SEARCH · PubMed Health

Results for “MESENTERIC VESSELS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,261 records · Page 70Linked to original sources

PubMed1983

Serotoninergic neurons in human fetal intestine: an immunohistochemical study.

The distribution of 5-hydroxytryptamine-like immunoreactivity was studied in whole-mount preparations of intestine from human fetuses. Immunoreactive nerve cell bodies were located in the myenteric plexus and were occasionally found in the submucous plexus; they were often seen to have long processes. Varicose fibers were found in the ganglia and internodal strands of the myenteric and submucous plexuses, in the deep muscular plexus of the circular muscle, and in the walls of some small mesenteric blood vessels immediately outside the intestine. This study provides evidence for the presence of serotoninergic nerves in the human intestine.

Colon↗

PubMed1981

Pharmacological studies of the antihypertensive effect of nitrendipine.

1,4-Dihydro-2,6-dimethyl-4(3-nitrophenyl)-3,5-pyridine carboxylic acid, 3-ethyl-5-methyl ester (nitrendipine, Bay e 5009) is a new vasodilatory calcium antagonist with pronounced hypertensive efficacy. Doses of 0.3-31.5 mg/kg p.o. lower the blood pressure of rats with spontaneous, renal and desoxycorticosterone acetate (DOCA)-hypertension. Doses of 0.03-10.0 mg/kg p.o. lower the blood pressure of dogs with renal hypertension. The hypotensive effect is about 10 times less in normotensive rats. No increase in tolerance occurred during therapeutic studies lasting 5 weeks in hypertensive rats and several days in hypertensive dogs. There were no signs either of acquired tolerance developing during these studies. Dogs in fentanyl analgesia respond to i.v. administration of 0.001-0.03 mg/kg with a reduction in peripheral vascular resistance and an increase in cardiac output and heart rate. The stroke volume remains unchanged. The vasodilatory effect occurs at different degrees in different vascular beds. The most pronounced increases in vascular flow were measured in the muscular vessels of the hind quarters and in the coronary vessels. The mesenterical, skin and brain blood flows were much less affected.

Animals↗

PubMed1994

Immunochemical localization of inducible nitric oxide synthase in endotoxin-treated rats.

BACKGROUND: Administration of endotoxin to rodents produces widespread tissue induction of nitric oxide synthase (NOS). To understand the mechanisms of the resulting endotoxin shock, it is important to know the cellular distribution of the inducible NOS (iNOS). EXPERIMENTAL DESIGN: We have investigated the localization and time course of expression of iNOS in rats at time 0 (control) and 3, 6, 9, and 24 hours after administration of endotoxin and also in endotoxin- and cytokine-stimulated RAW 264 murine macrophage and A7r5 aortic smooth muscle cells. We have used a rabbit antiserum to a synthetic peptide selected from the deduced sequence of the cloned macrophage enzyme (residues 47-71) and immunochemical techniques. RESULTS: The antiserum reacted with an approximately 130-kilodalton protein (the molecular weight of iNOS) in Western blots of total cytoplasmic proteins from livers of endotoxin-treated rats, RAW 264 murine macrophages stimulated with endotoxin and combinations of cytokines, and purified liver iNOS, but not in control, untreated tissues. Strong cytoplasmic immunostaining was seen in RAW 264 murine macrophages and A7r5 rat aortic smooth muscle cells after stimulation, but not in nonstimulated cells. Three hours after endotoxin treatment in rats, iNOS immunoreactivity was detectable in many tissues and was at its strongest at 6 and 9 hours after stimulation. Staining was detected predominantly in macrophages distributed abundantly in heart, lung, liver, and kidney. It was also present in Kupffer cells and hepatocytes, biliary epithelium, mesangial cells, airway epithelium, and nerves supplying mesenteric blood vessels but was not detected in any vasculature. By 24 hours there was a reduction in the number of cells stained compared with that seen at 6 and 9 hours. In addition, at 24 hours after endotoxin treatment, granulomatous lesions showing iNOS staining were evident, particularly in the liver. CONCLUSIONS: Antiserum raised to macrophage NOS recognizes an inducible enzyme in a wide variety of cells. Macrophages are the major site of iNOS expression in endotoxin-treated rats and show greatest staining between 6 and 9 hours after treatment. Although staining was not seen in vascular cells in vivo, levels of the enzyme that are below the immunocytochemistry detection limit cannot be excluded.

