Leukocyte-endothelial interactions in pial arterioles and venules on development of cerebral ischemia in rats

In vivo microscopy was used to study the interaction between leukocytes and the pial venular and arteriolar endothelium in rats during cerebral ischemia evoked by bilateral ligation occlusion of the carotid arteries. Specimens were obtained from 40 arterioles and 30 venules (diameter up to 40 μm) of the pia mater from Wistar rats (n = 7) subjected to ischemia for 5 h to respiratory arrest. The experimental data demonstrated significant differences in changes in the adhesion of leukocytes to the endothelium of arterial and venous microvessels during the development of hypoxia. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 94, No. 1, pp. 45–52, January, 2008.     

Morphodynamic analysis of the role of leukocytes in the microcirculation disorder of the cerebral cortex

The aim of this work was to establish the reasons for the disturbances of microcirculation (no reflow) during various kinds of oxygen starvation of the brain. Using contact optics and video-recording, direct observations were performed and leukocyte and erythrocyte displacement was monitored in the blood vessels of rat cerebral cortex in vivo in normoxia, during the development of various kinds of oxygen deficiency up to the terminal periods of life of an organism. In normoxia leukocytes were shown to decelerate erythrocyte movement in capillaries and to cause the irregularity of the capillary blood flow. Using the color videofilm recording it was shown that at deep stages of brain oxygen deficiency the disturbances of microcirculation up to its complete cessation were explained by the occlusion of venous microvessels as a result of massive adhesion of leukocytes to the inner surface of venules and the smallest veins. The co-adhesion of leukocytes was also found to take place. The latter leads to the formation of large leukocyte aggregates in venous vessels, results in "no reflow" effect. Leukocyte aggregates in veins block the venous outflow from the brain and may become the immediate cause of organism death as a result of disruption of circulation and oxygen deficiency.     

Studies of cerebral circulation in series experiments by means of changes in the blood pressure gradient in vessels supplying the brain

Summary A method of graphic a recording of arterial blood pressure in the aorta and the circle of Willis in series experiments on dogs is described. Measurements were taken in the common carotid artery brought out into a skin flap, to which 3 cuffs were attached: medial, recording variations in the pulse, one placed caudad and one cephalad from the medial cuff, occluding corrspondingly the blood flow from the aorta and the circle of Willis. The blood pressure in the bead occluding collar corresponded to the blood pressure in the circle Willis, after disappearance of aorta during complete occlusion of the inflow of blood from the aorta. The cortic blood pressure was determined by the appearance of the first pulse beat in decrease of the pressure in “thoracic” cuff with preserved occlusion of the “head” portion of the common carotid artery. The changes of the gradient of the fall of blood pressure from aorta to the blood vessels of the circle of Willis served as an indication of changes of the lumen of blood vessels of the brain (Hurthle's principle). Presented by Active Member AMN SSSR N. A. Rozhansky     

多器官衰竭早期血小板粘附与血管内皮细胞的改变

用失血再灌流加内毒素造成多器官衰竭（ＭＯＦ）的方法，在３００～１５００倍显微镜下观察血小板粘附和内皮损伤的改变，探讨血小板粘附和血管内皮损伤对微循环的影响。结果表明ＭＯＦ早期细静脉内皮上除有较多血小板贴壁或粘附在变形性差的白细胞上，细动脉内皮增厚，内皮表面出现较多血小板粘附，管腔内壁粗糙，可见到血流中的血小板迅速地粘附在损伤的内皮上，堆积、溶合形成壁栓。管腔内还有纤维蛋白形成丝网状粘附在血管腔的中间。血小板和纤维蛋白缠络在一起，形成棉絮状的团块在血管内流动。ＭＯＦ的早期细静脉内皮水肿、管壁增厚并有空泡形成，大的空泡占满整个管腔，造成血流受阻。这些改变都是造成ＭＯＦ发生的重要原因。     

Responses of cerebral arteries and arterioles to acute hypotension and hypertension

