Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources
PubMed1986

Effects of salicylate and steroid on neutrophil migration and corneal blood vessel growth.

Cauterization of the cornea results in emigration of neutrophils from the limbal blood vessels into the corneal tissue. Blood vessel proliferation follows, the stimulus for which is unknown. In this study, 0.1 M sodium salicylate drops administered topically to cauterized rat corneas over a 48-h period had an inhibitory effect on the migration of neutrophils from the limbal vessels 6 h after injury, but this was not maintained at 48 h. After 6 days of treatment, the salicylate had no effect on vessel growth into the cauterized rat cornea. Application of prednisolone disodium phosphate ointment to cauterized corneas also inhibited neutrophil migration at 6 h, but increased the extravascular neutrophils at 48 h. After 6 days of treatment, corneal blood vessel growth was significantly reduced. It was concluded that there is no consistent relation between the number of extravascular neutrophils at the corneal limbus and the extent of corneal blood vessel growth.

Animals↗
PubMed2003

A novel in vitro model of trophoblast-mediated decidual blood vessel remodeling.

In vivo the extravillous trophoblasts (EVTs) penetrate the decidua and the first third of the myometrium to remodel the uterine spiral arteries and achieve the high-flow, low-resistance circulation characteristic of the intervillous space of the term placenta. Much of our understanding of these processes comes from histologic analysis of placental bed biopsies, a limited tissue source and one that can provide only a snapshot of a dynamic process. To better characterize these cellular interactions, we have developed an in vitro co-culture system in which first trimester villous explants are cultured at low oxygen tension in contact with 2-mm(2) sections of decidua parietalis from the same patient. Hematoxylin eosin counterstaining of paraffin sections shows that EVT columns form at the tips of the placental villi and adhere and penetrate the decidual surface. The decidual blood vessels in the path of the EVT show morphologic disruption. Immunohistochemical analysis of the co-cultures using both an endothelial specific anti-CD31 and an anti-smooth muscle actin antibody show a disruption of the integrity of the vessel lining together with a complete loss of organized smooth muscle actin surrounding the blood vessels. In contrast control decidua samples in the absence of placental villi exhibit blood vessels with a complete endothelial lining and an organized muscular sheath. Using both an anti-cytokeratin-7 and anti-Cdx-2 antibody specific to trophoblasts, we show that these changes coincide with invasion of the vessels by endovascular trophoblasts and penetration of the decidua by interstitial EVTs. No EVTs were found in the control decidua. Thus we conclude that this in vitro model mimics the physiologic change observed in vivo during trophoblast invasion into maternal decidual tissues, and as such it may provide useful information concerning the interactions between EVTs and decidual cells and vessels during early gestation.

Actins↗
PubMed2003

VEGF(121) and VEGF(165) regulate blood vessel diameter through vascular endothelial growth factor receptor 2 in an in vitro angiogenesis model.

Vascular endothelial growth factor (VEGF) is essential for the induction of angiogenesis and drives both endothelial cell (EC) proliferation and migration. It has been suggested that VEGF also regulates vessel diameter, although this has not been tested explicitly. The two most abundant isoforms, VEGF(121) and VEGF(165), both signal through VEGF receptor 2 (VEGFR-2). We recently optimized a three-dimensional in vitro angiogenesis assay using HUVECs growing on Cytodex beads and embedded in fibrin gels. Fibroblasts provide critical factors that promote sprouting, lumen formation, and vessel stability. Using this assay, we have examined the role of VEGF in setting vessel diameter. Low concentrations of both VEGF(121) and VEGF(165) promote growth of long, thin vessels, whereas higher concentrations of VEGF remarkably enhance vessel diameter. Placental growth factor, which binds to VEGFR-1 but not VEGFR-2, does not promote capillary sprouting. Moreover, specific inhibition of VEGFR-2 signaling results in a dramatic reduction of EC sprouting in response to VEGF, indicating the critical importance of this receptor. The increase in vessel diameter is the result of cell proliferation and migration, rather than cellular hypertrophy, and likely depends on MEK1-ERK1/2 signaling. Both phosphatidylinositol 3-kinase and p38 activity are required for cell survival. We conclude that the diameter of new capillary sprouts can be determined by the local concentration of VEGF and that the action of VEGF on angiogenic EC in this assay is critically dependent on signaling through VEGFR-2.

