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PubMed1982

The effect of surgical procedures on blood vessel innervation. A fluorescence histochemical study of degeneration and regrowth of perivascular adrenergic nerves.

Four commonly used surgical procedures have been shown to cause extensive damage to the sympathetic nerves which supply and accompany blood vessels. One of these procedures, which produced a localised crush lesion, was shown by fluorescence microscopy to cause extensive degeneration of adrenergic nerves in two densely innervated blood vessels of different character in the guinea pig: the elastic carotid artery and the muscular mesenteric artery. The extent of denervation was different in the two vessels: in the carotid artery the crush lesion destroyed all the nerves near the lesion, but left undamaged sparse nerves which reached the vessel wall along its length with the vasa vasorum; in the mesenteric artery all the nerves ran with the artery, consequently denervation could be extensive (at least 2 cm distal to the crush), although the largest nerve bundles were resistant to crush injury. The regrowth rate of nerves in the mesenteric artery was faster than that found in the carotid artery. A plexus of normal density and appearance was re-established between 3 and 8 weeks, and hyperinnervation was observed in some specimens. In the carotid artery this process was usually not complete by 8 weeks and involved both the regrowth of injured fibres and collateral sprouting distal to the lesion of the sympathetic nerve fibres that had not been injured. Axon sprouting was observed in both vessels near the lesion site. Explanations for these differences are discussed.

Adrenergic Fibers↗
PubMed1978

Special problems in pulmonary atresia with ventricular septal defect: extreme hypoplasia of intrapericardial pulmonary arteries and autofocal collateral vessels.

4 patients with pulmonary atresia and ventricular septal defect are presented, who were selected from a group of 50 patients in whom intrapericardial pulmonary arteries were present. In 2 patients the pulmonary arteries were not only extremely hypoplastic but also displayed only minimal anastomoses with the arterial hilar vessels. They were considered not to be accessible for corrective surgery. In another patient about 50% of the pulmonary perfusion were supplied by collateral vessels not connected to the intrapericardial pulmonary arteries. The question is discussed, to what extent the systemic vessels are necessary for pulmonary perfusion and whether they may be all ligated at the time of corrective surgery. In the last patient anastomoses between 2 systemic vessels and the pulmonary arteries could be demonstrated, the right one of which was very hypoplastic. In this case a right-sided shunt operation combined with ligation of the collateral vessels seemed to be advisable to promote adaption of the pulmonary artery and to simplify the subsequent corrective procedure.

Adolescent↗
PubMed1981

Effect of monosodium glutamate on retinal vessel development and permeability in rats.

Monosodium glutamate (MSG) administered to neonatal rats on postnatal days 1 to 10 caused a generalized degeneration of the inner retinal layers. MSG administered only on postnatal days 8, 9, 10, and/or 11 caused a retinopathy limited to more peripheral retinal areas corresponding to currently existing regions of immature retinal vessels. Ink-injected retinal vessel studies showed a delay in development of the retinal vessel network but no alterations in vessel patency. Fluorescence microscopic examination of freeze-dried tissues revealed to abnormalities of the blood-retinal barriers to sodium fluorescein. We conclude, as demonstrated by these methods, that MSG retards development of the retinal vessels but does not affect development of the blood-retinal barriers. The retinotoxic effect of MSG apparently results from a mechanism(s) other than a breakdown of the blood-retinal barrier.

Age Factors↗
PubMedDate not supplied

Endothelial cell seeding onto the extracellular matrix of fibroblasts for the development of a small diameter polyurethane vessel.

A variety of experiments of endothelial cell seeding on artificial vessels have been performed. To improve endothelialization, one or two extracellular matrix components have been used as an underlying matrix. Although these methods have succeeded in in vitro experiments, they have not performed well in vivo. In this study, the authors used the whole extracellular matrix (ECM) excreted from fibroblasts as an underlying matrix. Fetal human fibroblasts were cultured on a polyurethane (PU) sheet. After confluence was attained, the cytoskeleton and the nuclei of the fibroblasts were destroyed using Triton-X, mitomycin, and irradiation. Omental microvascular endothelial cells from adult humans were seeded on various supports. After 12 days in culture, the cells were counted. The authors found that the ECM treated by irradiation had the highest cell number. In addition, the cells on this support exhibited the best morphologic appearance. Finally, the authors performed preliminary animal experiments. The PU vessels (inner diameter: 1.5 mm) treated with ECM were implanted in the arteries of rats. After the vessels had been implanted for 5 weeks, the authors found that the surface of the PU vessels were completely covered with endothelial cells. On the basis of these results, the authors conclude that the whole ECM makes a better underlying substrate for the endothelialization of small diameter artificial vessels.

