异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响

目的 探讨异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响。方法 选择SD雄性大鼠20只,随机分为两组,制备提睾肌微循环模型。吸入异氟醚、七氟醚麻醉后,分别记录吸入异氟醚、七氟醚1．5MAC3h内微循环、小动脉A1的直径和血流速度,微循环毛细血管后微静脉的白细胞滚动和粘附数量。结果 吸入异氟醚、七氟醚1．5MAC3h内HR,MAP,CVP和A1的直径和血流速度无明显改变（P＞0．05）。微循环毛细血管后微静脉的白细胞流动和粘附数量显著增加（P＜0．01）。结论 长时间吸入异氟醚、七氟醚后,可引起大鼠骨骼肌微循环毛细血管后微静脉的白细胞滚动和粘附数量显著增加。     

羟乙基淀粉对内毒素血症大鼠肠系膜细静脉白细胞活化和血管通透性的影响

目的 探讨羟乙基淀粉(HES 130/0.4)对内毒素血症早期大鼠肠系膜细静脉白细胞活化及血管通透性的影响.方法 雄性Wistar大鼠36只,体重200～250 g,随机分为3组(n=12):对照组(C组)静脉注射生理盐水0.5 ml后,静脉输注生理盐水16 ml·kg-1·h-1;内毒素组(LPS组)静脉注射LPS 2 mg/ks(溶于生理盐水0.5 ml)后,静脉输注生理盐水16 ml·kg-1·h-1;HES组静脉注射LPS 2ms/kg(溶于生理盐水0.5 ml)后,静脉输注HES 16 ml·kg-1·h-1.各组补液时间60 min.观察给药前及补液期间和补液后30 min内肠系膜细静脉白细胞滚动数、粘附数、游出数、肥大细胞脱颗粒情况及细静脉血管通透性情况,检测外周血白细胞粘附分子CD11b和CD18的表达.结果 与C组比较,LPS组沿肠系膜细静脉内滚动、粘附和游出的白细胞增加,肥大细胞脱颗粒率增加,LPS组和HES组CD11b、CD18表达上调,细静脉血管通透性增加(P＜0.05).与LPS组比较,HES组上述指标均降低(P＜0.05).结论 HES 130/0.4可抑制内毒素血症早期大鼠肠系膜细静脉白细胞沿血管壁滚动、粘附和游出,抑制肥大细胞脱颗粒及血管通透性的增加,从而改善微循环障碍.     

降钙素基因相关肽对急性胰腺炎胰腺微循环的影响

目的 研究降钙素基因相关肽（CGRP）对急性胰腺炎（AP）胰腺微循环及血管通透性的作用。方法 测定各组SD大鼠胰腺血流、微血管通透性，并对胰腺病理切片进行评分、对比。结果 （1）AP时胰腺血流发生显著改变；在AP模型建立前及过程中皮下注射CGRP，胰腺血流量、血液流速显著增加，胰腺病变程度减轻；在AP模型建立后注射CGRP，上述指标无改善。（2）AP时皮下注射CGRP，可使胰腺微循环血管通透性显著降低。结论 在AP模型建立前或同时皮下注射CGRP可以增加胰腺的血流量、血液流速，降低微血管通透性，减轻胰腺组织的损伤程度。     

兔后肢缺血再灌注后足背肌腱表面微循环变化

应用活体显微镜技术，观察了兔后肢常温止血带缺血２ｈ（ｎ＝８）及５（ｎ＝８）再灌注后最初１ｈ期间足背肌腱表面微循环动态变化，尤其是白细胞内皮粘附及微血管灌注状况的变化，旨在探讨缺血再灌注损伤的发生机制，从而指导临床治疗。结果表明：①肢体缺血再灌注后缺血组织微静脉内皮上粘附的白细胞数显著增加，而且缺血时间越长，增加越显著。②肢体缺血５ｈ再灌注后，缺血组织的微循环并不能均匀恢复，部分区域发生＂无复流现象＂，包括原发性无复流和继发性毛细血管灌注衰竭两种形式。提示：①白细胞内皮粘附参与了缺血再灌注损伤的病理生理过程。②肢体缺血５ｈ再灌注后发生的局部组织损伤并非皆属缺血再灌注损伤，部分区域可能系单纯缺血性损伤，部分区域则可能属缺血再灌注一继发性缺血损伤。     

