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At least 919 records · Page 51Linked to original sources
PubMed1988

Peptide-containing nerves around blood vessels of stroke-prone spontaneously hypertensive rats.

The distribution and density of nerves containing vasoactive intestinal polypeptide, substance P, and neuropeptide Y around the cerebral and peripheral blood vessels of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were studied using an indirect immunofluorescence technique. Neonatal sympathectomy of SHRSP with anti-nerve growth factor and guanethidine was also carried out to study the effect of sympathectomy on the distribution of these nerves. Vasoactive intestinal polypeptide nerve density was higher in the veins and superior mesenteric artery of SHRSP than of WKY and lower in the cerebral arteries of SHRSP than of WKY, but no difference was found in the muscular mesenteric arteries. Sympathectomy reduced the density of these nerves in all the peripheral vessels but had little effect on the cerebral arteries. Density of substance P nerves was similar between SHRSP and WKY in the peripheral vessels but higher in the cerebral arteries of WKY than of SHRSP. Sympathectomy reduced the density of these nerves in the peripheral vessels but increased the density in some cerebral arteries of SHRSP. Neuropeptide Y nerve density was higher in the peripheral blood vessels of SHRSP than of WKY, and no difference was found in the cerebral arteries. Sympathectomy almost completely removed these nerves in the peripheral vessels but had no effect on the cerebral arteries. We suggest that some of the differences in nerve density between SHRSP and WKY, especially those in the peripheral blood vessels, may be related to the development of hypertension in the SHRSP.

Animals↗
PubMed1999

Localization and expression of tissue kallikrein and kallistatin in human blood vessels.

Tissue kallikrein releases kinins by specific proteolysis, an activity inhibited by kallistatin. In this study, kallikrein and kallistatin were localized to endothelial and smooth muscle cells of large, medium, and small normal blood vessels by immunohistochemical techniques. Immunostaining for both proteins was strong in the endothelium of all sizes of blood vessels and was more intense in medial smooth muscle cells of small and medium-sized blood vessels than in elastic arteries. The sites of synthesis by endothelial and smooth muscle cells were demonstrated in normal blood vessels of all sizes by in situ hybridization histochemistry. Kallikrein and kallistatin levels were measured by immunoassays in homogenates of human aorta, vena cava, and iliac artery and vein. Tissue kallikrein and kallistatin transcripts were identified in human blood vessels by RT-PCR followed by Southern blot analysis with specific oligonucleotide probes. The results demonstrated the expression and co-localization of tissue kallikrein and kallistatin in human vessels and suggest a potential role of kallistatin in regulating tissue kallikrein in blood vessels.

Blood Vessels↗
PubMed1989

Small coronary vessel disease and sudden coronary death.

In an attempt to determine the importance of atherosclerosis in medium-sized coronary arteries, the hearts of 20 patients dying of cardiac disease, within 24 hours of the onset of symptoms, were compared with 19 controls. Post-mortem coronary angiograms were performed and the coronary arteries dissected in detail. Severe stenoses, or complete occlusions, were present in 34 of 80 major coronary arteries in the sudden cardiac death (SCD) group and 5 of 76 in the controls. Medium-sized branch vessels were severely stenosed or occluded in 20.5 per cent (37 of 180 vessels) in the SCD group and 6.4 per cent (11 of 171 vessels) in the controls. Forty of the 48 diseased branch vessels arose from the left anterior descending artery. In the SCD group, 18 patients died from major coronary artery atheroma, one from hypertensive heart disease and only one from disease of a branch vessel. We conclude that, in most cases of SCD, careful macroscopic examination of the major coronary vessels will provide an adequate explanation for death. Detailed dissection of all medium-sized branch vessels is unlikely to be of value as a routine procedure but, at the very least, pathologists should identify and dissect the first septal and diagonal branches of the left anterior descending artery in every post-mortem.

Coronary Disease↗
PubMed2002

Retinal Vessel Analysis--new possibilities.