Anastomosis, Surgical↗
PubMed1993

[Endothelin-1-induced vasoconstriction in retinal blood vessels in the rabbit].

Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide which is synthesized in retinal vessels. In order to investigate its effect on retinal blood vessels, we injected ET-1 intravitreally (10(-12), 3 x 10(-12), 10(-11), 3 x 10(-11), 10(-10) mole) and examined the change in diameters of retinal arteries in rabbits by fundus photography. After injection of a high dose (10(-10) mole) of ET-1, fluorescein angiography was used to investigate whether complete occlusions of retinal blood vessels occurred or not. 3 x 10(-12) mole ET-1 induced contraction of retinal arteries and the contraction of those induced by 10(-10) mole ET-1 showed complete occlusion. A medium dose (10(-11) mole) of ET-1 caused repeated vasospasms and segmental vasoconstrictions of retinal blood vessels. Fluorescein angiograms revealed that retinal blood flow was interrupted transiently by injection of a high dose (10(-10) mole) of ET-1. These findings suggested that intravitreal injection of ET-1 could provide a new model of experimental transient occlusion of retinal vessels in rabbits.

Animals↗
PubMed1993

Laparoscopic injury of abdominal wall blood vessels: a report of three cases.

BACKGROUND: Operative laparoscopy is being used for an increasing number of applications. Many of these innovative techniques require the insertion of large trocars through the anterior abdominal wall at points lateral to the midline. Because of the rich vascular supply of the anterior abdominal wall, the incidence of abdominal wall vessel injuries appears to be increased by these techniques. CASES: Three cases are reported in which abdominal wall blood vessels were injured during operative laparoscopy. Case 1 describes laceration of the inferior epigastric artery above the pubic crest. Despite initial hemostasis with a transabdominal suture ligation, postoperative blood loss necessitated transfusion and reoperation to control bleeding. Case 2 describes hematoma formation after unrecognized injury to one of the epigastric vessels. The hematoma resolved without sequelae with conservative treatment. Case 3 describes hematoma formation under a laparoscopic trocar incision lateral to the umbilicus that progressed to an abscess and was treated with drainage, irrigation, and antibiotics. CONCLUSIONS: Choosing appropriate trocar types and insertion sites based on a thorough understanding of anterior abdominal wall anatomy may minimize the risk of vessel injury during operative laparoscopy. However, because of anatomical variation, strategies for managing vessel injuries and their sequelae are also necessary.

Abdominal Muscles↗
PubMed1996

Calcium dependence of indolactam-mediated contractions in resistance vessels.

The protein kinase C activator, (-)-indolactam, has been shown to enhance reactivity of arterioles by a mechanism not requiring an increase in intracellular Ca++ (Ca++i). The aim of this study was to characterize the Ca++ requirement for indolactam-induced contraction of resistance vessels. Studies were performed in small mesenteric arteries (diameter, 260 +/- microm), using intact segments or after permeabilization with alpha-toxin (500 U/ml). Additional studies were preformed using isolated smooth muscle cells to allow electrophysiological assessment of the effect of indolactam on voltage-gated Ca++ entry. Intact and permeabilized vessel segments showed dose-dependent constriction to indolactam. Studies of Fura 2-loaded vessels and permeabilized segments maintained at low Ca++i, showed that the constriction occurred without an overt increase in Ca++i. That Ca++ was required was evident by near maximal relaxation after the removal of Ca++. Patch clamp studies indicated that indolactam potentiated voltage-gated Ca++ entry; however, nifedipine (0.5 microM) and La (0.2 or 1 mM) were relatively ineffective in reversing the contraction, indicating that voltage-gated Ca++ entry was not an absolute requirement. In intact vessel segments, the myosin light chain (MLC) kinase inhibitors, ML-7 and ML-9, reversed the indolactam contraction, suggesting the requirement of the MLC chain phosphorylation pathway. Furthermore, indolactam caused by a significant increase in MLC phosphorylation in permeabilized vessels, despite clamping of Ca++i at pCa 7.0. The data are consistent with the suggestion that the protein kinase C activator, indolactam, acts to modulate the Ca++ sensitivity of the smooth muscle contractile process such that higher than expected levels of MLC phosphorylation exist for a given level of Ca++i.