The responses of cerebral precapillary vessels to changes in arterial blood pressure were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation of the parietal cortex. Vessel responses were found to be size dependent. Between mean arterial pressures of 110 and 160 mmHg autoregulatory adjustments in caliber, e.g., constriction when the pressure rose and dilation when the pressure decreased, occurred only in vessels larger than 200 micron in diameter. Small arterioles, less than 100 micron in diameter, dilated only at pressures equal to or less than 90 mmHg; below 70 mmHg their dilation exceeded that of the larger vessels. When pressure rose to 170- 200 mmHg, small vessels dilated while the larger vessels remained constricted. At very high pressures (greater than 200 mmHg) forced dilation was frequently irreversible and was accompanied by loss of responsiveness to hypocapnia. Measurement of the pressure differences across various segments of the cerebral vascular bed showed that the larger surface cerebral vessels, extending from the circle of Willis to pial arteries 200 micron in diameter, were primarily responsible for the adjustments in flow over most of the pressure range.     

Bioactive Hydrogel Substrates: Probing Leukocyte Receptor–Ligand Interactions in Parallel Plate Flow Chamber Studies

The binding of activated integrins on the surface of leukocytes facilitates the adhesion of leukocytes to vascular endothelium during inflammation. Interactions between selectins and their ligands mediate rolling, and are believed to play an important role in leukocyte adhesion, though the minimal recognition motif required for physiologic interactions is not known. We have developed a novel system using poly(ethylene glycol) (PEG) hydrogels modified with either integrin-binding peptide sequences or the selectin ligand sialyl Lewis X (SLe^X) within a parallel plate flow chamber to examine the dynamics of leukocyte adhesion to specific ligands. The adhesive peptide sequences arginine–glycine–aspartic acid–serine (RGDS) and leucine–aspartic acid–valine (LDV) as well as sialyl Lewis X were bound to the surface of photopolymerized PEG diacrylate hydrogels. Leukocytes perfused over these gels in a parallel plate flow chamber at physiological shear rates demonstrate both rolling and firm adhesion, depending on the identity and concentration of ligand bound to the hydrogel substrate. This new system provides a unique polymer-based model for the study of interactions between leukocytes and endothelium as well as a platform to develop improved scaffolds for cardiovascular tissue engineering.     

Micropatterned surfaces for controlling cell adhesion and rolling under flow

Cell adhesion and rolling on the vascular wall is critical to both inflammation and thrombosis. In this study we demonstrate the feasibility of using microfluidic patterning for controlling cell adhesion and rolling under physiological flow conditions. By controlling the width of the lines (50–1000 μm) and the spacing between them (50–100 μm) we were able to fabricate surfaces with well-defined patterns of adhesion molecules. We demonstrate the versatility of this technique by patterning surfaces with 3 different adhesion molecules (P-selectin, E-selectin, and von Willebrand Factor) and controlling the adhesion and rolling of three different cell types (neutrophils, Chinese Hamster Ovary cells, and platelets). By varying the concentration of the incubating solution we could control the surface ligand density and hence the cell rolling velocity. Finally by patterning surfaces with both P-selectin and von Willebrand Factor we could control the rolling of both leukocytes and platelets simultaneously. The technique described in this paper provides and effective and inexpensive way to fabricate patterned surfaces for use in cell rolling assays under physiologic flow conditions.     

Direct in vivo observations of P-selectin glycoprotein ligand-1-mediated leukocyte–endothelial cell interactions in the pulmonary microvasculature in abdominal sepsis in mice

Objective

P-selectin glycoprotein ligand-1 (PSGL-1) has been shown to play a significant role in septic lung injury. However, the detailed role of PSGL-1 in the pulmonary leukocyte recruitment remains elusive. We have developed a method based on intravital fluorescence microscopy of the lung microcirculation to examine the role of PSGL-1 in the extravasation process of leukocytes in septic lung damage.

Methods

Male C57BL/6 mice were treated with a control antibody or an anti-PSGL-1 antibody prior to cecal ligation and puncture (CLP). Leukocyte–endothelium interactions and microvascular hemodynamics were studied in pulmonary arterioles, capillaries and venules 4 h after CLP.