丹参对随意型皮瓣活力影响的微循环观察实验研究

选用兔背部随意型皮瓣模型，长宽比例为３：１，用微循环观察仪直接观察，静脉滴注丹参注射液后，在不同的比例处观察微循环变化，辅以激光多普勒血流测定及组织学观察。结果表明：皮瓣的远端坏死是由于血管灌注压逐渐下降所致的微循环障碍引起，丹参可以明显改善皮瓣微循环状况，从而提高皮瓣成活长度。     

颈椎通治疗颈椎病机理的实验研究

本文采用具有活血化瘀作用之颈椎通胶囊进行大鼠血液流变学（A），兔离体主动脉（B），兔颈内动脉（C），犬椎动脉（D），大鼠肠系膜活体微循环（E）实验。结果表明：颈椎通胶囊具有降低大鼠血液粘度，直接舒张兔离体血管，显著增加兔颈内动脉与犬椎动脉血流量，明显改善大鼠肠系膜微循环等作用。其中颈椎通对B、C、D的作用优于颈复康，对E的作用与复方丹参相似。     

骨碎补总黄酮的活血化瘀作用及对实验性微循环障碍和骨质疏松症的影响

目的观察骨碎补总黄酮胶囊对大鼠的活血化瘀作用及对实验性微循环障碍、实验性骨质疏松症的影响.方法利用盐酸肾上腺素注射液造成大鼠"血瘀"模型,观察骨碎补总黄酮对大鼠血液黏度、红细胞功能、血小板聚集、粘附等血液流变学指标和大鼠肠系膜微循环的影响,利用维甲酸造成大鼠实验性骨质疏松症模型,观察骨碎补总黄酮对大鼠骨密度的影响.结果实验表明骨碎补总黄酮胶囊具有降低大鼠血液黏度、抑制血小板聚集的作用,与对照组比较差异有显著性(P＜0.01).骨碎补总黄酮对肾上腺素造成大鼠微动脉收缩具有抑制作用,并抑制微动脉血流的减慢,使血流状态得到改善;并提高大鼠的骨密度含量,提高大鼠的血钙浓度.结论骨碎补总黄酮具有一定的活血化瘀、抑制血小板聚集的作用;并能促进微循环的血流,对肾上腺素引起的微循环障碍有良好的预防和改善的作用;具有升高大鼠的骨密度和提高血钙含量的作用.     

梗阻性黄疸大鼠小肠肠系膜微循环变化及意义

目的以肠系膜为微循环观测窗，探讨梗阻性黄疸（简称梗黄）对肠系膜微循环的影响。方法将60只SD大鼠均分为对照组和梗黄组，每组分1、3、7d三个观测时相。将大鼠腹腔内一段回肠袢肠系膜平铺于恒温灌流盒作为微循环观察窗，用微循环显微镜及视频图像分析系统观测肠系膜微循环的动态变化并记录结果。结果梗黄组大鼠肠系膜微循环从微血管形态、微血管流态及微血管周围状态三个方面均发生明显变化，主要表现为毛细血管与微静脉扩张，血流减慢，红细胞聚集，微栓形成、毛细血管通透性增加及出血等，与对照组各相同时相比较差异均有统计学意义（P〈0．05）。结论梗阻性黄疸可引起大鼠肠系膜微循环障碍。     

TNFα、IL—1在白细胞与EC间粘附中的作用

目的：探讨IL－1、TNFα对白细胞与EC间粘附的影响。方法：分3组，（1）^51Cr标记白细胞＋EC＋M199培养液；（2）^51Cr标记白细胞＋EC＋TNFα或IL－1；（3）^51Cr标记白细胞＋人重组TNFα抗体预处理的EC＋TNFα。放免法测定TNFα和IL－1以及拮抗后EC与白细胞粘附率。结果：不同时间、不同浓度TNFα和IL－1作用下白细胞与EC间粘附率明显增加，具有时间依赖性和浓度依赖性，但具有时间差异性，TNFα引起的粘附率增高3h达到高峰，而IL－1是在6h，拮抗后EC与白细胞粘附率明显下降。结论：IL－1和TNFα均明显增加了白细胞与EC间粘附率，人重组TNFα单抗可消除TNFα引起的粘附。     