Retinal Vessel Analysis is a new technique to assess behavior of large retinal vessels based on diameter measurements. The Retinal Vessel Analyzer (RVA) measures continuously on-line obtaining data in relation to time and local position. Possible analysis tools include (a) Time Course Analysis of physiological, pathological, or therapy induced changes; (b) Local Course Analysis to recognize local narrow or wide vessel segments along the vessel; (c) Vasomotoric Analysis to determine vasomotions and blood pressure related diameter changes; (d) Functional Analysis to examine dynamic behavior e.g. the ability to autoregulate and (e) Functional Imaging to visualize functional parameters of vessels in single vessel segments. RVA is thus able to recognize and study different autoregulation mechanisms.

Fluorescein Angiography↗
PubMed2003

3-Nitrotyrosine in atherosclerotic blood vessels.

The effect of peroxynitrite on the development of atherosclerosis is one of the major foci of recent studies. Here, the cytotoxic effect of peroxynitrite was investigated by quantitatively measuring nitrated tyrosine, 3-nitrotyrosine (3-NT) levels in atherosclerotic blood vessels. Atherosclerotic vessels were obtained from the patients who underwent either coronary artery or peripheric artery bypass surgery. Internal thoracic arteries of the patients were treated as non-atherosclerotic control vessels. 3-NT was measured by reverse-phase HPLC and plasma nitrite-nitrate levels were measured by spectrophotometry. 3-NT levels were significantly elevated in atherosclerotic vessels (46.6 +/- 23.3 nmol/mg protein, n = 15; p < 0.001) in comparison to control vessels (15.8 +/- 2.5 nmol/mg protein, n = 10). Vessel 3-NT correlated weakly with plasma nitrate levels (r = 0.38). Thus, atherosclerotic arteries have higher 3-NT levels than non-atherosclerotic blood vessels.

Arteriosclerosis↗
PubMed2006

Lymphangiogenic growth factor responsiveness is modulated by postnatal lymphatic vessel maturation.

Lymphatic vessel plasticity and stability are of considerable importance when attempting to treat diseases associated with the lymphatic vasculature. Development of lymphatic vessels during embryogenesis is dependent on vascular endothelial growth factor (VEGF)-C but not VEGF-D. Using a recombinant adenovirus encoding a soluble form of their receptor VEGFR-3 (AdVEGFR-3-Ig), we studied lymphatic vessel dependency on VEGF-C and VEGF-D induced VEGFR-3 signaling in postnatal and adult mice. Transduction with AdVEGFR-3-Ig led to regression of lymphatic capillaries and medium-sized lymphatic vessels in mice under 2 weeks of age without affecting collecting lymphatic vessels or the blood vasculature. No effect was observed after this period. The lymphatic capillaries of neonatal mice also regressed partially in response to recombinant VEGFR-3-Ig or blocking antibodies against VEGFR-3, but not to adenovirus-encoded VEGFR-2-Ig. Despite sustained inhibitory VEGFR-3-Ig levels, lymphatic vessel regrowth was observed at 4 weeks of age. Interestingly, whereas transgenic expression of VEGF-C in the skin induced lymphatic hyperplasia even during embryogenesis, similar expression of VEGF-D resulted in lymphangiogenesis predominantly after birth. These results indicate considerable plasticity of lymphatic vessels during the early postnatal period but not thereafter, suggesting that anti-lymphangiogenic therapy can be safely applied in adults.

Adenoviridae↗
PubMed2006

Vascular endothelial growth factor-A mediates ultraviolet B-induced impairment of lymphatic vessel function.

