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 649 records · Page 36Linked to original sources

PubMed1995

Influence of some hydrodynamic factors of thrombus formation in microvessels.

The effect of mean blood velocity on thrombus formation parameters was studied using mesenteric vessels of white rats. An advanced phenomenological theory, explaining the relationship between mean blood velocity and thrombus growth rate, is presented. The qualitative analysis of theoretical and experimental data have shown that the main observed features in thrombus formation can be described by the theory with two phenomenological parameters.

Animals↗

PubMedDate not supplied

Bromelain proteases reduce human platelet aggregation in vitro, adhesion to bovine endothelial cells and thrombus formation in rat vessels in vivo.

The thiol protease, bromelain, an extract from pineapple stem, was suggested to have antithrombotic and anticoagulant activities in vivo. We studied the effects of bromelain on cell size distribution of isolated human platelets in vitro by Coulter Counter measurements. Preincubation of platelets with bromelain (10 micrograms/mL) completely prevented the thrombin (0.2 U/mL) induced platelet aggregation. Papain was less active in preventing platelet aggregation. In vitro, bromelain (0.1 microgram/mL) reduced the adhesion of bound, thrombin stimulated, fluorescent labeled platelets to bovine aorta endothelial cells. In addition, preincubation of platelets with bromelain, prior to thrombin, activation, reduced the platelet adhesion to the endothelial cells to the low binding value of unstimulated platelets. On the basis of mass concentrations, the proteases papain and trypsin were as effective as bromelain. Using a laser thrombosis model, the in vivo effects of orally and intraveneously applied bromelain on thrombus formation in rat mesenteric vessels were studied. Bromelain, orally applied at 60 mg/kg body weight, inhibited the thrombus formation in a time dependent manner, the maximum being after 2 hours in 11% of arterioles and 6% of venoles. Intravenous application at 30 mg/kg was slightly more active in reducing thrombus formation in arterioles (13%) and venoles (5%), suggesting that orally applied bromelain is biologically active. These results may help to explain some of the clinical effects observed after bromelain treatment in patients with thrombosis and related diseases.

Adult↗

PubMed1991

Computed tomography in superior mesenteric artery syndrome.

This is the first report of the use of computed tomography (CT) in a patient with classic features of superior mesenteric artery (SMA) syndrome. CT was able to simultaneously demonstrate the characteristic duodenal distension and the close proximity of superior mesenteric vessels and aorta. In addition, it was possible to show that CT signs improved after clinical symptoms disappeared during adequate nutritional therapy. CT together with anthropometric data indicated that the deposition of fat did not play the expected role in the resolution of SMA syndrome.

Adolescent↗

PubMed1987

Percutaneous transcatheter steel-coil embolization of a large proximal post-traumatic superior mesenteric arteriovenous fistula.

Arteriovenous fistulae affecting the proximal portions of the superior mesenteric vessels are extremely rare. We are reporting one such fistula which occurred in a young male as a sequel to a stab in the epigastrium. The arteriovenous fistula was successfully treated by percutaneous steel coil embolization.

Abdominal Injuries↗

PubMed1979

Grey-scale ultrasonic characteristics of carcinoma of the pancreas.

Fifty-five sonograms were performed on 25 cases of surgically and histologically proven carcinoma of the pancreas. The sonographic appearances of the tumour were determined. A diffuse echogenic pattern with irregular margin was the most common appearance. Displacement and indentation of the inferior vena cava and superior mesenteric vessels, greatly assist in localizing the tumour to the pancreas. A reliable prediction of tumour size and resectability cannot be determined by sonography alone. Sonography is helpful in assessing the response of unresectable pancreatic carcinoma to therapy. A more sonolucent appearance of the tumour occurs following chemotherapy.

Adult↗

PubMed2003

Only weak vasorelaxant properties of loop diuretics in isolated resistance arteries from man, rat and guinea pig.

Besides their diuretic action, loop diuretics may induce a rapid vasodilator effect that contribute to their short-term therapeutic properties. We examined the effects of furosemide (10(-6)-10(-3) mol l(-1)) in comparison with bumetanide (10(-6)-10(-4) mol l(-1)) on isolated resistance arteries from rat and guinea pig mesentery and human subcutaneous fat, and investigated the mechanism of the acute direct vasorelaxant action on an isometric microvascular myograph. Both loop diuretics induced concentration-dependent relaxation of resistance vessels irrespective of membrane potential. The maximal effect of furosemide was greatest in rat and least in human arteries. Both diuretics caused a rightward shift in the concentration-response curve to extracellular Ca(2+). Incubation with indomethacin (2 x 10(-5) mol l(-1)) or mechanical removal of the endothelium did not inhibit the loop diuretic-induced relaxation. At high concentrations (10(-4)-10(-3) mol l(-1)) loop diuretics exert only weak direct relaxant effects on isolated human subcutaneous resistance arteries compared to the vasorelaxant effects in rat and guinea pig mesenteric vessels.