Animals↗
PubMed1997

Ultrastructural changes in cerebral cortical blood vessels of immature and adult rats after a single episode of neonatal hypoxia.

Newborn rats were exposed to a single episode of neonatal hypoxia and were studied at intervals from 4 hours to 3 months after the exposure. Endothelial cells showed unusual darkening of the cytoplasm, and protrusion of the soma into the lumen of the vessels. Fibroblasts showed unusually dilated cisternae of rough endoplasmic reticulum. The perivascular cells were also unusual, in that they had an 'activated' appearance as suggested by the presence of large vacuoles and secondary lysosomes, and were often connected to the vessel walls by only a thin foot process. The basal lamina often gave off long extensions into the neuropil or incompletely surrounded the cells of the vessel walls. The astrocytic foot processes were swollen and contained many glycogen granules and loosely packed glial filaments. All the above changes were present even at 3 months posthypoxia. The discontinuous basal lamina could allow substances to pass more easily from the bloodstream into the neuropil. It is also possible, in view of the frequent observations of perivascular cells that were connected to the vessel walls by only a thin foot process, that these extensions could be places where perivascular cells leave the vessels to enter the neuropil. It is postulated that increased movement of 'activated' perivascular cells into the neuropil could result in increased pruning of neuronal processes in the neuropil, after the episode of neonatal hypoxia.

Aging↗
PubMed1997

Immunohistochemical localization of defensin in human coronary vessels.

Neutrophil defensins comprise a family of cationic peptides that possess potent antimicrobial activity. Defensins are normally sequestered in cytoplasmic granules with their primary site of action in phagolysosomes, although some peptide is released into the circulation during the course of infection or inflammation. In view of the fact that neutrophils adhere to the endothelium and that defensins have been reported to bind to human endothelial cells in vitro, we used immunohistochemistry to study the distribution of these peptides in normal and in atherosclerotic human coronary arteries. Defensin was found primarily in the intima of normal and atherosclerotic vessels, most prominently in association with intimal smooth muscle cells. Both large- and small-vessel endothelium stained focally for defensin. Defensin was also found in the media near the external elastic lamina and in some periadventitial vessels. The same distribution was seen in vessels that had been perfusion fixed immediately upon procurement, excluding diffusion of defensin from PMNs ex vivo. These data indicate that neutrophil defensin is present in the walls of human coronary arteries. The deposition of defensin in vessels may contribute to the pathophysiological consequences of inflammation in addition to their role in host defense.

Anti-Infective Agents↗
PubMed1998

Ultrastructure of blood vessel regression in involution of foreign-body granuloma.

The diversity of endothelial cell deletion in regressing blood vessels during involution of granulation tissue was investigated in foreign-body granulomas induced by a collagen sponge implanted into the dorsum of the rat. Small blood vessel density counts were performed to determine the degree of blood vessel regression in the involution of granulation tissue in foreign-body granuloma. The density of these small blood vessels significantly decreased between 100 and 130 days after sponge implantation. The detachment of endothelial cells from their underlying basement membrane and the consequent protrusion into and/or out of the lumen in the vascular network of granulation tissue was observed by electron microscopy. Based on the pattern of manifestation in the endothelium and the characteristic deformation of nuclei, the detached endothelial cells were classified into two groups: 1) the endothelial cell apoptosis group and 2) the endothelial cell degeneration group. The essential difference between the two groups was easily distinguishable as the nucleus of the former group displayed chromatin condensation and margination as the hallmark of early apoptotic changes, while the nucleus of the latter group displayed a pinch structure and intranuclear pocket formation. However, the process by which the detached endothelial cells were shed into the vascular lumen and eventually eliminated from circulation was the same in both groups. The occurrence of both groups increased on the 90th day after sponge implantation and reached a maximum on the 110th day, indicating that the appearance of the groups was synchronized. These results suggest that the two major processes of apoptosis and degeneration of endothelial cells occur during endothelial cell deletion as a mechanism contributing to blood vessel regression.