急性胰腺炎时内皮素和一氧化氮变化及丹参治疗作用研究

目的：研究急性胰腺炎时血浆内皮素（ET），一氧化氮（NO）变化和丹参对其影响，并探讨丹参对急性胰腺炎（AP）治疗作用，方法：急性胰腺炎71例，随机分为治疗组36例（A组），观察组35例（B组），A组用基础治疗＋丹参＋654－2；B组除丹参外治疗方法与A组相同。两组治疗前后均应用放射免疫分析方法测定血浆ET，NO和血尿淀粉酶（somogyi)，同时以健康体检者15例（C组）作对照，结果：急性胰腺炎时血浆ET，NO较C组明显增高，其增高程度与AP病变程度相关，A组经丹参活动后血浆ET，NO变化较B组具有显著性差异（P＜0．01），血尿淀粉酶恢复正常值时间，病程的缩短和治疗费与B组相比亦具统计学意义，结论：血浆ET，NO异常变化可能是AP发生，发展主要因素之一，丹参具有改善胰腺微循环和拮抗ET，NO产生，对AP有一定治疗作用。     

Isoflurane pretreatment supports hemodynamics and leukocyte rolling velocities in rat mesentery during lipopolysaccharide-induced inflammation

We hypothesized that the protective effects of isoflurane (ISO) pretreatment on the vasculature may be attributed, in part, to altered leukocyte-endothelial interactions. Rats were anesthetized with pentobarbital and then randomized into four groups: control, ISO-control (pretreatment with 30 min of 1.4% ISO), lipopolysaccharide (LPS; 10 mg/kg IV), and ISO-LPS (ISO pretreatment and then LPS). The mesentery was prepared for intravital videomicroscopy. Mean arterial blood pressure (MAP), along with microcirculatory variables that included postcapillary venular and arteriolar blood flow velocity and leukocyte dynamics (number of rolling and adherent leukocytes and individual rolling leukocyte velocities), were measured hourly (baseline and at 0-4 h). In LPS rats, ISO pretreatment significantly (P < 0.05) attenuated the decrease in MAP at 2 and 4 h after LPS and increased leukocyte rolling velocities after 2-4 h. Four hours after LPS, leukocyte rolling velocities were >200% more rapid (63.7 +/- 27.6 microm/s versus 19.8 +/- 6.4 micro m/s) in ISO-LPS versus LPS rats. In control rats, ISO pretreatment had no effect on MAP or leukocyte rolling velocities but increased the number of rolling leukocytes. ISO pretreatment had no effect on arteriolar and postcapillary venular blood flow velocity in LPS rats or leukocyte adherence in LPS or control rats. In conclusion, ISO pretreatment supported hemodynamics and increased leukocyte rolling velocities but did not alter the number of rolling or adherent leukocytes in the mesenteric microcirculation during LPS-induced inflammation. IMPLICATIONS: Isoflurane pretreatment supported hemodynamics and increased leukocyte rolling velocities in the mesenteric microcirculation during lipopolysaccharide-induced inflammation. Faster rolling velocities may reduce the incidence of inflammation by decreasing leukocyte-endothelial interactions and cellular injury.     

Leukocyte-Endothelium Interaction in the Rat Mesenteric Microcirculation during Halothane or Sevoflurane Anesthesia

Background: The effects of inhalational anesthetics on the microcirculation, including leukocyte dynamics, remain to be clarified. The authors investigated halothane and sevoflurane anesthesia to determine if these agents evoked leukocyte adhesion through endothelial cell-dependent mechanisms involving such adhesion molecules.

Methods: Rats were anesthetized with halothane or sevoflurane in 100% oxygen and the lungs were mechanically ventilated. Leukocyte behavior in mesenteric venules was recorded through intravital video microscopy under monitoring microvascular hemodynamics. To examine the mechanisms for leukocyte rolling and adhesion, these studies were repeated after animals were pretreated with a monoclonal antibody against P-selectin (MAb PB1.3) or against intracellular adhesion molecule-1 (ICAM-1; MAb 1A29): P-selectin required for rolling of circulating leukocytes and ICAM-1 for firm adhesive interactions with leukocyte integrins.

Results: Under baseline anesthetic conditions (1 minimum alveolar concentration [MAC]), venular wall shear rates, an index of the disperse force on marginating leukocytes, in the sevoflurane-treated rats were about two times higher than those with halothane. At 2 MAC, halothane caused a marked arteriolar constriction and decreasing shear rates concurrent with an increasing density of venular leukocyte adhesion. Sevoflurane at 2 MAC induced leukocyte rolling and adhesion, which were attenuated by PB1.3 and 1A29, without alterations in the wall shear rates. Halothane-induced leukocyte adhesion was not prevented by PB1.3 but it was by 1A29.     