Amino Acid Oxidoreductases↗

PubMed1993

Platelet-activating factor promotes shear rate-dependent leukocyte adhesion in postcapillary venules.

Reductions in shear rate are generally associated with a recruitment of rolling and adherent leukocytes within the microcirculation. In this study, we determined if platelet-activating factor (PAF) affects shear rate-dependent leukocytes adhesion in cat mesenteric venules and whether the adhesion glycoproteins CD11/CD18 and ICAM-1 contribute to this process. Shear rate was varied in postcapillary venules (25-35 microns) by graded occlusion of the superior mesenteric artery. Vessel diameter, red blood cell velocity, leukocyte rolling velocity, and the number of rolling and adherent leukocytes were measured at each shear rate either in the presence or absence of PAF superfusion. PAF superfusion resulted in an increased number of adherent, but not rolling, leukocytes at basal and reduced venular shear rates. A monoclonal antibody (MAb) directed against CD11/CD18 prevented the PAF-induced recruitment of adherent leukocytes, while an ICAM-1 specific MAb had no effect. These results indicate that PAF increases shear rate-dependent leukocyte adhesion, presumably through activation and/or increased surface expression of CD11/CD18 on granulocytes.

Animals↗

PubMed1994

Characterization of ovine lymphatic endothelial cells and their interactions with lymphocytes.

The interaction of blood-borne lymphocytes with blood vascular endothelial cells is a fundamental component of lymphocyte circulation. The role of lymphatic endothelial cells is less certain. These studies describe the isolation, characterization and lymphocyte binding capacity of efferent lymphatic endothelial cells from ovine mesenteric lymphatic vessels. Lymphatic endothelial cells had anti-thrombin 3, von Willebrand Factor and MHC I on their surface. The cells also actively metabolized acetylated low density lipoprotein. The morphological appearance was indistinguishable from blood vascular endothelium but quite different from cultured smooth muscle cells. Lymphocyte binding to lymphatic endothelial cells was not significantly different from binding to carotid artery or jugular vein endothelial cells. The degree of binding in all cases could be enhanced by incubating endothelial cells in medium containing rh TNF-alpha (recombinant human tumor necrosis factor alpha).

Acetylation↗

PubMed1996

Schistosoma mansoni induces in the Kenyan baboon a novel intestinal pathology that is manifestly modulated by an irradiated cercarial vaccine.

Light and scanning electron microscopic study of intestines of 5 baboons (Papio anubis) in a state of acute schistosomiasis mansoni after exposure to 800 cercariae was made. In addition to overt granulomatous inflammation in the mucosa of the colon and ileum, more subtle microscopic lesions consisting of smooth muscle hypertrophy and villous atrophy were present. The intensity and distribution of these lesions were less marked in 5 baboons previously vaccinated with 40,000 30-krad-attenuated cercariae and presenting a 39% mean protection level measured as a percent reduction in adult worms recovered from mesenteric vasculature at perfusion. No similar lesions were observed in 2 normal uninfected and nonvaccinated baboons. These results are comparable to what has been reported in mice infected by Schistosoma mansoni. The data indicate that villous atrophy, hypertrophy of muscularis mucosa, nd goblet cell hyperplasia are important pathological changes to be included in the evaluation of the efficacy of schistosomiasis vaccines in the baboon model, together with the routine adult worm recovery from mesenteric blood vessels and the overt liver and bowel pathology.

Acute Disease↗

PubMed1997

Lazaroid U-74500A for warm ischemia and reperfusion injury of the canine small intestine.