Angiogenesis Inducing Agents↗
PubMed2005

Noninvasive in vivo assessment of vessel characteristics in capillary vascular malformations exposed to five pulsed dye laser treatments.

BACKGROUND: The treatment of capillary vascular malformations by pulsed dye laser results in fading of these disfiguring lesions in the majority of patients. In only a minority, however, is full clearance of the lesion achieved. It is believed that the capillary composition of a capillary vascular malformation is an important determinant of whether it will respond to further laser treatment. Moreover, by determining the type, size, and depth of the ectatic capillaries within a capillary vascular malformation, it may be possible to target these vessels with specific laser parameters. METHODS: The noninvasive technique of depth measurement videomicroscopy was used to delineate the capillary structure of 22 previously untreated capillary vascular malformations and examine how this structure changes after five treatments with a 0.45-msec pulse duration using a 585-nm pulsed dye laser. RESULTS: After one and five treatments, there was a statistically significant lightening (p < 0.02 and p < 0.001, respectively) of the lesions, as seen on Munsell Color Chart testing. Before any laser treatment, the majority (59 percent) of capillary vascular malformations displayed a superficial type 1 or mixed capillary pattern, whereas after five laser treatments, the majority displayed a deep type 2 pattern (81 percent). After five laser treatments, there was a statistically significant increase in the depth of the remaining capillaries within the lesion compared with normal skin (p < 0.02) and a statistically significant reduction in the vessel diameters (p < 0.001). CONCLUSIONS: The authors found that vessels with a diameter greater than 50 mum were adequately treated, whereas those smaller than 50 microm appeared resistant to laser treatment. These data would suggest that pulse durations longer than 0.45 msec are not required to treat large ectatic capillary vascular malformation vessels. The authors suggest that the failure to treat very-small-diameter vessels is attributable to thermal dissipation from the target vessels, whose thermal relaxation time is much shorter than the pulse duration of the laser used.

Capillaries↗
PubMed2004

Detection of crossing vessels as the cause of ureteropelvic junction obstruction: the role of antegrade pyelography prior to endopyelotomy.

PURPOSE: To review the utility of antegrade pyelography in detecting crossing vessels as the cause of uretero-pelvic junction (UPJ) obstruction prior to planned endopyelotomy. MATERIALS AND METHODS: A retrospective review of the medical records, surgical reports, and medical images was performed in 109 consecutive adult patients in our practice who underwent antegrade pyelography just prior to planned endopyelotomy for symptomatic UPJ obstruction between January 1996 and December 2002. RESULTS: Fourteen patients were identified in whom a specific antegrade pyelographic appearance was detected in the diagnosis UPJ obstruction caused by crossing vessels. Surgical plans were changed in all 14 patients from antegrade endopyelotomy to open surgical pyeloplasty, during which the anterior (ventral) crossing vessels causing obstruction were confirmed. An additional three patients in the reviewed endopyelotomy group clinically failed their initial endopyelotomy procedure and were shown at the time of subsequent open or laparoscopic reconstructive surgery to have UPJ obstruction caused by anterior crossing vessels, but that diagnosis was missed at the time of the initial antegrade pyelogram. CONCLUSION: A specific antegrade pyelographic appearance was identified to diagnose UPJ obstruction caused by anterior crossing vessels with a sensitivity of 82.4% and a specificity of 100%. The direct obstructing effect of the vessels on the ureter is defined with pyelography as an acute posteriorly angulated ureteral deformity just below a patent UPJ. Recognition of this specific antegrade pyelographic appearance permits use of an appropriate surgical technique for UPJ obstruction repair.

Adolescent↗
PubMed2005

Cerebral small vessel diseases: cerebral microangiopathies.