Animals↗

PubMed1978

[Acid-base state disorders and their correction in acute mesenteric vascular obstruction].

The results of the investigation of main indices of acid-base equilibrium in 28 patients with acute obstruction of the mesenteric vessels are set forth. 12 patients out of 28 developed subcompensated or decompensated metabolic acidosis. The authors believe that the correction of acid-base equilibrium disorders is an efficacious factor of intense therapy and recommend to use it at all the stages of the treatment.

Acid-Base Imbalance↗

PubMed2006

Detection of venous invasion in surgical specimens of colorectal carcinoma: the efficacy of various types of tissue blocks.

BACKGROUND: Venous invasion (VI) is an important prognosis predictor after colorectal carcinoma (CRC) resection, enabling more accurate staging and influencing postoperative management. AIMS: To assess/compare various tissue block types (perpendicular, tangential, across mesentery (AM), from major vessels or lymph nodes (LNs)) for VI detection in CRC. METHODS: Fifty two CRCs (51 colectomies, one polypectomy) were studied. Tumours were measured, surface area calculated, and colorectum and bowel wall sites recorded. Weigert's staining for elastin facilitated VI detection. VI sites, type, and amount were recorded. Ratios of relative yield of tissue block types to their frequency were calculated. RESULTS: Average numbers of tissue blocks/colectomy specimen were: perpendicular, 10.2; tangential, 9.1; AM, 3.3; from major vessels, 2.1. Average number of LNs examined was 16.47. VI was detected in 22 tumours. Overall, VI was detected in 16 perpendicular, seven tangential, five AM, and two LN blocks. VI was detected in eight, two, one, and three tumours in perpendicular, tangential, LN, and AM blocks alone, respectively. In seven tumours, VI was identified in multiple tissue block types. The average number of blocks obtained was 39.7, 42.1, and 38 from all tumours, VI positive, and VI negative tumours, respectively (p = 0.0497). Efficacy to detect VI was 2.151, 2.088, 1.092, 0.172, and 0 for AM, perpendicular, tangential, LN, and mesenteric vessel blocks, respectively. CONCLUSIONS: VI was identified most frequently and in eight cases only in perpendicular blocks. However, extramural VI was detected in six tumours only in blocks cut tangentially, AM, or from harvested LNs. Hence, all these types of blocks should be submitted routinely and scanned for VI.

Adult↗

PubMed1990

Mechanism of cyclosporin potentiation of vasoconstriction of the isolated rat mesenteric arterial bed: role of extracellular calcium.

Hypertension is a serious side-effect of the clinical use of Cyclosporin A (CsA). One notion is that alterations of vascular reactivity contribute to this hypertension. In this study we used the isolated rat mesenteric vascular bed to test the specific hypothesis that CsA modifies vascular calcium regulation to potentiate vascular contractility. Mesenteric vessels from CsA-treated rats (10 mg/kg/day i.m. for 7 days) exhibited significantly greater vasoconstrictor responses to exogenous norepinephrine (NE) and potassium-induced depolarization than those of vehicle-treated animals. Similarly, in vitro CsA (8.3 X 10(-8) to 8.3 X 10(-6) M) augmented in a concentration-dependent manner both the sensitivity and the maximum response to NE and potassium. This effect of CsA on vasoconstriction was critically dependent on the presence of external calcium [( Ca++]o). The degree of vasoconstriction potentiation correlated significantly with the [Ca++]o which was used during exposure of the mesenteric bed to CsA. Reapplication of external calcium in the presence of CsA to "calcium-depleted" preparations increased significantly the amplitude of subsequent NE responses in a calcium-free medium. Thus, CsA-potentiated NE responses, once established, were not reversed by removing external calcium; however, attenuation occurred with the intracellular calcium antagonist dantrolene. Verapamil and nifedipine blocked potassium-elicited responses, but failed to prevent the CsA effect on NE-induced vasoconstriction. We conclude that CsA potentiation of vasoconstriction depends on extracellular calcium, and results from an enhanced transmembrane calcium transport. We speculate that CsA also increases the filling of intracellular stores of releasable calcium. These effects lead to greater calcium influx and greater intracellular calcium release upon stimulation.