UVB irradiation of the skin induces erythema, epidermal hyperplasia, vascular hyperpermeability, and edema formation. Previous studies have revealed that the cutaneous blood vasculature plays a critical role in the mediation of photodamage. In contrast, the role of lymphatic vessels, which play an essential role in the maintenance of tissue fluid balance, in the response to UVB irradiation has remained unknown. We report here that both acute and chronic UVB irradiation of murine skin results in prominent enlargement of lymphatic vessels. Surprisingly, these enlarged lymphatic vessels were functionally impaired and hyperpermeable, as detected by intravital lymphangiography. The expression levels of vascular endothelial growth factor (VEGF)-A but not of the known lymphangiogenesis factors VEGF-C or VEGF-D, were enhanced in UVB-irradiated epidermis. Targeted overexpression of VEGF-A in the epidermis of transgenic mice led to increased enlargement and leakage of lymphatic vessels after acute UVB irradiation, whereas systemic blockade of VEGF-A signaling largely prevented lymphatic vessel abnormalities and photodamage induced by UVB. Together, these findings identify lymphatic vessels as novel targets for UVB-induced cutaneous photodamage and suggest that VEGF-A mediates impairment of lymphatic vessel function, thereby contributing to the adverse effects of UVB irradiation on the skin.

Animals↗
PubMed1991

A semi-empirical model of apparent blood viscosity as a function of vessel diameter and discharge hematocrit.

A semi-empirical model is developed to describe the dependence of apparent viscosity of blood on vessel diameter (2.7 to 500 microns) and vessel discharge hematocrit (5% to 60%). The blood flow is modeled as a cell-rich core and a cell-free marginal layer in the larger vessels and an axial-train in the smaller vessels. Laminar (Poiseuille) flow is assumed in all cases. An equation is derived in which apparent viscosity is a function of vessel diameter, core viscosity, and width of marginal layer. This is then complemented by empirical equations in which core viscosity varies exponentially with discharge hematocrit while the width of marginal layer varies linearly with discharge hematocrit. The model correlates well with several sets of experimental data and behaves according to the Fahraeus-Lindqvist effect. Predicted apparent viscosity tends to the expected finite value for large vessel diameters. Dependence of apparent viscosity on vessel diameter is realistically smooth in the whole diameter range.

Blood Vessels↗
PubMed2002

Vascular endothelial growth factors C and D and their VEGFR-2 and 3 receptors in blood and lymphatic vessels in healthy and arthritic synovium.

OBJECTIVE: To localize vascular endothelial growth factor C (VEGF-C) and VEGF-D in synovial specimens in relation to their VEGFR-2 and VEGFR-3 receptors in blood and lymphatic vessels. METHODS: Immunohistochemical staining and messenger RNA analysis from control and arthritic synovial membrane specimens. RESULTS: Quantitative RT-PCR disclosed that VEGF-C mRNA copy numbers were higher than VEGF-D mRNA copy numbers in the rheumatoid arthritis (RA), osteoarthritis, and control patient groups studied (p < 0.01). Immunohistochemical staining localized VEGF-C to synovial lining cell layer, pericytes, and smooth muscle cells of blood vessels. The number of VEGF-C positive cells was increased in the synovial lining of ankylosing spondylitis (AS) and RA compared to control synovium. However, in contrast to control synovial lining, little if any VEGF-D was detected in AS or RA synovial lining. VEGFR-2 expressing stromal blood vessels, also positive for the vascular endothelial marker PAL-E and the basement membrane marker laminin, were more abundant in RA and AS than in controls. Interestingly, the lymphatic endothelial receptor VEGFR-3 was also expressed in most synovial vessels, especially in the sublining capillaries and venules. CONCLUSION: VEGF-C is strongly expressed in the hypertrophic synovial lining of arthritic joints, whereas VEGF-D expression is very low in AS and RA. The expression of VEGF-C and VEGF-D in pericytes and smooth muscle cells suggests that these factors may have a role in maintaining vascular homeostasis. The VEGF receptors VEGFR-2 and VEGFR-3 are present in most of the sublining blood vessels. The expression of the lymphatic marker VEGFR-3 in the sublining blood vessels may relate to fluid filtration and/or fenestrations. The relatively few lymphatic vessels along with increased vascular permeability in RA may contribute to the development of tissue edema and joint stiffness.

Arthritis↗
PubMed2002

Comparison of dilatation mechanism and long-term vessel remodeling between directional coronary atherectomy and balloon angioplasty assessed by volumetric intravascular ultrasound.