Animals↗
PubMed1998

The 67-kd laminin receptor is preferentially expressed by proliferating retinal vessels in a murine model of ischemic retinopathy.

Endothelial cell association with vascular basement membranes is complex and plays a critical role in regulation of cell adhesion and proliferation. The interaction between the membrane-associated 67-kd receptor (67LR) and the basement membrane protein laminin has been studied in several cell systems where it was shown to be crucial for adhesion and attachment during angiogenesis. As angiogenesis in the pathological setting of proliferative retinopathy is a major cause of blindness in the Western world we examined the expression of 67LR in a murine model of hyperoxia-induced retinopathy that exhibits retinal neovascularization. Mice exposed to hyperoxia for 5 days starting at postnatal day 7 (P7) and returned to room air (at P12) showed closure of the central retinal vasculature. In response to the ensuing retinal ischemia, there was consistent preretinal neovascularization starting around P17, which persisted until P21, after which the new vessels regressed. Immunohistochemistry was performed on these retinas using an antibody specific for 67LR. At P12, immunoreactivity for 67LR was absent in the retina, but by P17 it was observed in preretinal proliferating vessels and also within the adjacent intraretinal vasculature. Intraretinal 67LR immunoreactivity diminished beyond P17 until by P21 immunoreactivity was almost completely absent, although it persisted in the preretinal vasculature. Control P17 mice (not exposed to hyperoxia) failed to demonstrate any 67LR immunoreactivity in their retinas. Parallel in situ hybridization studies demonstrated 67LR gene expression in the retinal ganglion cells of control and hyperoxia-exposed mice. In addition, the neovascular intra- and preretinal vessels of hyperoxia-treated P17 and P21 mice labeled strongly for 67LR mRNA. This study has characterized 67LR immunolocalization and gene expression in a murine model of ischemic retinopathy. Results suggest that, although the 67LR gene is expressed at high levels in the retinal ganglion cells, the mature receptor protein is preferentially localized to the proliferating retinal vasculature and is almost completely absent from quiescent vessels. The differential expression of 67LR between proliferating and quiescent retinal vessels suggests that this laminin receptor is an important and novel target for future chemotherapeutic intervention during proliferative vasculopathies.

Animals↗
PubMed1983

Baring of a circumlinear vessel in glaucoma.

We independently examined 144 optic disc stereophotographs. Despite a preliminary learning trial, we were able to agree about the presence of a circumlinear vessel in only 73% of eyes and about baring of a vessel, if present, in only 71% of eyes. Bared vessels were present in 73% of 22 glaucomatous eyes, 41% of 71 ocular hypertensive eyes, and 14% of 51 normal eyes. During several years of follow-up of 44 ocular hypertensive eyes with bared circumlinear vessels, visual field defects developed in only three. We conclude that baring of a circumlinear vessel is a difficult sign for trained observers to detect with certainty and, although present frequently in glaucoma, is of low specificity as a sign or predictor of glaucomatous damage.

Glaucoma↗
PubMed2002

Flutamide induces relaxation in large and small blood vessels.