活血化瘀注射液（HHI—I）对大鼠脑微循环、血-脑屏障和小鼠抗缺氧能力的有益影响

目的：研究HHI—I对大鼠脑微循环、血-脑屏障和小鼠抗缺氧能力的有益作用。方法：将探头放置软脑膜或插入脑实质用激光多普勒血流计测定大鼠脑徽循环血流.除了对两部位微循环的药理作用进行观察外还研究了HHI—I对高分子右旋糖酐（10％,9mL/kg,静脉注射）引起的大鼠脑微循环障碍的保护作用。应用5％氧浓度缺氧箱研究了HHI—I对小鼠抗致死性缺氧的保护作用。应用苯肾上腺素引起大鼠高血压性血-脑屏障通透性破坏,以伊文思蓝为标记物研究了静脉注射HHI—I对通透性的影响。结果：HHI—I能增加大鼠脑微循环血流,并对脑微伯环障碍有某些保护作用。HHI—I能降低小鼠致死性缺氧过程中的脑水肿。在增加脑血流的同时,HHI—I还能降低大鼠血-脑屏障通透性。结论：HHI—I对大鼠脑微循环、血-脑屏障和小鼠抗缺氧能力有一定的有益作用.     

L-selectin and leukocyte function in skeletal muscle reperfusion injury.

HYPOTHESIS: Treatment with anti-L-selectin monoclonal antibody will reduce venular neutrophil-endothelial rolling (flux and velocity) and adhesion associated with ischemia reperfusion injury in rat skeletal muscle. DESIGN: Prospective, randomized experimental trials. SETTING: Basic science research laboratory. MATERIALS: Male Wistar rats weighing 109 +/- 5 g (mean +/- SEM). INTERVENTIONS: Gracilis pedicle muscle flaps were elevated and microcirculation was observed by intravital microscopy. Two groups were evaluated: (1) the control group, which received 4 hours of global ischemia, and (2) the experimental group, which received 4 hours of global ischemia, plus treatment with anti-L-selectin monoclonal antibody 30 minutes before reperfusion. MAIN OUTCOME MEASURES: The number of rolling and adherent leukocytes in postcapillary venules were counted in the 2 groups at baseline and at 1 through 5, 10, 15, 20, 30, 45, and 60 minutes of reperfusion. RESULTS: Treatment with the monoclonal antibody to L-selectin significantly reduced the number of rolling leukocytes (flux) at 2 through 5, 20, 30, 45, and 60 minutes of reperfusion compared with controls (P<.05). Use of the monoclonal antibody significantly reduced the number of adherent neutrophils at 5, 10, 15, 20, 30, 45, and 60 minutes of reperfusion (P<.05). There was no significant difference in leukocyte velocity. CONCLUSION: L-Selectin plays a significant role in leukocyte rolling and adherence to venular endothelium in rat skeletal muscle ischemia reperfusion injury.     

An anti-inflammatory property of aprotinin detected at the level of leukocyte extravasation

BACKGROUND: Aprotinin is a serine protease inhibitor used extensively in cardiac operations to reduce postoperative bleeding. It has also been used in trials aimed at reducing the systemic inflammatory response to cardiopulmonary bypass. It remains unclear whether the anti-inflammatory action of aprotinin is related to its general ability to suppress leukocyte activation or whether aprotinin can exercise effects during the leukocyte-endothelial cell adhesion cascade. METHODS: We used intravital microscopy to study the 3 main stages of the adhesion cascade (leukocyte rolling, firm adhesion, and extravasation) within the mesenteric microcirculation of rats. This in vivo technique allows leukocyte recruitment to be viewed directly through the transparent mesentery of anesthetized animals. RESULTS: Aprotinin, given by continuous infusion at a clinically relevant dose, exerted no effect on the rolling or firm adhesion responses toward local chemoattractant N -formyl-methyl-leucyl-phenylalanine but significantly inhibited extravasation of leukocytes (73% at 40 minutes, P =.04) into surrounding tissues. In parallel in vitro experiments, aprotinin (used at 200, 800, and 1600 kIU/mL) dose dependently inhibited neutrophil transmigration through cultured endothelial cells in response to 3 different chemoattractants: N -formyl-methyl-leucyl-phenylalanine (P <.001 at 800 and 1600 kIU/mL), interleukin 8 (P <.05 at 200 kIU/mL and P <.001 at 800 and 1600 kIU/mL), and platelet-activating factor (P <.05 at 1600 kIU/mL). CONCLUSIONS: Our studies have therefore revealed a novel anti-inflammatory mechanism of aprotinin operating at the level of leukocyte extravasation. These findings may be relevant in the prevention of systemic inflammation after cardiopulmonary bypass through the use of protease inhibitors.     