Although acute and late outcomes of coronary interventions have been determined by coronary angiography, this method cannot determine changes in vessel and plaque volume. Volumetric intravascular analysis has the potential to evaluate the morphology and redistribution of plaque after coronary intervention as well as longitudinal vessel remodeling. We used 3-dimensional intravascular ultrasound (3-D IVUS) to delineate the mechanism of coronary dilatation and long-term (> 1 year) remodeling in 25 patients. Ten patients underwent directional coronary atherectomy (DCA), and 15 underwent balloon angioplasty (POBA). No patients exhibited restenosis at 6-month angiographic follow-up. Validated Netra 3-D IVUS was performed pre- and post-intervention, at 6-months and at > 1-year. There were some differences in mechanism of dilatation and time course of change in vessel size between DCA and POBA patients. The principal mechanism was vessel stretching and longitudinal plaque redistribution in the POBA group and plaque debulking in the DCA group. In the POBA group, vessel volume increased just after the procedure; this increase was maintained at 6 months and at > 1-year. However, in the DCA group, vessel volume increased initially 6 months after the procedure. 3-D IVUS revealed a difference in mechanism of dilatation between POBA and DCA; this difference might affect late-term vessel remodeling even in patients without restenosis.

Aged↗
PubMed1975

[Vessels of the microcirculatory bed of the heart in myocardial infarction].

Vessels of the microcirculatory bed of the heart in myocardial infarction were studied on the basis of the material of 21 section observations using histological, histochemical methods and the technique of impregnation of films of the epicardium developed by V. V. Kupriyanov. In the ischemic stage in the zone of ischemia and in perifocal areas there were noted signs of increased vascular permeability and impairment of hemodynamics: plethora of the venous department of the microcirculatory system, stasis of the blood in capillaries, spasm and paresis of vessels of the microcirculation. In the necrotic stage in the zone of necrosis there were observed destruction of vessels of the microcirculatory bed; in the peri-infarction zone--drastic plethora of veins, venules and capillaries, higher vascular permeability, leucostasis, leucopedesis, perivascular cellular infiltrates, destruction of vessels of the microcirculatory bed, dilatation of lymphatic vessels; in the intact zone--venous plethora and elevated permeability. In cases of shocks and collapses in vessels of the microcirculatory bed of the heart beyond the zone of necrosis aggregations of erythrocytes were found. In the reparative stage newly formed vessels in the granulation tissue were observed; In the post-infarction scars sinusoid vascular cavities and arteries of the closing type were noted.

Aged↗
PubMed1992

Most peripheral, node-negative, non-small-cell lung cancers have low proliferative rates and no intratumoral and peritumoral blood and lymphatic vessel invasion. Rationale for treatment with wedge resection alone.

We investigated the tumor aggressiveness (intratumoral and peritumoral lymphatic and blood vessel invasion by tumor emboli) and proliferative activity (mitotic count) of 45 patients with peripheral, superficially seated, node-negative (T1-2 N0 M0), non-small-cell lung cancer treated with wedge resection alone between January 1982 and June 1988. Most patients were male (n = 39) with T1 (n = 25), small (mean diameter, 2.6 +/- 0.8 cm), squamous (n = 24), right-sided (n = 29) tumors located in either upper lobe (n = 35). The surgical specimens were studied by immunohistochemical staining with a monoclonal antibody targeting the factor VIII-related antigen. None of the tumors had lymphatic peritumoral or intratumoral invasion. Seven neoplasms (15%) harbored blood vessel invasion by tumor cells; all but one of these invasions were within the substance of the tumor. The median mitotic count was 8 mitoses per 10 high-power fields (range, 1 to 42 mitoses), significantly (p = 0.003) higher in patients with blood vessel invasion than in those without. With a 24-month minimum follow-up, projected 3- and 5-year survivals are 79% and 68%, respectively. Eleven patients had relapses and died of their tumors because of either local (n = 5) or extrathoracic (n = 6) recurrence; three patients died without tumors of comorbidity. Among the six tumors recurring in extrathoracic sites, five (83%) harbored intratumoral (n = 4) or peritumoral (n = 1) blood vessel invasion. Both recurrence of disease and death from non-small-cell lung cancer were significantly (p = 0.0009) higher for tumors with blood vessel invasion. By univariate analysis, significant predictors of survival were tumor stage (T1 vs T2, p = 0.008), size (< or = 2.6 cm vs > 2.6 cm, p = 0.039), mitotic count (< or = 8 vs > 8 mitoses, p = 0.0007), and blood vessel invasion (absence vs presence, p = 0.0001). By multivariate analysis, however, only blood vessel invasion retained its level of prognostic significance (p = 0.006). Data demonstrate that peripheral, node-negative non-small-cell lung cancers have a low metastatic potential. Whenever anatomically feasible, wedge resection seems to be an appropriate method of primary treatment.

