The craniocervical venous system in relation to cerebral venous drainage.
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BACKGROUND AND PURPOSE: Passing from the supine to the upright position favors cerebral venous outflow into vertebral venous systems rather than into the internal jugular veins. We sought to determine venous connections between dural venous sinuses of the posterior cranial fossa and craniocervical vertebral venous systems. METHODS: Corrosion casts of the cranial and cervical venous system were obtained from 12 fresh human cadavers, and anatomic confirmation was made by dissection of three previously injected fresh human specimens. MR venography was performed to provide radiologic correlation. RESULTS: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins were found to represent the venous connections between the dural venous sinuses of the posterior cranial fossa and the vertebral venous systems. This study revealed the nearly constant presence of the anterior condylar confluent (ACC) located on the external orifice of the canal of the hypoglossal nerve. The ACC offered multiple connections with the dural venous sinuses of the posterior cranial fossa, the internal jugular vein, and the vertebral venous system. All these structures were shown by MR venography. CONCLUSION: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins connect the dural venous sinuses of the posterior cranial fossa with the vertebral venous systems. These connections are clinically relevant, because encephalic drainage occurs preferentially through the vertebral venous system in the upright position. The ACC is a constant anatomic structure that may play an important role in the redirection of cerebral blood in the craniocervical region. (+info)
Interactions between trophoblast cells and the maternal and fetal circulation in the mouse placenta.
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Mammalian embryos have an intimate relationship with their mothers, particularly with the placental vasculature from which embryos obtain nutrients essential for growth. It is an interesting vascular bed because maternal vessel number and diameter change dramatically during gestation and, in rodents and primates, the terminal blood space becomes lined by placental trophoblast cells rather than endothelial cells. Molecular genetic studies in mice aimed at identifying potential regulators of these processes have been hampered by lack of understanding of the anatomy of the vascular spaces in the placenta and the general nature of maternal-fetal vascular interactions. To address this problem, we examined the anatomy of the mouse placenta by preparing plastic vascular casts and serial histological sections of implantation sites from embryonic day (E) 10.5 to term. We found that each radial artery carrying maternal blood into the uterus branched into 5-10 dilated spiral arteries located within the metrial triangle, populated by uterine natural killer (uNK) cells, and the decidua basalis. The endothelial-lined spiral arteries converged together at the trophoblast giant cell layer and emptied into a few straight, trophoblast-lined "canals" that carried maternal blood to the base of the placenta. Maternal blood then percolated back through the intervillous space of the labyrinth toward the maternal side of the placenta in a direction that is countercurrent to the direction of the fetal capillary blood flow. Trophoblast cells were found invading the uterus in two patterns. Large cells that expressed the trophoblast giant cell-specific gene Plf (encoding Proliferin) invaded during the early postimplantation period in a pattern tightly associated with spiral arteries. These peri/endovascular trophoblast were detected only approximately 150-300 microm upstream of the main giant cell layer. A second type of widespread interstitial invasion in the decidua basalis by glycogen trophoblast cells was detected after E12.5. These cells did not express Plf, but rather expressed the spongiotrophoblast-specific gene Tpbp. Dilation of the spiral arteries was obvious between E10.5 and E14.5 and was associated with a lack of elastic lamina and smooth muscle cells. These features were apparent even in the metrial triangle, a site far away from the invading trophoblast cells. By contrast, the transition from endothelium-lined artery to trophoblast-lined (hemochorial) blood space was associated with trophoblast giant cells. Moreover, the shaping of the maternal blood spaces within the labyrinth was dependent on chorioallantoic morphogenesis and therefore disrupted in Gcm1 mutants. These studies provide important insights into how the fetoplacental unit interacts with the maternal intrauterine vascular system during pregnancy in mice. (+info)
Collateral arteries grow from preexisting anastomoses in the rat hindlimb.
