍ，外径２．２±０．７ｍｍ。８８．９％的骨膜支来自肌动脉，经股中间肌与股内侧肌之间的间隙，达股骨中段前份。骨膜支干长３６±１１ｍｍ，外径１．５±０．４ｍｍ。以肌动脉为蒂，     

改善微循环和促进创伤愈合的新途径:功能型医用敷料

观察在纤维中纺入无机超细粉粒,能释放出远红外线的新型医用功能敷料对微循环和创面愈合的效应。方法：用显微电视微循环观察系统、红细胞跟踪仪、电视测微仪测定新型功能敷料作用前后大鼠微循环血流的变化,用病理切片光镜观察新型功能敷料对家兔切割创面愈合的效应。结果：１层、３层、５层新型功能纱布作用大鼠肠系膜２０ｍｉｎ,分别使微动脉血流量增加５１.７％±８．１％、９２.１％±９．１％、９２．７％±９．６％,它显著高于普通纱布对照组的的０．５％±９．６％（Ｐ＜０.０１）。用功能纱布一侧的家兔切割创面,其水肿、白细胞浸润和渗出物均比普通纱布覆盖的另一侧创面要轻微。伤后５天功能纱布组创面表皮已完全修复平坦,而对照一侧尚未完全修复。结论：新型功能敷料能显微改善微循环,并有加速创伤愈合的特殊效应。     

雌激素拮抗胰岛素在中枢胆碱能神经的生物效应

雌性ＳＤ大白鼠２０只，于鼠脑顶皮质作宽２ｍｍ的冠状损伤切口，分为胰岛素脑室内注射组（０．６ｕ／次／３日），雌二醇肌注射组（１００μｇ／ｋｇ／２日），胰岛素和雌二醇联合应用组（用药同前），损伤对照组和正常对照组。术后存活４周，用Ｈｅｄｒｅｅｎ推荐的染色方法显示ＡＣｈＥ阳性纤维，结合网格计算分析切口嘴、尾侧区胆碱能纤维的再生和抽芽情况．结果是：（１）胰岛素用药组嘴、尾侧纤维密度（１５９．９±１６．８，９２．７±１１．７）和雌二醇用药组嘴、尾侧的纤维密度（１５０．４±１６．５，８０．１±１１．０）均高于损伤对照组（１３６．９±１１．６，６８．３±７．１）（Ｐ＜０．０１）；（２）胰岛素和雌二醇联合用药组嘴、尾侧纤维密度（１００．８±１４．１，４８．９±８．６）低于损伤对照组（Ｐ＜０．０１）。提示：胰岛素、雌激素对皮质胆碱能纤维损伤后的再生和抽芽有促进作用，但联合应用雌激素和胰岛素显示出拮抗效应，结果使损伤后皮质胆碱能纤维的再生和抽芽受到抑制．     

人脑颞叶组织中类固醇5a－还原酶同功酶活性分布研究

本文采用酶放射分析法对新鲜人脑颞叶组织中５ａ－还原酶同功酶的活性分布进行研究。结果显示：（１）在颞叶脑组织中，５ａ－还原酶１和５ａ－还原酶２主要分布在灰质，其酶活性（５ａ－还原酶１，３３．６±４．５ｐｍｏｌ·ｈ_（－１）／ｍｇ蛋白，ｎ＝１２；５ａ－还原酶２，１３．８±２．９ｐｍｏｌ·ｈ_（－１）／ｍｇ蛋白，ｎ＝１１）明显高于分布在白质中的酶活性（５ａ－还原酶１，１４．７±２．０ｐｍｏｌ·ｈ_（－１）／ｍｇ蛋白，ｎ＝１２，Ｐ＜０．００１；５ａ－还原酶２，５．２±０．９ｐｍｏｌ·ｈ_（－１）／ｍｇ蛋白，ｎ＝１１，Ｐ＜０，０１）；（２）在灰质中，５ａ－还原酶活性主要来自于５ａ－还原酶１，其酶活性（３４．９±２．５ｐｍｏｌ·ｈ_（－１）／ｍｇ蛋白，ｎ＝３２）明显高于５ａ－还原酶２（１５．０±２．３ｐｍｏｌ·ｒ_（－１）／ｍｇ蛋白，ｎ＝１８，（Ｐ＜０．００１）；（３）５ａ－还原酶１和５ａ－还原酶２的活性在男女性之间差异不显著，且与年龄无相关关系。     