PURPOSE OF REVIEW: Small vessel diseases of the brain are still clinically underrecognized whereas their burden is increasing steeply. The most frequent is acquired degenerative small vessel disease. Many hereditary or idiopathic small vessel diseases have also been identified, of which cerebral autosomal-dominant arteriopathy with stroke and ischaemic leukoencephalopathy (CADASIL) is the most prominent. In this review, we will highlight current evidence on pathophysiology and genetics, new imaging tools, and treatment options. RECENT FINDINGS: Recent imaging studies have stressed the disruption of white matter connections in the pathogenesis of cognitive impairment in acquired small vessel disease. Clinical trials suggest a therapeutic benefit of acetylcholinesterase inhibitors. CADASIL is caused by mutations in the Notch3 gene. Current basic research has identified Notch genes to be important for endothelial and smooth muscle cells to form arteries and veins. Diagnosis can now be made reliably by magnetic resonance brain imaging, skin biopsy, or genetic testing. The so-called retinocerebral vasculopathies share the involvement of both retinal, cerebral and cochlear arterioles (e.g. Susac's syndrome). Cerebral amyloid angiopathy, occurring either sporadically or as a cause of various gene mutations, predisposes to lobar haemorrhages caused by rupture of affected small cortical vessels. Other rare cerebral microangiopathies, such as mitochondrial cytopathies, Fabry's disease and toxemic vasculopathy, offer established or new therapeutic options. SUMMARY: Cerebral small vessel diseases are highly variable in their aetiopathogenesis and clinical course. Current pathophysiological insights will help develop better treatment modalities; new imaging tools will provide surrogate markers for monitoring disease progression and treatment effects.

CADASIL↗
PubMed1997

The LKLF transcription factor is required for normal tunica media formation and blood vessel stabilization during murine embryogenesis.

The transcriptional programs that regulate blood vessel formation are largely unknown. In this paper, we examine the role of the zinc finger transcription factor LKLF in murine blood vessel morphogenesis and homeostasis. By in situ hybridization and immunohistochemistry, we show that LKLF is expressed as early as embryonic day 9.5 (E9.5) in vascular endothelial cells throughout the developing mouse embryo. To better understand the function of LKLF, we used homologous recombination in embryonic stem (ES) cells to generate LKLF-deficient (LKLF-/-) mice. Both angiogenesis and vasculogenesis were normal in the LKLF-/- mice. However, LKLF-/- embryos died between E12.5 and E14.5 from severe intra-embryonic and intra-amniotic hemorrhaging. This bleeding disorder was associated with specific defects in blood vessel morphology. Umbilical veins and arteries in the LKLF-/- embryos displayed an abnormally thin tunica media and aneurysmal dilatation before rupturing into the amniotic cavity. Similarly, vascular smooth muscle cells in the aortae from the LKLF-/- animals displayed a cuboidal morphology and failed to organize into a compact tunica media. Consistent with these findings, electron microscopic analyses demonstrated endothelial cell necrosis, significant reductions in the number of vessel-wall pericytes and differentiating smooth muscle cells, and decreased deposition of extracellular matrix in the LKLF-/- vessels. Despite these defects, in situ hybridization demonstrated normal expression of platelet-derived growth factor B, Tie1, Tie2, transforming growth factor beta, and heparin-binding epidermal growth factor in the vasculature of the LKLF-/- embryos. Therefore, LKLF defines a novel transcriptional pathway in which endothelial cells regulate the assembly of the vascular tunica media and concomitant vessel wall stabilization during mammalian embryogenesis.

Animals↗
PubMed2005

Do xylem fibers affect vessel cavitation resistance?

Possible mechanical and hydraulic costs to increased cavitation resistance were examined among six co-occurring species of chaparral shrubs in southern California. We measured cavitation resistance (xylem pressure at 50% loss of hydraulic conductivity), seasonal low pressure potential (P(min)), xylem conductive efficiency (specific conductivity), mechanical strength of stems (modulus of elasticity and modulus of rupture), and xylem density. At the cellular level, we measured vessel and fiber wall thickness and lumen diameter, transverse fiber wall and total lumen area, and estimated vessel implosion resistance using (t/b)(h)(2), where t is the thickness of adjoining vessel walls and b is the vessel lumen diameter. Increased cavitation resistance was correlated with increased mechanical strength (r(2) = 0.74 and 0.76 for modulus of elasticity and modulus of rupture, respectively), xylem density (r(2) = 0.88), and P(min) (r(2) = 0.96). In contrast, cavitation resistance and P(min) were not correlated with decreased specific conductivity, suggesting no tradeoff between these traits. At the cellular level, increased cavitation resistance was correlated with increased (t/b)(h)(2) (r(2) = 0.95), increased transverse fiber wall area (r(2) = 0.89), and decreased fiber lumen area (r(2) = 0.76). To our knowledge, the correlation between cavitation resistance and fiber wall area has not been shown previously and suggests a mechanical role for fibers in cavitation resistance. Fiber efficacy in prevention of vessel implosion, defined as inward bending or collapse of vessels, is discussed.