Blood Vessels↗
PubMed2004

Acoustic intensity for a long vessel with noncircular cross section.

The acoustic intensity distribution around and within long vessels of noncircular cross section was investigated for parameters typical of biomedical ultrasound and blood vessels. We have developed a collocation method for finding the acoustic field when a uniform plane wave is obliquely incident on a long, not necessarily cylindrical, impedance interface. Results are presented for vessels of noncircular cross section and for vessels with thick walls of nonuniform thickness. The intensity in the vicinity of the vessel, throughout the lumen, and in the wall, is calculated for intermediate length scales, i.e., vessel radius and wall thickness in the range 1 to 10 wavelengths. The intensity distribution is an interference pattern, with complicated regions of increased and decreased intensity. These results are compared with approximate intensity obtained using ray theory. Effects not predicted by ray theory and intensity variations that will be significant in any close ultrasonic investigation of these vessels are revealed.

Anatomy, Cross-Sectional↗
PubMed2005

The approach to small vessels in the era of drug-eluting stents.

The treatment of small-vessel disease will occupy an increasingly important part of interventional cardiology practice and this raises several issues. The definition of "small vessels" has great implications for device size selection, and knowledge of "normal" small-vessel dimensions is important. Stents have been applied in the setting of smaller-vessel disease and future iterations of small-vessel stents will need to address several design factors. Stent strut thickness might impact on subsequent restenosis as well as late lumen loss. There has been great interest in the use of drug-eluting stents for small vessels. Randomized clinical trials of sirolimus-eluting versus bare metal stents in the treatment of small-vessel disease have shown significant improvements in the rates of target lesion revascularization and restenosis with sirolimus-eluting stents. These improvements in restenosis rates are attributable to the low levels of late loss with the drug-eluting stent.

Blood Vessel Prosthesis Implantation↗
PubMed2005

[Management of blood vessels in the vascularized autogenous submandibular gland transfer for severe keratoconjunctivitis sicca].

OBJECTIVE: To summarize the management of blood vessels in the transfer of vascularized autogenous submandibular gland. METHODS: Sixty-eight cases of vascularized transfer of autogenous submandibular gland for severe keratoconjunctivitis sicca performed from August 1999 to April 2004 were reviewed. Data collected for each patient included general items, donor and recipient vessels, vessel crisis, salvage of the vessel thrombosis, and survival of transferred glands. RESULTS: Among the 68 cases, all the donor and recipient arteries were facial artery and superficial temporal artery respectively. For donor veins, 55 were facial veins, 1 was vein near the duct, and 12 were venae comitantes of facial artery. For recipient veins, 62 were superficial temporary veins and five were veins in the upper neck, one was deep temporary vein. Vessel thromboses occurred in 10 cases, 9 were venous and 1 were arterial. The salvage rate was 10.0%, with the overall survival rate of 86.8% of transferred gland. CONCLUSIONS: Variation in venous outflow is common in microvascular transfer of submandibular gland, and anastomosis between venae comitante of facial artery and superficial temporal vein is most dependable. Vessel anastomosis under microscope may reduce the vessel thrombosis rate after operation.