尿毒症患者血液透析前后的甲襞微循环

观察１８例慢性肾功能不全尿毒症终末期患者甲襞微循环的改变及其中１１例用血液透析治疗的患者第一次血透前与血透４～８次（平均５．９次）后甲襞微循环的变化，结果表明，尿毒症患者甲襞微循环加权积分综合判断，中度异常者占８３．３％，重度异常者占１６．７％。其中１１例作血透的患者在治疗前与治疗后总积分值分别为６．９０±０．７２与５．１０±０．７０，二者有非常显著差异。提示尿毒症患者甲襞微循环障碍经血透治疗后可有明显改善，但仍在中度异常范围。给尿毒症患者进行甲襞微循环检查，对其病情的估价有着一定的临床意义。     

正常人消化间期胃肠移行性复合运动规律的观察

对１６例健康志愿者用连续灌注导管系统进行胃十二指肠测压，以了解消化间期移行性复合运动（ＭＭＣ）的规律，检测时间４～６ｈ，结果显示ＭＭＣＩ期持续时间１２７．６±５６．４ｍｉｎ，Ⅱ期为１９．９±６．１ｍｉｎ，Ⅲ期胃窦部为３．４±１．１ｍｉｎ，十二指肠为４．６±２．０ｍｉｎ，近端空肠为５．８±３．０，近端空肠与胃窦部比Ｐ〈０．０１），由胃窦至空肠Ⅲ期收缩频率呈上升趋势，波幅明显下降。ＭＭＣ平均周期为１８     

溃疡病患者胃肠运动功能障碍及表皮生长因子的变化

用连续灌注导管测压，并测定胃液和血清的表皮生长因子（ＥＧＦ）的含量，为了解十二指肠球溃疡（ＤＵ）患者消化间期移行性复合运动（ＭＭＣ）的规律，及其胃液和血清中的表皮生长因子含量的变化。结果显示：１、６０％ＤＵ患者缺乏ＭＭＣⅢ期，与正常人比Ｐ＜０．０５。２、ＤＵ患者ＭＭＣⅢ期持续时间（２．９±１．９ｍｉｎ）比正常人（４．３±１．１ｍｉｎ）缩短，（Ｐ＜０．０５）。３、ＤＵ患者ＭＭＣⅢ用十二指肠近端及远端的运动波幅较正常人减低（Ｐ＜０．０１）。４、ＤＵ患者的胃液和血清的表皮生长因子含量显著降低，分别为１９９．２７±１４７．８１ｐｇ／ｍＬ和１４８．６７±１２４．３１ｐｇ／ｍＬ，（Ｐ＜０．０１）。说明消化间期移行性复合运动和表皮生长因子在十二指肠球溃疡发病机理上起一定作用。     

An ultrastructural analysis of endothelial change paralleling platelet aggregation in a light/dye model of microvascular insult

Those microvascular endothelial events that parallel the evolution of platelet aggregation were evaluated in a well-controlled animal model. Cat pial microvessels were observed through a cranial window while local platelet aggregation was produced by intravenous injection of sodium fluorescein and simultaneous exposure of the pial vessels to light from a filtered mercury lamp that excited the fluorescein. The vessels were fixed in situ when the in vivo observations of a preselected vessel indicated early, intermediate, or advanced aggregation in that vessel. The preselected vessel was then harvested for ultrastructural study together with adjacent vessels from the illuminated field. These vessels and appropriate controls were compared in semiserial thin sections. The onset of platelet aggregation in both venules and arterioles was accompanied by focal endothelial lucency, vacuole formation, luminal membrane rupture, and swelling of the nuclear envelope. These changes were not found in control material. With intermediate aggregation these changes were more common, while with advanced aggregation these abnormalities occurred together with focal endothelial denudation. Thus, in this model denudation occurred only with advanced aggregation and was not a prerequisite for aggregation.     