Effect of salvianolic acid B on TNF-a induced cerebral microcirculatory changes ina micro-invasive mouse model

Purpose: To investigate the effects of salvianolic acid B (SAB) on tumor necrosis factor a (TNF-a) induced alterations of cerebral microcirculation with a bone-abrading model. Methods: The influences of craniotomy model and bone-abrading model on cerebral microcirculation were compared. The bone-abrading method was used to detect the effects of intracerebroventricular application of 40 mg/kg$bw TNF-a on cerebral venular leakage of fluorescein isothiocyanate (FITC)- albulmin and the rolling and adhesion of leukocytes on venules with fluorescence tracer rhodamine 6G. The therapeutical effects of SAB on TNF-a induced microcirculatory alteration were observed, with continuous intravenous injection of 5 mg/kg$h SAB starting at 20 min before or 20 min after TNF-a administration, respectively. The expressions of CD11b/CD18 and CD62L in leukocytes were measured with flow cytometry. Immunohistochemical staining was also used to detect E-selectin and ICAM-1 expression in endothelial cells. Results: Compared with craniotomy method, the bone-abrading method preserved a higher erythrocyte velocity in cerebral venules and more opening capillaries. TNF-a intervention only caused responses of vascular hyperpermeability and leukocyte rolling on venular walls, without leukocyte adhesion and other hemodynamic changes. Pre- or post-SAB treatment attenuated those responses and suppressed the enhanced expressions of CD11b/CD18 and CD62L in leukocytes and E-selectin and ICAM-1 in endothelial cells induced by TNF-a. Conclusions: The pre- and post-applications of SAB during TNF-a stimulation could suppress adhesive molecular expression and subsequently attenuate the increase of cerebral vascular permeability and leukocyte rolling.     

In vivo assessment of acute microvascular injury after reperfusion of ischemic tibialis anterior muscle of the hamster

The purposes of this study were to develop an in vivo model of skeletal muscle ischemia--reperfusion to assess the patterns of microvascular injury, to evaluate a scoring system that permits quantitation of this injury, and to determine in vivo the extent of white blood cell adhesion within the microcirculation during the acute postreperfusion period. Syrian golden hamsters underwent 3.0 or 4.5 hr of lower extremity ischemia without anticoagulation. The microcirculation of the tibialis anterior muscle was visualized by fluorescent intravital microscopy (700X). During the first 1.5 hr of reperfusion the microvascular injury was scored by a grading system based upon the extent of extravasation of fluorescein-labeled albumin and the degree and level of microvessel obstruction. To correlate the observed changes in the microcirculation to changes in the whole muscle, in a separate group of animals, pH changes in the tibialis anterior muscle were measured at the same time intervals under identical experimental conditions as the microvascular measurements. White blood cells were transiently fluoresced at 1.5 hr after reperfusion by intravenous acridine red and the number of white blood cells rolling (rollers) or sticking (stickers) to the endothelium during a 30-sec observation period was recorded. Two distinct patterns of microvascular injury were seen: after 3.0 hr of ischemia there was a progressive extravasation, some capillary but no arteriolar or venular obstruction, flow velocities increased over time; after 4.5 hr of ischemia there was a greater heterogeneity of injury, primary "no reflow," extensive capillary, arteriolar, and venular obstruction, as well as a progressive decline in flow velocities. Thrombosis of microvessels was rare. There was no inflow vessel thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

C1-esterase inhibitor and its effects on endotoxin-induced leukocyte adherence and plasma extravasation in postcapillary venules