Results

Immunoneutralization of PSGL-1 decreased CLP-induced leukocyte rolling in pulmonary arterioles and venules significantly. Inhibition of PSGL-1 had no effect on leukocyte adhesion in venules, whereas the number of adherent leukocytes in lung arterioles and the number of trapped leukocytes in capillaries were markedly decreased. Moreover, immunoneutralization of PSGL-1 improved microvascular perfusion in the lung of septic animals.

Conclusions

Taken together, these results document that PSGL-1 mediates leukocyte rolling in arterioles and venules. However, inhibition of PSGL-1 only decreases leukocyte adhesion in arterioles, suggesting that leukocyte rolling is not a prerequisite for pulmonary venular adhesion of leukocytes in sepsis. In addition, our data show that capillary trapping of leukocytes is dependent on PSGL-1 function.     

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.     

Metabolic control of large-bore arterial resistance vessels,arterioles, and veins in cat skeletal muscle during exercise

The metabolic control of the vascular bed in cat gastrocnemius muscle during exercise was studied with a new technique (Björnberg et al. 1988) permitting continuous and simultaneous recordings of arteriolar and capillary pressures, and of resistances in the following consecutive vascular section: proximal arterial resistance vessels > 25 μm, arterioles < 25 μm, and on the venous side. The study thereby provided quantitative data for resistance and active intrinsic tone in these vascular segments at rest, during graded exercise vasodilatation, and in the post-exercise period. Slight activation of the metabolic control system by low-frequency somatomotor nerve stimulation (light exercise') caused inhibition of intrinsic tone and decreased vascular resistance selectively in the arteriolar section. At increasing workloads, arteriolar resistance was further decreased, but resistance and tone in the proximal arterial resistance vessels and the veins then became clearly reduced as well. This difference in effectiveness of the metabolic control system on the different segments of the vascular bed was expressed quantitatively in terms of a ‘metabolic vasodilator index’. Graded activation of the metabolic control system led to a marked segmental redistribution of intrinsic vascular tone, in turn resulting in an increased pressure drop across the proximal arterial vessels and the veins and a decreased pressure drop over the arterioles. The observed decrease in the pre- to post-capillary resistance ratio caused, at a constant arterial pressure of 100 mmHg, a graded increase in capillary pressure with increasing workloads, at maximum vasodilatation by an average value of 14 mmHg above the resting control value of 15.4 ± 0.6 mmHg. In the post-exercise period, recovery of vascular tone to control was more rapid in the proximal arterial resistance vessels and the veins than in the arteriolar segment.     

Development of brain vessels in human embryos and fetuses in conditions of prenatal exposure to alcohol

Light and electron microscopy were used to study the characteristics of the formation of brain vascular structures at the early stages of development in conditions of maternal alcoholization during pregnancy. Computer morphometric methods using the Scion Image system for image analysis showed that fetuses at 11–12 weeks of development in conditions of prenatal alcohol exposure showed a decrease in the mean absolute cross-sectional area of vessels in the intermediate layer of the brain, with an increase in their relative area and an increase per unit area of sections, as compared with the control group. Vessels started to differentiate into arteries and veins from 10 weeks of development. __________ Translated from Morfologiya, Vol. 131, No. 2, pp. 63–66, March–April, 2007.     

Resistance and capacitance functions of veins in the gastrocnemius muscle during electrical stimulation of ventral subdivisions of medulla oblongata

Perfusion of blood vessels in the gastrocnemius muscle with autoblood under local electrostimulation of pressure zones of ventral part of the medulla oblongata revealed increments in resistance to blood flow in the muscle veins and arteries, which were respectively, 83 and 81% of the constrictor reactions of these vessels in response to a supramaximum electrostimulation of the sympathetic chains, while decrease in the venous blood filling was 33%. In response to electrostimulation of VMO depressor zones, the venous blood filling did not increase, while in the muscle arteries and veins the resistance to blood flow decreased by 60 and 130% in comparison with the dilator reactions of these vessels after dissection of sciatic nerve in the muscle preparation. Both quantitative and qualitative aspects of resistance and capacitance function of venous and resistive arterial vessels are shown to depend on individual features in the regulation of veins and arteries at the central and peripheral level. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 125, No. 5, pp. 493–496, May, 1998     