HYPOTHESIS: Flutamide, a testosterone receptor antagonist, produces various beneficial effects in male rats following hemorrhagic shock, possibly as a result of a direct vasodilating effect on large and small vessels in the rat. DESIGN, INTERVENTIONS, AND MAIN OUTCOME MEASURES: The aorta and the small intestine were isolated from normal male and female Sprague-Dawley rats. Isolated aortic rings were placed in the organ bath and constricted by 2 x 10(-7)M norepinephrine bitartrate (Sigma, St Louis, Mo). Flutamide-induced and testosterone-induced vascular relaxation dose-response curves were then determined. The dose-response curves of flutamide were also determined in the small blood vessels of the isolated small intestine under conditions of constant flow following preconstriction induced by 5 x 10(-6 )M norepinephrine bitartrate. The effects of prior incubation with testosterone (8 x 10(-5)M) and sex differences on flutamide-induced vascular relaxation were also examined in aortic rings and in the small intestine. Moreover, flutamide-induced relaxation in endothelium-denuded aortic rings and in aortic rings from animals subjected to trauma and hemorrhagic shock was examined. RESULTS: Flutamide induced significant relaxation in aortic rings and small intestinal blood vessels in healthy males. The flutamide-induced relaxation in vessels from normal males was partially attenuated by prior incubation with the male sex steroid testosterone, and was significantly lower in females. Flutamide-induced vascular relaxation in the aorta was partially attenuated by endothelium removal, but it was not significantly affected by trauma and hemorrhagic shock in male rats. CONCLUSIONS: Flutamide has a direct vasodilating effect on large and small vessels in rats, which involves sex-dependent mechanisms. Thus, the beneficial effects of flutamide on cardiovascular responses in males following trauma and hemorrhagic shock may be due to the direct vascular relaxation induced by this agent.

Androgen Antagonists↗
PubMed1995

The prognostic value of lymphatic and blood vessel invasion in operable breast cancer.

BACKGROUND: This study assessed the prognostic effect of lymphatic and blood vessel invasion (LVI and BVI) on survival in a retrospective sample of 1408 patients with breast cancer. METHODS: Survival analysis was evaluated by univariate (Kaplan-Meier product limit method and log rank test) and multivariate (Cox model) analysis. Correlations among variables were studied by contingency tables and statistical significance was evaluated by chi-square test. RESULTS: Lymphatic vessel invasion was present in 34.2% of cases, and BVI in 4.2%. Lymphatic vessel invasion correlated with BVI (P < 0.0001), and both were correlated with metastatic axillary lymph nodes and increasing tumor size and grade; BVI was sporadic (only 10 cases) among lymph node negative patients. Although LVI was more frequent among premenopausal patients and those with ductal carcinomas, BVI was unrelated to menopausal status and tumor type. Lymphatic vessel invasion and BVI were associated with poor survival by univariate analysis (P < 0.0001). By multivariate analysis, relative risk of death was significantly increased when LVI was present both in the whole series as well as in the lymph node negative and lymph node positive subgroups; the prognostic role of LVI was independent of menopausal and lymph node status, tumor size, tumor grade, or adjuvant treatment. In the lymph node negative sample, LVI had strong prognostic power. In the lymph node positive sample, the prognostic role of LVI was also independent of the number of lymph nodes with metastases. Blood vessel invasion had no prognostic role in any subgroup. CONCLUSION: The prevalence of BVI was particularly low in this study, and the question of its possible prognostic role for patients with breast cancer should be assessed with methods that amplify its detection. LVI is a strong prognostic factor for operable patients with breast cancer. In lymph node negative patients, LVI is a predictor of poor prognosis for those who are consequently candidates for adjuvant therapy. Similarly, in lymph node positive patients, LVI is a predictor for a high risk of death for those who are candidates for highly intensive adjuvant strategies.

Adult↗
PubMed2000

Effect of vascular freezing on the histopathology of dissected small vessels in the rat: vascular freezing does induce intimal hyperplasia in arteries and veins.

Intimal hyperplasia is the primary response of a vessel wall after injury. It may be the single most significant factor affecting long-term patency. The purpose of this study was to find out whether freeze injury, inflicted on rat microvessels, would be followed by intimal hyperplasia. Toward this aim, we exposed the superficial femoral vessels in the rat. On one side they were frozen using liquid nitrogen spray. The other side was dissected as the control. Vessel segments, harvested immediately and after 1, 2, 3, and 5 months, were studied light microscopically for the occurrence and content of intimal hyperplasia. In the arteries a considerable intimal hyperplasia was found within a 4-week interval, persisting for at least 5 months, as a result of the freeze injury. In the veins, the intimal hyperplasia was much less marked but was nevertheless demonstrable. These findings are not in agreement with earlier studies, in which freezing of injured rat microarteries with liquid nitrogen spray was followed by complete regeneration of the vessel wall, without intimal hyperplasia taking place. The factors contributing to these differences are discussed. It is concluded that freezing of a vessel wall is followed by intimal hyperplasia, which is part of the normal healing process.