Animals↗

PubMed2005

Insulin resistance in spontaneously hypertensive rats is associated with endothelial dysfunction characterized by imbalance between NO and ET-1 production.

Insulin stimulates production of NO in vascular endothelium via activation of phosphatidylinositol (PI) 3-kinase, Akt, and endothelial NO synthase. We hypothesized that insulin resistance may cause imbalance between endothelial vasodilators and vasoconstrictors (e.g., NO and ET-1), leading to hypertension. Twelve-week-old male spontaneously hypertensive rats (SHR) were hypertensive and insulin resistant compared with control Wistar-Kyoto (WKY) rats (systolic blood pressure 202 +/- 11 vs. 132 +/- 10 mmHg; fasting plasma insulin 5 +/- 1 vs. 0.9 +/- 0.1 ng/ml; P < 0.001). In WKY rats, insulin stimulated dose-dependent relaxation of mesenteric arteries precontracted with norepinephrine (NE) ex vivo. This depended on intact endothelium and was blocked by genistein, wortmannin, or N(omega)-nitro-l-arginine methyl ester (inhibitors of tyrosine kinase, PI3-kinase, and NO synthases, respectively). Vasodilation in response to insulin (but not ACh) was impaired by 20% in SHR (vs. WKY, P < 0.005). Preincubation of arteries with insulin significantly reduced the contractile effect of NE by 20% in WKY but not SHR rats. In SHR, the effect of insulin to reduce NE-mediated vasoconstriction became evident when insulin pretreatment was accompanied by ET-1 receptor blockade (BQ-123, BQ-788). Similar results were observed during treatment with the MEK inhibitor PD-98059. In addition, insulin-stimulated secretion of ET-1 from primary endothelial cells was significantly reduced by pretreatment of cells with PD-98059 (but not wortmannin). We conclude that insulin resistance in SHR is accompanied by endothelial dysfunction in mesenteric vessels with impaired PI3-kinase-dependent NO production and enhanced MAPK-dependent ET-1 secretion. These results may reflect pathophysiology in other vascular beds that directly contribute to elevated peripheral vascular resistance and hypertension.

Animals↗

PubMed1990

A tribute to the late Dr. Ryo Shimazu: a chronic bowel allograft model in the rat.

A chronic model of bowel allotransplantation is described. End-to-end microvascular anastomosis between superior mesenteric vessels was utilized. The recipient splenic vein was preserved to avoid postoperative pancreatitis. Euro-Collins solution was used to flush the vasculature in the lumen of the transplant. Low-dose cyclosporine was used for immunosuppression. With experience, 89% long-term survival was achieved.

Anastomosis, Surgical↗

PubMed2003

Leukocyte trafficking in experimental autoimmune uveitis: breakdown of blood-retinal barrier and upregulation of cellular adhesion molecules.

PURPOSE: To clarify the order of events occurring in the breakdown of the blood-retinal barrier (BRB) in experimental autoimmune uveoretinitis (EAU) and in particular to study the relationships between increased vascular permeability, upregulation of endothelial cell adhesion molecules, and leukocyte adhesion and infiltration during EAU. METHODS: B10.RIII mice were immunized with human interphotoreceptor retinoid binding protein (IRBP) peptide 161-180. Changes in the retinal microvasculature were examined on days 3, 6, 7, 8, 9, 10, 16, and 21 postimmunization (pi). Evans blue dye was administered intravenously to assess vascular permeability. Expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, P-selectin, E-selectin, and platelet endothelial cell adhesion molecule (PECAM)-1 was evaluated by in vivo administration of antibody and subsequent immunostaining of retinal wholemounts. Lymphocytes from inguinal lymph nodes of normal and chicken ovalbumin (OVA)- or IRBP peptide-immunized mice at day 5, 6, 7, 8, and 15 pi were labeled in vitro with calcein-AM (C-AM) and infused intravenously into syngeneic recipient mice, which had been immunized with peptide at the same corresponding time point. Wholemount preparations of retinas were observed 24 hours later by confocal microscopy to determine the adhesion and infiltration of lymphocytes. RESULTS: The first observation of an increase in vascular permeability occurred at day 7 pi and was restricted to focal areas of the retinal postcapillary venules of the inner vascular plexus. This progressively extended to the outer vascular plexus at day 9 pi. Specific adhesion of leukocytes to the endothelium of retinal venules of the inner vascular plexus was first observed at day 6 pi. Leukocyte extravasation into the retinal parenchyma from these vessels began at day 8 pi and extended to the outer vascular plexus at day 9 pi. The expression of adhesion molecules increased progressively during the development of EAU. In particular, the adhesion molecules ICAM-1, P-selectin, and E-selectin were expressed predominately in retinal venules, the sites of BRB breakdown, cell adhesion, and extravasation, from day 7 pi. The increases in expression of ICAM-1 and P-selectin were associated both spatially and temporally with breakdown of the BRB, cell adhesion, and extravasation. No increase in expression of P-selectin and ICAM-1 was observed in either the mesenteric vessels of EAU mice or the retinal vessels of OVA-immunized mice. CONCLUSIONS: The sequence of events in EAU appears to be focal adhesion of leukocytes to discrete sites on postcapillary venules, followed by upregulation of adhesion molecules, especially ICAM-1 and P-selectin, and breakdown of the BRB, leading to transendothelial migration of leukocytes and recruitment of large numbers of cells to the retinal parenchyma. These changes occur over a short period of 6 to 9 days pi and initiate the process of tissue damage during the following 2 to 3 weeks.