Adhesion of HT-29 colon carcinoma cells to endothelial cells requires sequential events involving E-selectin and integrin β4

HT-29 colon carcinoma cells attach to TNFα-activated human umbilical vein endothelial cells (HUVECs) by their specific binding to E-selectin. This interaction activates, in the cancer cells, the MAPK SAPK2/p38, which leads to their transendothelial migration (Laferrière et al., J Biol Chem 2001; 276: 33762). In this study, we investigated the role of E-selectin in activating integrins to modulate adhesion and regulate integrin-mediated events. Blocking the integrins from HT-29 cells (α2, α3, α6, αvβ5, β1 and β4) with specific antibodies revealed a role for β4 integrin in their adhesion to TNFα-treated HUVEC. The β4 integrin-dependent adhesion was maximal after 30 min, whereas the-E-selectin-dependent adhesion was maximal after 15 min. Integrin β4 became quickly phosphorylated upon addition of HT-29 cells to endothelial cells and the effect was independent of the expression of E-selectin. Moreover, a recombinant E-selectin/Fc chimera did not induce the phosphorylation of β4. The phosphorylation of β4 is not required for adhesion since adhesion was not affected in HT-29 cells that express a truncated form of β4 that is deleted from its cytoplasmic phosphorylatable domain. However, the expression of the non-phosphorylatable deletant of β4 was associated with decreased transendothelial cell migration underscoring the key role for the cytoplasmic domain of β4 in cell migration. We suggest: 1) that the adhesion of HT-29 cells to activated endothelial cells follows at least two essential sequential steps involving the binding of E-selectin to its receptor on carcinoma cells and then the binding of β4 to its own receptor on endothelial cells; 2) that the phosphorylation of integrin β4 contributes to enhance the motile potential of cancer cells and increase their trans-endothelial migration. Overall, our results indicate that the interaction of metastatic cancer cells with endothelial cells implies a specific sequence of signaling events that ultimately leads to an increase in their efficient transendothelial migration. Abbreviations: ERK – extracellular signal-regulated kinase; GFP – green fluorescent protein; ICAM – intercellular adhesion molecules: JNK – c-Jun NH₂-terminal kinase; MAPK – mitogen-activated protein kinase; MAPKAP K2, MAP kinase-activated protein kinase 2; PI3K – phosphatidyl inositol 3-kinase; SAPK – stress-activated protein kinase; TNFα– tumor necrosis factor-α. This revised version was published online in July 2006 with corrections to the Cover Date.     

Increased distensibility in dependent veins following prolonged bedrest

Displacement of blood to the lower portion of the body that follows a postural transition from recumbent to erect is augmented by a prolonged period of recumbency (bedrest). Information is scarce as to what extent this augmented blood-volume shift to dependent veins is attributable to increased distensibility of the veins. Accordingly, we studied the effect of 5 weeks of horizontal bedrest on the pressure–distension relationship in limb veins. Elevation of venous distending pressure was induced by exposure of the body except the tested limb to supra-atmospheric pressure with the subject seated in a pressure chamber with one arm, or supine with a lower leg, protruding through a hole in the chamber door. Diameter changes in response to an increase of intravenous pressure (distensibility) from 60 to about 140 mmHg were measured in the brachial and posterior tibial veins using ultrasonographic techniques. Prior to bedrest, the distensibility was substantially less in the tibial than in the brachial vein. Bedrest increased (P < 0.01) pressure distension in the tibial vein by 86% from 7 ± 3% before to 13 ± 3% after bedrest. In the brachial vein, bedrest increased (P < 0.05) pressure distension by 36% from 14 ± 5% before to 19 ± 5% after bedrest. Thus, removal of the gravity-dependent pressure components that act along the blood vessels in erect posture increases the distensibility of dependent veins.     