BACKGROUND: Although lazaroids have been shown to protect various organs from ischemia/reperfusion injury, results obtained in the small intestine have been conflicting. STUDY DESIGN: The canine small intestine was made totally ischemic for 2 hours by occluding the superior mesenteric artery and the superior mesenteric vein with interruption of the mesenteric collateral vessels. A lazaroid compound, U74500A, or a citrate vehicle was given intravenously to each of the six animals for 30 minutes before intestinal ischemia. Intestinal tissue blood flow, lipid peroxidation, neutrophil infiltration, adenine nucleotides and their catabolites, and histologic changes after reperfusion were determined. RESULTS: Lazaroid treatment attenuated decline of the mucosal and serosal blood flow after reperfusion. Accumulation of lipid peroxidation products and neutrophils in mucosal tissues was markedly inhibited by the treatment. Postischemic energy resynthesis was also augmented by lazaroid. Morphologically, mucosal architectures were better preserved with lazaroid treatment after reperfusion, and recovered to normal by postoperative day 3 in the treated group and by postoperative day 7 in control animals. CONCLUSIONS: Lazaroids protect the canine small intestine from ischemia/reperfusion injury by inhibiting lipid peroxidation and neutrophil infiltration. Dogs are tolerant of 2-hour normothermic complete intestinal ischemia.

Animals↗

PubMed1997

[Unusual vascular lesions in the course of a colonic leishmaniasis in an HIV positive patient].

Patients with acquired immunodeficiency syndrome are often susceptible to atypical dissemination of visceral leishmaniasis. Digestive localizations seem to be relatively frequent. Colonic localizations reported in the literature are endoscopically normal or show superficial mucosal lesions. We describe an original case of leishmaniasis associated with a colonic pseudotumoral stenosis with perforated ulcer penetrating in the mesocolon. Striking inflammation of mesenteric blood vessels, even far from the ulcer, suggested an ischemic mechanism for the colonic stenosis. These findings raise the hypothesis that vasculitis is secondary to mucosal parasitic infection.

Adult↗

PubMed1997

[Bowel elongation technique by using omentum as vascular pedicle in beagle dogs].

Basing on the establishment of an isolated bowel segement (IBS) in Beagle dog by omentoenteropexy, the possibility of using omentum as vascular pedicle in bowel elongation was investigated. Five young Beagle dogs (3 females, 2 males) with a body weight of 5-9 kg were used. A longitudinal incision (15 cm long) was made down to the seromuscular layer of the jejunal segment on the antimesenteric border, 20 cm distal to the duodenojejunal fold, the mucosal layer should never be injured. Then the free margin of the omentum was attached to the seromuscular border of the jejunum by interrupted sutures. One dog died from volvulus and necrosis of the bowel 3 days after operation. Seven weeks later, the mesentery was ligated in one dog and the bowel lengthening procedure was carried out in the other 3 dogs. The procedure consisted of longitudinal splitting of the isolated bowel segment anteroposteriorly, thus two separated segments of bowel were obtained, each received its own blood supply from either omental or mesenteric blood vessels. Either of the longitudinally splitting segments was rebuilt into one intestinal canal by 3/0 non-traumatic sutures. Then isoperistaltic end-to-end anastomosis of these two isolated segments was carried out, and an jejunostomy was established. The free jejunal ends were rejoined together to restore the continuity of the bowel lumen. Two weeks later, the blood supply of the experimental bowel segment was observed. It was shown that the IBS and elongated bowel segment (EBS) appeared viable, and there was good collateral circulation between the bowel segment and the omentum. The regeneration of lymphatics was observed from injection of methylene blue. It was concluded that a viable IBS and EBS could be established by using omentoenteropexy technique. The application of the this model in the management of short bowel syndrome needed to be further investigated.

Anastomosis, Surgical↗

PubMed2002

Thromboxane A2 in vasomotor effects of phenylephrine, acetylcholine, and bradykinin in rat mesenteric bed.