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Previous findings have suggested that collateral arteries grow from preexisting arteriolar anastomoses ("arteriogenesis"). To investigate whether collateral growth occurs without preceding angiogenesis, we obtained vascular casts and postmortem angiographies 3, 7, and 21 days after unilateral femoral artery occlusion in the rat. Proliferation kinetics were determined after 5'-bromo-2'-desoxyuridin infusion. A preexisting anastomosis was identified. Proliferation of this vessel began 24 h after femoral artery occlusion, increased maximally during the first 3 days, and reached 60% at day 7. Cell division was restricted to preexisting anastomoses and occurred neither in directly neighboring arterial vessels nor in capillaries. Collateral vessels doubled their diameter within 7 days and assumed a typical corkscrew appearance (increase of length: 21%). After 7 days of occlusion, we measured a further increase of length (14%) but no proliferation or increase of diameter. We conclude that arteriogenesis is a biphasic process involving rapid proliferation of preexisting arteriolar shunts followed by pronounced remodeling processes. Arteriogenesis occurs independently of angiogenesis and denotes a separate entity of vascular proliferation. (+info)
Effects of efonidipine hydrochloride on renal arteriolar diameters in spontaneously hypertensive rats.
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Efonidipine, a calcium antagonist, has been reported to dilate not only afferent but also efferent arterioles, thereby reducing glomerular hydrostatic pressure. We investigated the effect of chronic treatment with efonidipine or lisinopril on the afferent and efferent arteriolar diameters by the vascular cast technique. Four-week-old spontaneously hypertensive rats (SHR) were divided into three groups: untreated, efonidipine (25 mg/kg/day)-treated, and lisinopril (3 mg/kg/day)-treated. At 22 weeks of age, the renal vasculatures were fixed at the maximally dilated condition. The morphometrical measurements showed that the treatments with efonidipine and lisinopril caused structural alteration of the vasculature, resulting in significantly greater efferent arteriolar diameters than in untreated SHR. In addition, lisinopril-treated rats had wider afferent lumina. The renoprotective effect of efonidipine and lisinopril might be partly due to the structurally larger efferent arteriolar lumen. (+info)
A Rho-associated kinase mitigates reperfusion-induced change in the shape of cardiac capillary endothelial cells in situ.
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OBJECTIVE: We have previously demonstrated that ischaemia and reperfusion of the myocardium alter capillary dimensions and endothelial cell shape and that these changes are likely to be effected by the actomyosin contractile system in endothelial cells. Rho GTPases are involved in the regulation of cytoskeletal re-organization and in cell contraction. Rho-associated kinase regulates the sensitivity of myosin light chain to Ca(2+) in smooth muscle but not in cardiac or skeletal muscle myocytes. This study investigated the role of Rho-associated kinase in endothelial cell shape change induced by cardiac ischaemia and reperfusion. The role of Rho proteins in endothelial cell shape change in situ in the myocardial capillary bed has to date not been investigated. METHODS: Ischaemia and reperfusion were induced in Langendorff perfused rat hearts at constant flow. Electron microscopy and immunofluorescence studies localized the beta Rho-associated kinase isotype in capillary endothelial cells. Whole capillary and luminal cross-section areas, luminal and abluminal membrane lengths were measured to monitor changes in cell dimensions. We used a ROCK inhibitor, Y-27632, to investigate the role of this protein in endothelial cell shape change. RESULTS: ROCK1 localized primarily to intracellular membranes in endothelial cells. Morphometric analysis and a study of capillary lumen resin casts demonstrated that inhibition of the activity of this kinase with Y-27632 ablated the change in shape of endothelial cells induced by ischaemia and reperfusion. CONCLUSION: These results suggest that ROCK1 is involved in cardiac capillary endothelial cell shape change in situ and that targeting the contractile system in this way may be useful in ameliorating reperfusion injury. (+info)
Embryonic development of coronary vasculature in rats: corrosion casting studies.