Three-dimensional cytoarchitecture of rat pulmonary venous walls: a light and scanning electron microscopic study

 The three-dimensional architecture of the rat pulmonary veins was studied by light microscopy (LM) and scanning electron microscopy (SEM). For LM, the left lungs were fixed with formalin, sectioned and immunostained with an anti-α-smooth muscle actin (α-SMA) antibody in addition to conventional staining. For SEM, the specimens were fixed with glutaraldehyde and immersed in 30% KOH solution for 8 min followed by treatment of collagenase solution for more than 5 h. By LM, the smooth muscle cells stained with anti-α-SMA showed discontinuous, periodical thickenings of circular bundles in the wall of the venules, but they became thin and continuous in the larger vessels (or veins) that had a cardiac muscle layer on the outside. Under SEM, the smooth muscle cells formed circular-oriented bundles at constant intervals along the venules less than 100 μm in diameter. These bundles had circumferential constrictions in the lumen. The cardiac muscle cells, which appeared in large pulmonary veins of more than 100 μm, ran in a circular or oblique direction and completely surrounded the vessel wall outside of the thin continuous layer of smooth muscle cells. The muscle arrangements were considered to play a significant role in the return blood flow in rat pulmonary veins. Accepted: 15 June 1998     

Immunology: Distribution of cell adhesion molecules on CD56++, CD3-, CD16- large granular lymphocytes and endothelial cells in first-trimester human decidua

Human decidua exhibits a unique infiltrate of large granularlymphocytes (LGL) with a natural killer (NK) cell phenotype(CD56++, CD16–, CD3–). The mechanisms underlyingthe binding of circulating LGL to vascular endothelium in thedecidua and their migration into the decidual stroma were investigatedimmunohistochemically in first-trimester decidua with antibodiesagainst endothelial adhesion molecules and their counter-receptorson leukocytes. Decidual and peripheral blood LGL were also investigatedby flow cytometry. In the immunohistochemical investigations,moderate to large numbers of lymphoid cells in the decidua werefound to express the ₄ and _L integrin subunits, platelet endothelialcell adhesion molecule (PECAM) and intercellular adhesion molecule-1(ICAM-1). PECAM and ICAM-1 were found on the endothelium oflarge numbers of decidual blood vessels of all types. Vascularcell adhesion molecule (VCAM), however, was found on the endotheliumof only small to moderate numbers of arterioles and venulesand a few capillaries, the latter being the main site of migrationof leukocytes into the stroma. Weak staining for endothelialleukocyte adhesion molecule (ELAM) was seen only in a moderatenumber of blood vessels. Flow cytometry revealed expressionof the _L integrin subunit by 72 ± 10% and 97 ±3% of decidual and peripheral blood CD56+ LGL, respectively,of the 4 integrin subunit by 85 ± 7% and 90 ±5%, of PECAM by 40 ± 12% and 30 ± 15%, and ofICAM-1 by 22 ± 10% and 1 ± 1%. These findingssuggest that interaction between the integrin _2L and ICAM-1is the more important mechanism of binding to endothelium inthe migration of CD56+ LGL out of the peripheral blood intothe decidua.     

Morphological changes in hepatic vessels during modeling of pulmonary trunk stenosis and after its elimination

Experiments on dogs showed that pulmonary trunk stenosis increased the tone of arterial vessels in the liver and led to the development of veno-arterial and veno-venous reactions. The number of vessels with intimal musculature and myoelastic sphincters in the arterial bed increases, and muscle rolls in large hepatic veins are thickened. The walls are hypertrophic in all vessels. Elimination of the defect abolished the previously formed vascular adaptation reactions, the tone in afferent liver vessels decreased, which leads to regression of hypertrophic changes in their tunica media. The number of arteries with intimal musculature and sphincters decreases. Muscle rolls in the efferent hepatic veins are thinned. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 144, No. 9, pp. 342–345, September, 2007     

Pathways of macromolecular tracer transport across venules and small veins. Structural basis for the hyperpermeability of tumor blood vessels.