Biomechanical Phenomena↗
PubMed1995

Thermal relaxation of port-wine stain vessels probed in vivo: the need for 1-10-millisecond laser pulse treatment.

Although thermal relaxation times of cutaneous port-wine stain microvessels have been calculated and used to formulate laser selective photothermolysis, they have never been measured. A scheme to do so was devised by measuring the skin response to pairs of 585-nm dye laser pulses (250-360 microseconds each) as a function of the time interval between the two pulses, in five volunteers with port-wine stains. After a pump pulse delivering 80% of the fluence necessary for causing purpura, the fluence of a second probe pulse necessary to cause purpura was determined and was found to increase with the interval between the two pulses, in a manner consistent with thermal diffusion theory. Biopsy specimens were obtained from four of the five subjects to examine the nature and extent of vessel damage and to measure the port-wine stain vessel diameters. Using diffusion theory, the thermal relaxation time was calculated based on the measured vessel diameters. These calculated values are consistent with the increase in radiant exposure (fluence) of the probe pulse necessary to induce purpura for longer time delays. Two simple models for thermal relaxation of port-wine stain vessels are presented and compared with the data. The data and histologic assessment of the vessel injury strongly suggest that pulse durations for ideal laser treatment are in the 1-10-millisecond region and depend on vessel diameter. No dermatologic lasers presently used for port-wine stain treatment operate in this pulse width domain.

Adult↗
PubMed2006

Increased laser Doppler flow in skin tumors corresponds to elevated vessel density and reactive hyperemia.

BACKGROUND/PURPOSE: Tumor angiogenesis plays a key role in tumor growth and formation of metastasis. Quantitative analysis of tumor blood flow is a prerequisite for developing novel treatment strategies such as antiangiogenic and antivascular treatment options. Laser Doppler flow in malignant melanomas has been shown to be increased compared with normal skin and melanocytic nevi. This study investigated whether this phenomenon is originated by elevated blood vessel density or by reactive hyperemia. METHODS: Laser Doppler flow was studied in 35 melanocytic nevi, 22 malignant melanomas and three basal cell carcinomas. After excision digital imaging analysis was performed in microtome sections (factor VIII-associated antigen and CD 31 labelled). The ratio of vessel area in histological sections from tumor tissue and in non-lesional skin was calculated and related to Doppler flow values. RESULTS: Malignant melanomas demonstrated an enlargement of vessel cross-sectional area by factor 3.7+/-1.9 and of Doppler flow by factor 10.56+/-10.7, and melanocytic nevi accomplished increase of vessel cross-sectional area by factor 1.7+/-0.9 and of Doppler flow by factor 2.7+/-3.5. CONCLUSION: The laser Doppler flow is influenced by the number and the velocity of erythrocytes in the tissue. The greater increase of laser Doppler flow than of vessel density in histological sections demonstrates that the flow signal in skin tumors is caused by neovascularization as well as by functional hyperemia. Laser Doppler perfusion imaging is a useful method for non-invasive, repeated and quantitative assessment of tumor vascular network and effects of antiangiogenic treatment directed vs. tumor vasculature in vivo, but it cannot distinguish between increased vessel density and reactive hyperemia.

Adult↗
PubMed1996

Selective enhancement by tumor necrosis factor-alpha of vascular permeability of new blood vessels induced with agarose hydrogel-entrapped Meth-A fibrosarcoma cells.