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The aim of this study was to analyze the development of coronary vessels at different stages of embryonic life in rats using corrosion casts and scanning electron microscopy (SEM). We studied morphologic details of vessel maturation, expansion, and pattern formation from the stage of development when the coronary system forms patent connections with the aorta and the right atrium (embryonic day 16 (ED16)) to full-term fetus (ED21). The internal surface morphologies of the arterial and venous vessel walls were different and were dependent on the distance from the orifice and the capillary system. They also depended on the maturation state of a given vessel. In various branches of the coronary system we demonstrated round, fusiform or polygonal, endothelial cell imprints. The capillary network was dense, however, at the early stages of development, it formed a thin layer over the myocardium. By ED21 capillaries assumed an orientation parallel to the long axes of the cardiac myocytes. During all stages of development, different forms of angiogenesis by intussusceptive growth were observed. Splitting of the vessel wall occurred in two or three points along the vessel, forming two- or three-link chains. Certain areas of vessels resembled doughnuts, from which several sister vessels originated. The coronary arteries were situated deep within the myocardial wall. The major coronary veins were mostly located on the surface of the capillary plexuses of the myocardial wall. In conclusion, this method of vessel casting enables the detection of angiogenesis by intussusceptive growth, and the visualization of a capillary's position to the myocardial wall, thickness of the capillary plexuses, and the internal surface morphology of major vessels. (+info)
Pulmonary lymphatics and edema accumulation after brief lung injury.
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In a past study of hyperoxia-induced lung injury, the extensive lymphatic filling could have resulted from lymphatic proliferation or simple lymphatic recruitment. This study sought to determine whether brief lung injury could produce similar changes, to show which lymphatic compartments fill with edema, and to compare their three-dimensional structure. Tracheostomized rats were ventilated at high tidal volume (12-16 ml) or low tidal volume (3-5 ml) or allowed to breathe spontaneously for 25 min. Light microscopy showed more perivascular, interlobular septal, and alveolar edema in the animals ventilated at high tidal volume (P < 0.0001). Scanning electron microscopy of lymphatic casts showed extensive filling of the perivascular lymphatics in the group ventilated at high tidal volume (P < 0.01), but lymphatic filling was greater in the nonventilated group than in the group that was ventilated at low tidal volume (P < 0.01). The three-dimensional structures of the cast interlobular and perivascular lymphatics were similar. There was little filling and no difference in pleural lymphatic casts among the three groups. More edema accumulated in the surrounding lymphatics of larger blood vessels than smaller blood vessels. Brief high-tidal-volume lung injury caused pulmonary edema similar to that caused by chronic hyperoxic lung injury, except it was largely restricted to perivascular and septal lymphatics and prelymphatic spaces. (+info)
Capillary angiogenesis and degeneration in bovine ovarian antral follicles.
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Angiogenesis and capillary degeneration are both evident during ovarian follicle growth. However, the characteristics and distribution of thecal capillary proliferative and degenerative structures have not been fully defined. Indeed, the role of thecal microvasculature changes in follicular atresia is still a matter of debate. The present study examined the distribution of thecal capillary changes occurring during follicular growth and related the changes to capillary morphology (by scanning electron microscopy, SEM, on bovine ovarian corrosion casts) with the incidence of capillary apoptosis (TdT-mediated dUTP nick end-labelling, TUNEL) and follicular status (as confirmed by follicular fluid steroid concentrations). SEM demonstrated well-perfused vascular plexuses of small to large antral follicles with structural and functional changes to capillaries. Angiogenesis was evident mainly in the apical part of the inner capillary layer of medium follicles and the middle or basal part of the inner capillary layer of dominant follicles that exhibited high oestradiol:progesterone ratios. Degenerative capillaries were observed mainly in the outer vascular layers of small follicles, and in the inner and outer vascular layers of medium antral follicles. Although apoptotic structures were present only in the outer capillaries of the theca interna of morphologically healthy antral follicles, atretic follicles showed apoptotic structures in both the outer and inner thecal capillary layers. These results show that angiogenesis increases during bovine follicular growth and occurs unevenly in different inner theca regions of the follicles. The differential angiogenic and degenerative response of theca interna capillaries may reflect differences in the microenvironment of the follicles, which in turn determine the fate of the follicles (continued growth versus atresia). (+info)