心-肾反射在调节兔肾水钠排出功能中的作用

目的： 研究不同浓度盐溶液所致的心房及血容量扩张通过心-肾反射对肾排钠利尿功能的影响，探讨心-肾反射在肾脏功能调节中的作用。方法： 取健康家兔分为生理盐水和高渗盐溶液组。去窦弓神经，左肾神经在近肾门处切断。导管经右颈外静脉插至右心房，以10 mL/min输入15%血容量的生理盐水和1.8%氯化钠溶液前后，观察中心静脉压（CVP）、左肾交感神经传出活动（ERSNA）、左、右肾尿量和排钠系数的变化。结果： 输液后高渗盐和生理盐水组 CVP分别升高75.00%±27.40%和64.00%±15.56%；ERSNA频率分别减慢63.00%±12.49%和44.00%±13.64%，平均群集时间分别缩短37.00%±16.49%和31.00%±10.69%，平均群集间期分别延长68.00%±27.04%和60.00%±18.38%；左肾尿量分别增加640.00%±155.39%和158.00%±28.10%，排钠系数分别增加376.00%±121.72%和132.00%±35.23%；右肾尿量分别增加 1 343.00%±429.95%和192.00%±32.26%，排钠系数分别增加856.00%±261.48%和300.00%±76.99%。结论： 在去窦弓神经家兔，不同浓度溶液所致的心房及血容量扩张可刺激心肺感受器，通过心-肾反射活动抑制ERSNA，使肾的排钠和排水增多，进而调整和维持机体血容量的相对稳定。     

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.     

Development of pressurized retinal resistance-sized arteriolar preparation with special reference to acetylcholine-induced nitric-oxide-mediated vasodilatation

We examined the responses of pressurized bovine retinal functional arterioles (97-185 microm in diameter and approximately 3 mm long) to vasoactive substances and the mode of action of acetylcholine (ACh) on the pressurized arterioles. The retinal arterioles were cannulated at both ends with glass micropipettes and perfused at a constant pressure of 60 mmHg. Vasoconstrictions of the retinal arterioles were induced by prostaglandin F(2 alpha) (PG F(2 alpha)), U46,619, noradrenaline (NA), and 5-hydroxytryptamine (5-HT) in a dose-dependent manner. The decreasing order of potency (pD(2) value) in the constrictive responses was as follows: 5-HT = U46,619 > NA > PG F(2 alpha). On the other hand, sodium nitroprusside (SNP), isocarbacyclin (a stable prostaglandin I(2) analog), ACh, and isoproterenol (ISP) caused dose-dependent vasodilatation in the pressurized retinal arterioles preconstricted with high-potassium solution (40 mM K+). The decreasing order of potency in the vasodilative responses was as follows: isocarbacyclin > SNP > ACh. The ACh-induced vasodilatation was suppressed significantly by pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME) (3 x 10(-5) M). A treatment with L-arginine (10(-3) M) in the presence of 3 x 10(-5) M L-NAME reversed completely the L-NAME-induced reduction of the vasodilatation. These results suggest that ACh causes the production and release of endogenous nitric oxide or its related compounds, which results in vasodilatation of the pressurized bovine retinal functional arterioles.     

荧光显微镜观察电针对实验性急性出血性低血压脑微循环的作用

目的：研究电针对急性出血性低血压的大鼠软脑膜微循环的作用。方法：通过股动脉放血造成急性低血压的模型，经过开颅术后在软脑上安置颅窗，利用荧光显微镜观察软脑膜微循环和显微图像，我们分析了针刺过程对脑小动脉的作用。结果：电针前三里有增加脑血流的作用。血压（设ｙ为相对平均血压）－小动脉管径（设ｘ为相对直径）相互关系由以下公式描述：针刺组：ｙ＝１．３２８ ５ｘ~２．２ ８７６ ３ｘ＋ ２．４９３１，非针刺组；ｙ＝０．４７６ ６　ｘ~２－ ０．９７６ ２ｘ＋１．５０８ ４。结论：电针对急性出血性低血压的大鼠软脑膜微循环有明显的扩张小动脉血管的作用。     

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.     