BACKGROUND: C1-esterase inhibitor (C1-INH) has been shown to have beneficial effects in patients with sepsis. However, the microcirculatory effects of C1-INH during sepsis are unknown. This study investigated the influence of C1-INH on leukocyte-endothelial cell adhesion, vascular leakage, and venular microhemodynamics in postcapillary venules of rat mesentery during endotoxemia. METHODS: Thirty-two anesthetized Wistar rats randomly received 1 of 4 treatments: pretreatment with infusion of C1-INH in a concentration of 7.5 U.kg-1 body weight (C1-INH-7.5 group, n = 8) or in a concentration of 15 U.kg-1 body weight (C1-INH-15 group, n = 8) followed by continuous infusion of Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 8) was pretreated with saline solution 30 minutes before LPS infusion. The control group (n = 8) received equivalent amounts of saline infusion. Leukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules of rat mesentery were determined every 60 minutes during a period of 120 minutes using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from mean red blood cell velocity and vessel diameter. RESULTS: LPS infusion induced a decrease in venular wall shear rate and an increase in leukocyte adherence and vascular permeability in postcapillary venules of rat mesentery. All microcirculatory disturbances were attenuated by pretreatment with C1-INH, showing no significant difference between the 2 concentrations. CONCLUSIONS: Pretreatment with C1-INH attenuates endotoxin-induced leukocyte adherence and macromolecular leakage in postcapillary venules of rat mesentery, indicating that complement inhibition might be a therapeutic tool in the treatment of sepsis.     

Higher bypass temperature correlates with increased white cell activation in the cerebral microcirculation

OBJECTIVE: Cardiopulmonary bypass induces a systemic inflammatory response, which in turn promotes a cascade of leukocyte and endothelial cell activity. We investigated whether differences in bypass temperature and flow rate affect endothelial cell and leukocyte adhesion in the cerebral microcirculation. METHODS: Thirty-six piglets (13.0 +/- 1.1 kg) had a cranial window placed over the parietal cortex to evaluate the microcirculation by means of intravital microscopy. Animals were cooled to a temperature of 15 degrees C, 25 degrees C, or 34 degrees C on cardiopulmonary bypass with hematocrit levels of 20% or 30% by using pH-stat management, followed by 60 minutes of reduced flow (10, 25, or 50 mL.kg(-1).min(-1)). Rhodamine staining was used to observe adherent and rolling leukocytes in postcapillary venules. RESULTS: Higher bypass temperature correlated with significantly more adherent and rolling leukocytes during the full 60 minutes of low-flow bypass (P <.05). Poisson regression revealed more adherent leukocytes at 34 degrees C than at 15 degrees C and at a flow rate of 10 mL.kg(-1).min(-1) compared with a flow rate of 50 mL.kg(-1).min(-1). There was an inverse correlation between flow rate and the number of adherent and rolling leukocytes at 30, 45, and 60 minutes of low-flow bypass (P <.05). Temperature was a multivariable predictor of histologic score, with greater neurologic damage found after bypass at 34 degrees C (P <.01). CONCLUSIONS: Leukocyte activation in cerebral microcirculation is increased with higher temperature and lower flow rate, suggesting that these variables influence the inflammatory response during cardiopulmonary bypass.     

Local histamine release increases leukocyte rolling in the cerebral microcirculation of the mouse

Histamine mediated induction of leukocyte rolling and adhesion in the cerebral microcirculation was examined in two inbred strains of mice (SJL/J and BALB/c). A cranial window was surgically prepared for the visualization of the cerebral microcirculation using intra vital microscopy. Leukocyte rolling and adhesion to pial venular walls were assessed during off line video playback analyses. The surgical preparation of the cranial windows was found to trigger spontaneous leukocyte rolling, and this was attributed to disruption of dural mast cells and localized release of vasoactive histamine. This sponta neous leukocyte rolling was observed only in the SJL/J strain of mice, and could be prevented by pre surgical treatment with the mast cell stabilizer sodium cromoglycate. BALB/c mice did not show spontaneous leukocyte rolling or adhesion; this strain is known to have low numbers of CNS associated mast cells. Exogenous histamine, applied topically to the cerebral microcirculation via the cranial window in mice pretreated with sodium cromoglycate, produced significant dose dependent increases in leukocyte rolling and adhesion to pial venules in SJL/J mice, but not in BALB/c mice. Diphenhydramine (H₁ receptor antagonist), but not cimetidine (H₂ receptor antagonist), abolished both spontaneous and histamine induced leukocyte rolling. Anti-P-selectin antibody was found efficiently to block both spontaneous and histamine induced increases in leukocyte rolling, but not leukocyte adhesion.