In vessels, pharmacological agents displace the balance between relaxing and contracting factors. A cross-talk between those factors has been shown in some vascular beds. To examine whether NO may regulate the vascular tone by modulating prostanoid synthesis or release, we analyzed the response of resistance rat mesenteric arterial bed to vasoactive agents. Phenylephrine, bradykinin (BK), and acetylcholine (ACH) were administered in the absence or in the presence of either NO synthesis inhibition (N(G)-nitro-L-arginine methyl ester [L-NAME]), cyclo-oxygenase inhibition (indomethacin), and/or a thromboxane A2 (TXA2) receptor antagonist (S18886), or a combination thereof. In the presence of L-NAME, the response to phenylephrine was markedly increased. Indomethacin limited these changes, which are attributed to TXA2 release since they were abolished by S18886 and a marked increase in TXB2 release (stable metabolite of TXA2) was found during phenylephrine infusion under NO blockade. Similarly, BK response under NO blockade was markedly attenuated with an improved response with indomethacin and a restoration of vasorelaxation with S18886. In contrast, indomethacin decreased further the response to ACH during L-NAME treatment, and TXA2 inhibition had no effect. Thus, in pathophysiological conditions where an endothelial dysfunction is present, TXA2 stimulation induced by NO release impairment may contribute to an altered response to phenylephrine or BK.

Acetylcholine↗

PubMed1999

Acetylcholine-induced relaxation of peripheral arteries isolated from mice lacking endothelial nitric oxide synthase.

1. Acetycholine-mediated relaxations in phenylephrine-contracted aortas, femoral and mesenteric resistance arteries were studied in vessels from endothelial nitric oxide synthase knock-out (eNOS -/-) and the corresponding wild-type strain (eNOS +/+) C57BL6/SV19 mice. 2. Aortas from eNOS (+/+) mice relaxed to acetylcholine in an endothelium-dependent NG-nitro-L-arginine (L-NOARG) sensitive manner. Aortas from eNOS (-/-) mice did not relax to acetylcholine but demonstrated enhanced sensitivity to both authentic NO and sodium nitroprusside. 3. Relaxation to acetylcholine in femoral arteries was partially inhibited by L-NOARG in vessels from eNOS (+/+) mice, but relaxation in eNOS (-/-) mice was insensitive to a combination of L-NOARG and indomethacin and the guanylyl cyclase inhibitor 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). The L-NOARG/ODQ/indomethacin-insensitive relaxation to acetylcholine in femoral arteries was inhibited in the presence of elevated (30 mM) extracellular KCl. 4. In mesenteric resistance vessels from eNOS (+/+) mice, the acetylcholine-mediated relaxation response was completely inhibited by a combination of indomethacin and L-NOARG or by 30 mM KCl alone. In contrast, in mesenteric arteries from eNOS (-/-) mice, the acetylcholine-relaxation response was insensitive to a combination of L-NOARG and indomethacin, but was inhibited in the presence of 30 mM KCl. 5. These data indicate arteries from eNOS (-/-) mice demonstrate a supersensitivity to exogenous NO, and that acetylcholine-induced vasorelaxation of femoral and mesenteric vessels from eNOS (-/-) mice is mediated by an endothelium-derived factor that has properties of an EDHF but is neither NO nor prostacyclin. Furthermore, in mesenteric vessels, there is an upregulation of the role of EDHF in the absence of NO.

Acetylcholine↗

PubMed2004

[Role of adrenoreceptors in the effect of thyroliberin on lymphatic vessels].

Formerly we showed that TRH had simulative effect on mesenteric bovine and rat lymphatic vessels (LV) in very low concentration--10(-12)-10(-18) M. In present paper, participation of LV alpha- and beta-receptors in realization of TRH activity on rat mesenteric lymphatic vessels was studied in situ. Propranolol increased the stimulative effect of TRH, isoproterenol exerted an opposite effect. Phentolamine, prazosin eliminated the simulative effect of TRH, yohimbine resulted in additional gain of effect, which seems to testify 1) presynaptic action of TRH or 2) increase of the output of norepinephrine, which is potentiated by alpha 2-adrenoceptor antagonists. Also the participation of adrenergic receptors in positive chronotropic effects of mesenteric rat LV was studied using the method of selective destruction of dopamine-containing neurons after 6-OHDA infusion. As it occurred, desympathization hindered development of stimulating action of TRH. Thus, the efficiency of TRH as a stimulator of LV is connected with activation of adrenergic mechanisms.

Adrenergic Agonists↗

PubMed1994

Evaluation of vascular tone in portacaval shunts comparing the index of contractility and resistance in cats.