Adolescent↗
PubMed2005

[Study on distribution and drainage of lymphatic vessels of tongue].

OBJECTIVE: To investigate the distribution and drainage of lymphatic vessels of tongue, and to provide anatomical evidence for treatment of tongue cancer. METHODS: Indirect lymphatic injection was employed, combined with clearing method with winter green oil and corrosive cast technique, to study the distribution of lymphatic vessels of tongue. Anatomical methods were used to detect the sentinel lymph nodes in different region of tongue. RESULTS: The lymphatic vessels of dorsal mucosa composed of lymphocapillary vessels and anstomosing side branches were present by superficial and deep capillary networks. The distribution of lymphatic networks extend from tip to base and from one board to another, and was not influenced by the sulcus tenninalis and median lingual sulcus. Lymphatic vessels in the muscular portion communicated with lymphocapillary network of dorsal and ventral mucosa, which made the lymphatic vessels of tongue to be an integrity network structure. These characters of distribution influenced the lymphatic drainage of tongue. The results showed principal sentinel lymph nodes (SLNs) for anterior part of tongue were submental lymph nodes, submandibular lymph nodes and juguloomohyoid lymph nodes, for lateral part and middle part of tongue were submandibular lymph nodes, jugulodigastric lymph nodes and thyroid lymph nodes, and for root part of tongue were jugulodigastric lymph nodes. SLNs for every injection region were all presented at bilatral neck, but the frequency of stained SLNs at homolateral neck was more than that at contralateral neck. CONCLUSION: The lymphatic vessels of tongue arranged like a network, which made the lymphatic drainage at various ways and made the distribution of sentinel lymph nodes to be bilateral and dispersive.

Drainage↗
PubMed1990

[Treatment of coronary artery disease with poor left ventricular function: comparison of medical and surgical treatments in relation to the numbers of the diseased vessel].

The operative mortality and short-term (average 20 months) survival of 100 surgically or medically treated patients, who had coronary artery disease with poor left ventricular function, were examined. One hundred patients with myocardial infarction and radionuclide-documented left ventricular dysfunction (LVEF at rest less than or equal to 40%) were subjects of this study; 85 patients among them underwent simultaneous coronary arteriography. Fifty-six patients whose average age was 59.7 years, and an average LVEF was 30.0%, were treated medically; 44 patients with an average age of 56.0 years, and an average LVEF of 30.9%, were treated surgically, 41 with bypass grafts, two with left ventricular surgery, and one with both these procedures. The medically treated patients consisted of four groups. Group I comprised 15 patients, in whom coronary angiography was contraindicated. Their average age was 67.1 and an average LVEF was 26.2%, Group II, included six patients, who had no indication for surgery because of severely diseased distal coronary arteries. This group had an average age of 57.5 years and an average LVEF of 22.5%. There were one with two-vessel disease and five with three-vessel disease. Group III included five surgical candidates who refused surgery. Their average age and an LVEF were 67.0 and 35.0%, respectively. In this group, there were one with two-vessel disease and four with three-vessel disease. Group IV, comprised 22 patients who did not need surgical therapy. Their average age was 55.3 and average LVEF was 32.5%. They included 22 with one-vessel disease, seven with two-vessel disease and one with three-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Cryocoagulation of retinal vessels: an experimental model of intravascular coagulation.

Various amounts of cryothermy were applied to the posterior pole of rabbit eyes to determine changes in retinal tissue and vasculature. Four consecutive freezing and refreezing applications of -60 degrees was the most effective technique for achieving central retinal vessel occlusion. Electron microscopic observations of sequentially sectioned occlusion. Electron microscopic observations of sequentially sectioned occluded vessels showed that the vessels were occluded by a platelet plug distally and packed erythrocytes proximally. Fibrin formation was not found in the occluded retinal vessels but was seen within platelet plugs in choroidal vessels. Because cryocoagulation simulates the normal physiologic means of coagulation more closely than other vessel occluding techniques, cryocoagulation of the primary retinal vessels is suggested as an experimental model for intravascular coagulation.

Animals↗