We have previously developed a simple and quantitative method for assessment of in vivo tumor cell-induced angiogenesis by means of microencapsulation of tumor cells in agarose hydrogel and mouse hemoglobin ELISA (mHb-ELISA). In this article, we report that the new blood vessels induced with agarose-encapsulated tumor cells have the same sensitivity to tumor necrosis factor-alpha (TNF-alpha) as the original solid-tumor vessels. Agarose beads (average diameter = 200 microns), in which Meth-A fibrosarcoma cells were microencapsulated, were subcutaneously implanted in non-syngeneic ddY mice. Ten days later, extensive angiogenesis was observed on the implanted sites of Meth-A agarose heads, whereas no new blood vessels were induced with cell-free agarose heads. The vascular permeability of the new blood vessels induced with agarose-microencapsulated Meth-A cells was selectively and significantly enhanced by the i.v. injection of TNF-alpha, and it reached the maximum level at 2 h after the injection of TNF-alpha. At 4 h after the injection of TNF-alpha, the vascular permeability was reduced to the basal level. This permeability profile in Meth-A agarose beads in ddY mice is very similar to that in Meth-A solid tumor in syngeneic BALB/c mice. On the other hand, TNF-alpha-treatment did not affect the vascular permeability of other normal tissues or inflammatory tissue in ddY mice. These results strongly suggest that the new blood vessels induced with agarose-microencapsulated tumor cells have the specific characteristics of tumor vessels. Our in vivo angiogenesis assay system should be useful not only to screen anti-angiogenetic agents, but also to elucidate the mechanism of tumor angiogenesis.

Animals↗
PubMed1986

Transection of varicose vessels in the nasal mucosa of patients with recurrent epistaxis. A 2-year follow-up.

Twenty-two patients with recurrent nose bleeds and varicose vessels on the nasal septum were subjected to transection of the vessels and followed-up for 2 years. One month after the operation, it was not possible to identify the original vessels. In other locations new varicose vessels began to appear after 1 month, and at the end of the follow-up period were observed on 9 out of 10 operated sides. The transection resulted in an immediate decrease in the frequency of nose bleeds and at the end of the control period 12 (55%) of the patients had had less than 4 bleeds during the previous year in spite of the observed rapid formation of new vessels. Mucosal atrophy with symptoms of increased nasal crusting occurred in 3 patients. Transection of varicose vessels in patients with nose bleeds leads to a decrease in the number of bleeds.

Adult↗
PubMed2006

Relationships in Alzheimer's disease between the extent of Abeta deposition in cerebral blood vessel walls, as cerebral amyloid angiopathy, and the amount of cerebrovascular smooth muscle cells and collagen.

The relationship between degree of cerebral amyloid angiopathy (CAA) and the amount of smooth muscle cells (SMCs) and deposition of collagen IV fibres (COL IV) was investigated in the frontal and occipital cortex of 70 patients with autopsy confirmed Alzheimer's disease (AD). The extent of CAA was significantly greater in occipital than in frontal cortex, although SMC loss was greater in frontal than in occipital cortex. COL IV staining was significantly higher in occipital than in frontal cortex. The degree of SMC loss correlated with CAA, as Abeta40 but not as Abeta42 or total Abeta, in frontal cortex, but not in occipital cortex. Leptomeningeal arteries within occipital cortex showed significantly greater external diameter, greater wall thickness and greater luminal area than those in frontal cortex. The degree of CAA correlated with thickness of blood vessel wall and external diameter in frontal cortex, whereas extent of SMC loss correlated with thickness of blood vessel wall in occipital cortex. There were significant negative correlations between duration of disease and thickness of vessel wall, external diameter and luminal area. In patients with disease durations exceeding 10 years, external vessel diameter and thickness of the vessel wall were both halved compared with patients with durations less than 5 years; luminal area was reduced by about 75%. Blood vessels in AD undergo degenerative changes involving deposition of Abeta and COL IV with loss of SMC. SMC loss may relate to increasing Abeta deposition in early stages of disease, but this relationship may be lost with disease progression.

Aged↗
PubMed2006

Use of the ligaSure vessel sealing system in laparoscopic adrenalectomy.