A model of prehepatic chronic portal hypertension in cats was used to determine portacaval shunt responses to infused norepinephrine and to possible transmitter overflow into portal blood from nerves supplying the gut. Responses are compared using a new index of contractility. Four weeks after application of a slowly constricting occluder, the portal vein was completely occluded and acute experiments were carried out under pentobarbital anesthesia. Portal pressure was elevated to 15.0 +/- 0.9 mmHg and all portal flow passed through the shunts. In response to intraportal norepinephrine (0.25, 0.5 and 1.25 micrograms.min-1.kg-1) shunt resistance rose by 6% +/- 3%, 19% +/- 4% and 26% +/- 5%, respectively, whereas the index of contractility rose (by 22% +/- 8%, 46% +/- 10% and 89% +/- 20%, respectively), the distending blood pressure also rose (5% +/- 1%, 7% +/- 1% and 14% +/- 3%, respectively). The difference in percentage increase of resistance and the index of contractility is a result of the passive dilator effect of the elevated distending pressure acting on the distensible shunt vessels. Stimulation of mesenteric nerves caused the mesenteric artery to constrict, but the shunt vessels showed no effect. In conclusion, the shunt vessels respond actively to norepinephrine and passively to altered distending pressure. However, transmitter overflow from nerves supplying the intestines is unlikely to play a role in determining resistance in the shunts. Vascular resistance is affected by both active and passive effects, so that the active contractile responses are best evaluated using the index of contractility, which is not altered passively.

Animals↗

PubMed2003

CT findings in patients with familial Mediterranean fever during an acute abdominal attack.

The aim of this study is to present the abdominal CT findings of patients with familial Mediterranean fever (FMF) examined during an acute abdominal attack. CT scans of 17 patients (10 women and 7 men; age range 11-45 years) were retrospectively reviewed. Attention was directed to mesenteric or peritoneal abnormalities and to the presence of appendiceal pathology. Patients were divided into two groups; group A (n=14) consisted of patients with an acute abdominal attack caused by FMF, and group B (n=3) consisted of patients whose attack proved to be owing to a separate pathology requiring surgery. Characteristic CT findings of acute abdomen in FMF included mesenteric pathology (n=12), mainly of engorged vessels with thickened mesenteric folds, mesenteric lymphadenopathy (n=6) and ascites (n=6). Signs of focal peritonitis were found in four patients. Radiologists should be familiar with such CT findings of peritoneal irritation in patients with FMF during an acute attack, and may suggest this clinical diagnosis in the proper clinical setting in a patient who has not been previously diagnosed. Alternatively, the radiologist should be aware of the possibility of a concurrent acute appendicitis or other acute abdominal pathology in patients with known FMF and should search for it.

Abdomen, Acute↗

PubMedDate not supplied

Contrast-enhanced MR angiography of the mesenteric circulation: a pictorial essay.

Outstanding results have been achieved with magnetic resonance (MR) angiography, which has become competitive with conventional angiography as a vascular imaging technique. With the advances in gradient technology and the capability of imaging vessels in a single breath hold, one can track an intravenous bolus of paramagnetic contrast agent and evaluate the entire mesenteric circulation. Use of a breath-hold technique obviates the problem of motion artifact. Use of targeted maximum-intensity projection images from the three-dimensional (3D) volume data allows evaluation of the vascular anatomy at different phases (arterial and venous) of contrast enhancement. MR angiography performed with a contrast-enhanced breath-hold fat-suppressed 3D technique allows visualization of the superior mesenteric vessels, celiac artery, and portal vein in healthy subjects. Pathologic conditions of the mesenteric vessels that can be identified with this technique include stenosis or occlusion of the superior mesenteric artery, celiac artery aneurysm, thrombosis of the superior mesenteric vein, portal hypertension with varices, and vascular invasion by pancreatic carcinoma.

Adult↗

PubMed1997

Structural changes of small resistance arteries in spontaneously hypertensive rats after treatment with various doses of lacidipine.