BACKGROUND: Blood vessels supplying tumors are hyperpermeable to macromolecules, but the mechanisms responsible are poorly understood. EXPERIMENTAL DESIGN: To investigate the structural basis for the leakiness of tumor blood vessels, we performed a transmission electron microscopic study of three syngeneic transplantable carcinomas (mouse ovarian carcinoma and the line 1 and line 10 bile duct guinea pig carcinomas) at early intervals after intravenous injection of several macromolecular tracers. Tracers with widely differing physical properties were studied: horseradish peroxidase, ferritin, 150 kilodalton fluorescein isothiocyanate-dextran and gold-bovine serum albumin. RESULTS: All tracers leaked primarily from venules and small veins at the tumor-host interface, for the most part vessels lined by a continuous endothelium. The predominant pathway by which all four tracers exited venules in all three tumors was by way of a system of smooth membrane-bound, interconnecting vesicles and vacuoles; these tended to cluster together at irregular intervals in the endothelial cell cytoplasm to form organelle-like structures, vesiculo-vacuolar organelles (VVO). In favorable sections, VVO interfaced with both the luminal and abluminal surfaces of endothelial cells. HRP alone crossed venules and small veins through apposed inter-endothelial cell junctions. Tracers also exited vessels by way of endothelial fenestrae where these occurred (rarely) in mouse ovarian tumor-associated venules. VVO occurred with similar frequency and complexity in the continuous endothelium-lined venules and small veins that supplied the normal subcutis of either tumor-bearing or control animals. As in tumor-associated vessels, VVO provided the predominant pathway by which all four tracers exited normal vessels, but VVO labeling and extravasation were both much greater in tumor than in control vessels (p < 0.001 for ferritin). CONCLUSIONS: VVO are prominent structures in both tumor-supplying and control vessel endothelial cells and provide the primary pathway for macromolecular extravasation. The large increase in permeability characteristic of tumor vessels is likely attributable to upregulation of VVO function.     

Possible reversibility of structural changes in renal vascular bed after correction of experimental coarctation of the aorta

Renal vessels were studied in 22 puppies with induced coarctation of the aorta, 15 with corrected defect, and 12 controls by functional, histological, and morphometrical methods. Constriction of the isthmus of the aorta was associated with decreased pressure of blood flowing to the kidneys and pronounced morphological restructuring of the renal blood system components. Correction of the experimental defect triggers the mechanism of regression of previously induced changes and promotes appreciable recovery of the structure of renal arteries, veins, and glomeruli. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 142, No. 9, pp. 346–349, September, 2006     

Scanning electron microscopic studies of the vascular smooth muscle cells and pericytes in the rat heart

The cytoarchitecture of smooth muscle cells and pericytes in the rat cardiac vessels was studied by scanning electron microscopy after the removal of connective tissue matrices using a modified KOH-collagenase digestion method. The initial stem of the coronary arteries had groups of smooth muscle cells which ran in various directions on the outermost layer of the media. Although smooth muscle cells in coronary arteries of more than 100 microm in the outer diameter were arranged in a rough circle around the vessel axis, oblique and/or longitudinal muscle bundles were often present in the medio-adventitial border of the vessels. The presence of irregularly oriented muscular bundles is probably connected with resistance against the stretching force induced by the beating of the heart. As the vessel size decreased toward the periphery, almost all of the smooth muscle cells became spindle-shaped with several tiny processes and ran circularly or helicaly to the vessel axis. In the precapillary arterioles (6-12 microm), smooth muscle cells acquired various cytoplasmic processes which helicaly surrounded endothelial cells. Unmyelinated nerves were often associated with arterioles. Blood capillaries were morphologically divided into three segments: arterial capillaries which had pericytes with wide and circularly oriented processes, true capillaries whose pericytes extended long and thin primary processes bilaterally along the vessel axis, and venous capillaries surrounded irregularly and loosely by wide pericytic processes. The stellate pericytes in the postcapillary venules (10-30 microm) gradually changed into flat tape-like smooth muscle cells, which ran circularly in the collecting venules and veins (30-200 microm). The large collecting veins were finally overwhelmed by superficial thin layer of the myocardium, their own smooth muscle cells being very sparse. This suggests that large veins have poor ability to contract by themselves but are influenced by the surrounding myocardial cells.