Laparoscopic adrenalectomy is the operation of choice for benign adrenal lesions. During laparoscopic surgery, vessels are usually ligated with diathermy, ligaclips, staplers or ultrasonic coagulators. Use of the electrothermal bipolar vessel sealer (LigaSure; Valleylab, Boulder, CO, USA) has recently been described in a variety of procedures, not including adrenalectomy. This article is a retrospective study of 28 patients undergoing laparoscopic adrenalectomy within the University of Sydney Endocrine Surgical Unit at the Royal North Shore Hospital using the LigaSure vessel sealing system. Between July 2004 and August 2005, 28 consecutive patients underwent laparoscopic adrenalectomy using the LigaSure vessel sealing system to divide feeding adrenal vessels as well as the adrenal vein. There were no bleeding complications. The LigaSure vessel sealing system can be safely used to secure haemostasis, including division of the adrenal vein, in laparoscopic adrenalectomy.

Adrenalectomy↗
PubMed2005

Differential endostatin binding to bladder, prostate and kidney tumour vessels.

OBJECTIVES: To define the anti-angiogenic mechanism and causes of the heterogeneous influence of endostatin, one of a group of matrix-derived inhibitors of tumour angiogenesis of increasing significance in tumour treatment, on various tissue types. MATERIALS AND METHODS: Variations in the binding behaviour of endostatin with vessels were assessed in different tumours (bladder, prostate and kidney) and compared with benign tissue vessels. Biotinylated endostatin was used and detected using extravidin CY3 and extravidin-gold immunolabelling. RESULTS: There were significant differences in the number of vessels showing endostatin binding among benign and malignant bladder, prostate and kidney tissues. While there was distinct endostatin binding on a mean (sd) of 94.2 (3.0)% bladder and 73.8 (19.5)% prostate tumour vessels, there was less binding, at 11.32 (3.9)%, on kidney tumour vessels. There was less binding to vessels of benign bladder, prostate and kidney tissue, at 2.0 (1.5), 1.7 (1.7) and 1.5 (1.7)%, respectively. At the ultrastructural level, different binding sites were detected both inside and outside the endothelial cells. CONCLUSION: Endostatin binds more to all tumour tissues than to benign tissue, but the degree of binding in malignant kidney tissue was significantly less than that in malignant prostate and bladder tissues. These divergent vascular endostatin-binding patterns could be responsible for a tumour type-dependent anti-angiogenic effect attributable to endostatin. Such selective behaviour would have therapeutic consequences for future anti-angiogenic therapy, in which different kinds of tumours could be further classified into those responding to endostatin or not.

Aged↗
PubMed1991

Evidence for differing origins of the serotonergic innervation of major cerebral arteries and small pial vessels in the rat.

We have studied the nature and origin of the serotonergic innervation of two distinct anatomical cerebrovascular compartments, namely, small pial vessels and major cerebral arteries, in the rat. To this end, the levels of serotonin [5-hydroxytryptamine (5-HT)] and 5-hydroxyindoleacetic acid (5-HIAA) were measured by HPLC in both cerebrovascular compartments after either bilateral sympathectomy or destruction of the ascending serotonergic pathways, which originate from the raphe nuclei. We first showed that the small pial vessel samples were not contaminated by underlying cortical tissues through the use of an immunohistochemical approach that revealed the glia limitans, the most superficial cortical layer. Superior cervical ganglionectomy caused a marked decrease in noradrenaline concentrations in major cerebral arteries (-77%), although the reduction was less pronounced (-34%) in small pial vessels. Sympathectomy decreased by 33% 5-HT concentrations in the major cerebral arteries but was without effect on 5-HT levels in the small pial vessels. Destruction of the ascending serotonergic pathways (via local administration of 5,7-dihydroxytryptamine into the ventral tegmental area) produced a dramatic fall in 5-HT and 5-HIAA concentrations in both vascular compartments. To establish the authenticity of the serotonergic innervation, the synthesis of 5-HT [as assessed by measuring the accumulation of 5-hydroxytryptophan (5-HTP) after decarboxylase inhibition] was measured in the two vascular beds under control conditions and after destruction of the ascending serotonergic pathways. The rate of accumulation of 5-HTP was higher in the small pial vessels than in major cerebral arteries, an observation that indicates an important de novo synthesis of 5-HT in small pial vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMedDate not supplied

Evaluation of a vessel-sealing device for small intestinal resection and anastomosis in normal horses.