Neuropeptide Y: Immunocytochemical localization to and effect upon feline pial arteries and veins in vitro and in situ

Plexuses of nerve fibres containing neuropeptide Y (NPY)-like immunoreactivity invest pial arteries belonging to the circle of Willis, pial arterioles, occasionally penetrating arterioles and large veins. A more sparse supply of NPY-like fibres are observed around pial veins and venules. The NPY-immunoreactive fibres are located within the adventitia or at the adventitia-media border. Only occasional fibres are present in cerebral vessels of animals in which the superior cervical ganglion has been removed one week previously. Administration of NPY resulted in strong, concentration-dependent contractions of isolated feline middle cerebral arteries whereas administration of avian pancreatic polypeptide (APP) elicited weak contractions. In chloraloseanaesthetized cats, perivascular microapplication of NPY in situ resulted in marked concentration-dependent contractions of cerebral pial arterioles (34.7±6.6%; maximum decrease in calibre with NPY. Perivascular administration of NPY resulted in the constriction of pial veins but the magnitude of the venous calibre reductions was smaller than the response of arterioles at each reductions was smaller than the response of arterioles at each concentration examined. APP did not elicit contraction of pial arterioles or veins during in situ conditions. The pharmacological and immunocytochemical results strongly indicate the existence of a novel perivascular neuronal system containing NPY, which mediates contraction of cerebral blood vessels and NPY is colocalized with NA in sympathetic nerves.     

The effect of a nitric oxide donor, sodium nitroprusside, on the release of acetylcholine from the in vitro cat carotid body

The purpose of the present study was to determine the impact of a nitric oxide (NO) donor, sodium nitroprusside (SNP), on the release of acetylcholine (ACh), an essential excitatory neurotransmitter, from the in vitro cat carotid body (CB). Bilateral CBs were harvested from five deeply anesthetized cats according to the regulations contained in the policies of the Johns Hopkins Animal Care and Use Committee. After recovering from the surgical procedures for extraction and cleaning, the CBs were taken through a 15-step protocol in which they were exposed to a hyperoxic gas mixture (40% O2/5% CO2; 20 min), then a hypoxic gas mixture (6% O2/5% CO2; 20 min), and a final 10 min hyperoxic mixture. This sequence was applied twice, followed by the same sequence in the presence, first, of 5 microM SNP, and secondly in the presence of 10 microM SNP. After washing and a recovery period the CBs were again exposed to the gases as in the first two non-SNP trials. The SNP exposures significantly reduced the overall release of ACh by about 20% (P=0.039). Further, SNP significantly reduced the hypoxia-induced increase in ACh release (without SNP: 82.4+/-19.1 fmol/20 microL versus with SNP: 49.7+/-15.0 fmol/20 microL; mean+/-S.E.M.; P=0.032). Trials #1 and #2 which preceded the application of SNP and Trial #3 which followed SNP were statistically indistinguishable. The CBs had recovered their original status. The data support the hypothesis that the frequently reported NO-induced reduction in CB neural output during hypoxia is at least in part due to the reduction in ACh release. The results are consistent with a previous report in which l-arginine, an NO precursor, had the same reducing effect. Possible mechanisms are discussed.     

Radioactively Labelled Microspheres in Regional Cerebral Blood Flow Determinations A study on monkeys with 15 and 35 μm spheres

15 μm and 35 μm radioactive microspheres, differently labelled, were used simultaneously for rCBF-determinations in monkeys. Flow values calculated from data for 35 μm spheres were 27±7 g/min per 100 g higher for grey matter and 10±3 g/min per 100 g lower for white matter than flow values calculated from 15 μm spheres, while both sphere sizes resulted in similar values for the choroid plexus. A large number of 35 μm spheres were trapped in extracerebral pial arterioles. It is concluded that entrapment in relatively large arterioles of the 35 μm spheres explains the differences in flow values, and that this invalidates the use of 35 μm spheres, and larger, in rCBF-determinations.     

颅脑损伤与微循环障碍的实验研究

目的:研究颅脑损伤后的微循环障碍,借以讨论临床某些病人的脑功能紊乱。方法:用两种方法进行研究,一是压迫静脉造成颅内高压模型;另一种是应用荧光素钠作脑血管造影,观察脑外伤后荧光素自脑微血管内向外渗漏的范围。用家兔作实验,通过颅骨窗观察脑软膜的微循环变化。结果:高颅内压时脑微循环停流,当颅内压降低时脑微循环流态正常,无论微血流停流或复流过程均无粒摆流。脑外伤后荧光素自脑微血管中向外渗漏,标识出脑损伤的范围。结论:脑微循环障碍是颅高压的合并症,荧光素自脑微血管向脑组织通道渗漏可显示脑外伤的范围,对脑外伤后某些综合病征和后遗症有诊断价值。