OBJECTIVE: To evaluate the modifications of the morphology of mesenteric small resistance vessels in spontaneously hypertensive rats (SHR) induced by lacidipine treatment. METHODS: Lacidipine was administered at three different dosages, 20, 10, and 0.3 mg/kg per day. Fifty rats were studied. Nine SHR and 11 Wistar-Kyoto (WKY) rats were not treated. Each lacidipine dose was administered to 10 SHR. The drug and the placebo were administered by gavage from age 4 to age 12 weeks. The blood pressure was measured noninvasively every week. The animals were killed when they were aged 13 weeks, and the relative left ventricular mass (left ventricular weight plus septum weight/body weight) was calculated. Small mesenteric resistance vessels were dissected and mounted on a micromyograph (Mulvany's technique), and morphological parameters of the vessels were studied (media thickness and media: lumen ratio). RESULTS: The systolic blood pressure of SHR administered 20 and 10 mg/kg lacidipine per day was reduced significantly during the treatment period, whereas that of rats treated with 0.3 mg/kg lacidipine per day did not change. A significant reduction in media: lumen ratio was observed for all three groups of treated rats, including those to which 0.3 mg/kg lacidipine per day had been administered, and no reduction in systolic blood pressure could be detected. The relative left ventricular mass was reduced significantly only in rats to which 20 and 10 mg/kg lacidipine per day had been administered. CONCLUSION: A significant reduction in magnitude of vascular structural alternations was observed even in SHR treated with a low, nonhypotensive dose of lacidipine.

Animals↗

PubMed1985

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries.

We have investigated the effect of a synthetic 'atrial natriuretic factor' (ANF) on induced tone in rat isolated renal arcuate arteries (lumen diameter ca. 250 microns), and compared this with the effects of synthetic ANF on resistance vessels of similar size taken from the mesenteric, femoral, cerebral and coronary vasculature. Synthetic ANF was found to cause relaxation of the renal vessels when these were sub-maximally activated with K+, noradrenaline or 5-hydroxytryptamine, but had no effect on the responses of the other vessels to these agonists. Synthetic ANF had a near maximal effect (65% relaxation) at 100 nM, with an IC50 of 7.9 nM. The relaxant effect of synthetic ANF on the renal vessels was fully maintained for at least 15 min. Hydralazine (100 microM) caused relaxation of renal vessels (47%) and coronary vessels (42%), but had no effect on the other vessel types. By contrast, sodium nitroprusside (1 microM) relaxed all vessel types. The relaxant action of synthetic ANF on the renal vessels was seen in the presence of ouabain (1 mM), propranolol (1 microM), phentolamine (1 microM), atropine (1 microM) and felodipine (1 nM). In t renal vessels, synthetic ANF had no effect on membrane potential, measured with intracellular electrodes, despite the simultaneously measured relaxation. Synthetic ANF had no effect on the efflux of 22Na+ in either renal or mesenteric vessels. The results demonstrate that synthetic ANF has a specific and prolonged relaxant effect on renal small arteries, and are consistent with this effect being mediated through specific receptors.

Animals↗

PubMed1982

[Arterial vascular bed of the human mesenteric lymph nodes].

The anatomy of the blood vessels has been studied in 394 mesenteric lymph nodes macro- and microscopically. Morphometrical measurements of the size and diameter of the nodes have been performed in the intraorganic arteries of all orders of branching. Correlative connections existing between the size of the nodes and the number of the arteries supplying them with blood, between the size of the nodes and the diameter of the arteries feeding them, between the number of the hiluses and the number of the arteries supplying the lymph node with blood have been determined. As the results of the investigation demonstrate, the mesenteric lymph nodes having various localization differ in their size and form. The number and diameters of the arteries getting into the nodes via the hilus and the capsule vary within a wide range. There are two (often) or three (seldom) hiluses. One - three arteries get into one hilus. The structure of the intraorganic arterial vessels in the mesenteric lymph nodes is complex and variable, depended on the form of the nodes, number and position of the hiluses, on the type of blood supply and on the branching of the arteries getting into the nodes via the hiluses. In most of the mesenteric lymph nodes there are four orders of branching of the intraorganic arteries, each of them having a specific type of division into branches. All the intraorganic arteries either are situated within the trabecular connective tissue or are surrounded with elastic and collagenous fibres. The arteries of various order are differently connected with the structural-tissue elements of the lymph nodes. There are various variants in blood supply of the lymph node folliculi. The arterial vessels of the human mesenteric lymph nodes have a twisty course.

Adult↗