OBJECTIVES: To compare arterial bursting pressure after vessel closure using a vessel-sealing device (LigaSure Atlas Laparoscopic Sealer/Divider Instrument; Valleylab, Boulder, CO), a ligate-and-divide stapling device (LDS), and 2-0 polydioxanone suture. To evaluate the LigaSure Atlas as a method for ligation of the mesenteric vasculature during small intestinal resection in normal horses. STUDY DESIGN: Experimental study. ANIMALS: Part A: jejunal segments from 19 horses. Part B: 6 horses, aged 1 to 18 years, weighing 330 to 509 kg. METHODS: Part A: Jejunal segments with mesenteric vessels were collected from 19 horses. After closure by 1 of 3 methods (LigaSure Atlas, LDS, 2-0 polydioxanone) arteries were cannulated, and bursting pressure was measured by incrementally increasing intraluminal pressure until failure. Part B: Six horses had jejunal resection and anastomosis using a vessel-sealing device (LigaSure Atlas) to provide hemostasis of the mesenteric vasculature. Horses were monitored clinically for 4 weeks. RESULTS: Part A: Mean +/- SEM bursting pressure after 2-0 polydioxanone ligation (1,014.50 +/- 279.05 mm Hg) was significantly greater than mean bursting pressure after LigaSure (554.25 +/- 228.79 mm Hg), which was significantly greater than the mean bursting pressure after LDS (373.25 +/- 183.69). Part B: No major operative or postoperative hemorrhage occurred after application of the LigaSure Atlas for sealing and transecting mesenteric vasculature during small intestinal resection in normal horses. CONCLUSIONS: The LigaSure Atlas appears to be a safe method for hemostasis of the mesenteric vasculature during small intestinal resection in normal horses. CLINICAL RELEVANCE: Benefits of the LigaSure Atlas vessel-sealing device include reduced time required to provide hemostasis, acceptable arterial bursting pressure, no remaining foreign material, and no risk for ligature slippage. In our experience, use of the LigaSure Atlas during small intestinal resection and anastomosis in horses is safe for ligation of vessels less than or equal to 7-mm diameter.

Anastomosis, Surgical↗
PubMed1994

Perivascular neuropeptides (NPY, VIP, CGRP and SP) in human brain vessels after subarachnoid haemorrhage.

INTRODUCTION--Cerebral blood vessels are innervated by sympathetic nerve fibres storing neuropeptide Y (NPY), parasympathetic nerves storing acetylcholine, vasoactive intestinal peptide (VIP) and sensory afferent fibres containing calcitonin gene-related peptide (CGRP), substance P (SP) and neurokinin A. In experimental studies on subarachnoid haemorrhage (SAH) there are indications that perivascular peptides are involved. In the present study we have in man measured the levels of NPY, VIP, SP and CGRP in brain vessels of patients that have suffered a fatal SAH and compared this with the levels encountered in subjects that died of an extracerebral cause. MATERIAL AND METHODS--Vessels from patients who have died from SAH or nonSAH were obtained during autopsy performed within 24 hrs after death. The peptides were extracted and fractionated with reversed phase liquid chromatography (HPLC). The levels of NPY, VIP, SP, and CGRP were measured with radioimmunoassay. Vasomotor responses of human cerebral arteries were performed using a sensitive in vitro system. RESULTS--Human cerebral vessels contained NPY, VIP, CGRP and SP which eluted at the same positions as the authentic peptides. The level of CGRP was significantly lower (p < 0.01) in arteries removed from SAH patients as compared to control subjects. The level of SP was not changed, if anything it tended to be increased after SAH. The levels of NPY and VIP were not significantly altered after SAH. In isolated brain vessels alpha-CGRP was a potent vasodilator of arteries precontracted with whole blood, prostaglandin F2 alpha or endothelin. It had a poor effect on vessels precontracted with 60 mM potassium. CONCLUSION--The evidence suggest that the trigemino-cerebrovascular system, storing CGRP and SP, is to a differential degree involved in the pathophysiology of SAH in man and supports the hypothesis of an exhaustion of CGRP as one important factor in the development of late spasm occurring after SAH.

Adult↗