Animals↗
PubMed1978

An ultrastructural study of developing extracellular matrix in vitelline blood vessels of the early chick embryo.

This investigation was designed to describe the morphological events in embryonic development of peripheral blood vessels (vasculogenesis) and to relate this process to the appearance of extracellular matrix (ECM) during growth and maturation of these tissues. Extraembryonic vitelline vessels of the early chick embryo were chosen for this study and light, transmission, and scanning electron microscopy were carried out on vessels excised from chick embryos (Hamburger-Hamilton stages 8 through 23). Our data show that early (stage 10) vessels are composed of two distinct epithelial layers, an inner layer of presumptive endothelium surrounded by a layer of splanchnopleuric mesoderm. During development, the inner layer gives rise to mature vascular endothelium while splanchnopleuric mesoderm differentiates to form primitive vascular smooth muscle. Ultrastructural studies show the presence of collagen and basal lamina in the extracellular space between these two layers during initiation of endothelial and smooth muscle cytodifferentiation. Furthermore, ruthenium red-positive material is present on basal surfaces of developing vascular endothelium at this time, indicating possible glycosaminoglycans (GAG) or other polyanionic components of the ECM. These data suggest that the sequential production of basal lamina, collagen (s), and/or GAG's by developing peripheral vessel wall epithelia may be critical to their final differentiation.

Animals↗
PubMed1990

An investigation of lymphatic vessels in the feline dental pulp.

The existence of lymphatic vessels in the dental pulp has been a matter of continuing controversy. We have now used light microscopy to examine semithin transverse sections of perfusion-fixed incisors and canines in cats. Lymphatics were found in all the teeth studied. In most teeth they were present in the coronal, middle, and apical regions of the pulp; but in a few they were lacking coronally and in the middle. Within individual teeth, lymphatics were found in the subodontoblastic zone or more centrally in the pulp; but none were found in the odontoblast layer or in the pulp horns. Vessels located by light microscopy were subsequently examined by transmission electron microscopy. Their ultrastructural features were typical of lymphatics and included irregular, attenuated endothelium with adjacent cells joined in different ways. Occasional gaps connected the extracellular spaces with their lumens, and abluminal endothelial projections appeared to form open end bulbs. There was very little basement membrane, but anchoring filaments were found near the abluminal surface of the endothelium and near collagen fibrils. The total cross-sectional area of lymphatic vessels was measured in semithin sections and, with pulp area, increased from the coronal region to the middle. However, both areas decreased from the middle to the apical region suggesting either that lymph flows faster as it reaches the foramens of the apical delta or that some vessels leave the tooth through lateral root canals. Using the methods of light and transmission electron microscopy, therefore, we have shown that pulp lymphatic vessels exist. Questions remain, however, about their distribution within teeth, variations between teeth, and routes of exit from teeth.

Animals↗
PubMed1995

Amyloid beta-proteins 1-40 and 1-42(43) in the soluble fraction of extra- and intracranial blood vessels.

To investigate the process of amyloid beta-protein (A beta) accumulation in cerebral amyloid angiopathy (CAA), the levels of A beta were determined in the soluble fraction of extra- and intracranial blood vessels and leptomeninges obtained at autopsy. Two enzyme immunoassays were employed that are known to sensitively and specifically quantify two A beta species, A beta 1-40 and 1-42(43). A beta was detectable in the intracranial blood vessels and leptomeninges with the latter containing the highest levels, while it was undetectable in the extracranial blood vessels. Thus the levels of soluble A beta correlated well with the predilection sites for CAA. Among individuals aged 20 to 90, the A beta levels in the leptomeninges increased sharply in those aged 50 to 70 and thereafter tended to decline. However, only slight degrees of CAA were detected by immunocytochemistry, even when those leptomeninges contained high levels of A beta comparable with those in Alzheimer's disease. The level of A beta 1-42 was almost always severalfold that of A beta 1-40 in the soluble fraction of leptomeninges. This is in good agreement with the immunocytochemical result showing the presence of A beta 40-negative, A beta 42(43)-positive meningeal vessels. These results indicate that A beta 1-42 is the initially deposited species in CAA and that the disruption of A beta homeostasis precedes A beta deposition in the meningeal vessels.

Adult↗