Animals↗

PubMed1981

[Mesenteric vascular occlusion].

This report concerns 70 cases of occlusion of the mesenteric vessels, 32 arterial and 38 venous. Clinical symptoms and possibilities of therapy are discussed. Operative therapy was carried out in only 19 patients, 5 of whom survived. The time between the first symptoms and the operation essentially influences the prognosis. Postoperative anti-coagulation seems to be significant. The value of a 'second-look' operation is dubious.

Abdomen, Acute↗

PubMed1979

Comparison of the in vitro effects of prazosin, nifedipine, and dihydralazine in isolated human mesenteric and crural vessels.

The inhibitory and relaxing effects of prazosin, nifedipine, and dihydralazine on contractions induced by noradrenaline (NA), or potassium (K+), were investigated in isolated human crural and mesenteric arteries and veins. Vascular ring preparations were suspended in organ baths and isometric tension was recorded. Prazosin was the most potent of the drugs in counteracting NA-induced contractions in all types of vessels except crural veins, in which the effect of nifedipine was the more pronounced. On K+-induced contractions prazosin was completely devoid of relaxing or inhibitory effects, whereas nifedipine was by far the most effective of the investigated drugs. Nifedipine had a more marked effect in venous than in arterial preparations from the peripheral circulation, but no such difference was seen in mesenteric vessels. Dihydralazine was found to have a very low potency in all types of vessels, and no difference between the effects on arterial and venous preparations was found. The results suggest that the in vitro effects of prazosin, nifedpine, and dihydralazine are different from those observed in vivo. Thus, the balance between the effects on arteries and veins in vitro was quite different from those reported in clinical studies on the three vasodilatators. The results give no support to the hypothesis of an unspecific vasodilatating effect of prazosin. The clinical usefulness of dihydralazine cannot be explained from the poor in vitro effects of the unmetabolized drug.

Adolescent↗

PubMed1995

[Nonobstructive mesenteric ischemia--a diagnostic problem in internal intensive care].

Four cases of acute gut ischemia in elderly patients due to non-occlusive disease (NOD) are presented. Bowel necrosis occurred after episodes of hypotension in the course of myocardial infarction, arrhythmias and sepsis. Symptoms and clinical findings were blurred by the underlying extraintestinal disease. Angiography showed coexistent atherosclerosis but no occlusion of the major celiac and mesenteric vessels. At laparotomy (three cases) or autopsy (one case) extensive small and large bowel necroses were detected. Early laparotomy (possibly preceded by laparoscopy) is recommended for patients with suspected acute gut ischemia even if angiography fails to reveal occlusion of the large splanchnic arteries.

Aged↗

PubMed2003

Partial abdominal evisceration, ex vivo resection, and intestinal autotransplantation for the treatment of pathologic lesions of the root of the mesentery.

BACKGROUND: Resection of lesions of the root of the mesentery with established techniques is difficult and at times impossible because of their proximity to the blood supply of the intestine. Damage of the superior mesenteric vessels necessitates resection of the intestine, resulting in short bowel syndrome and intestinal failure. STUDY DESIGN: We describe a surgical technique drawn from our experience in intestinal transplantation in which the root of the mesentery (including the lesion) and the head or the entire pancreas, duodenum, small intestine, and part of the colon are excised en bloc and preserved in a cold solution. Resection of the lesion is performed in a bloodless field ex vivo, and the salvaged intestine is reimplanted in the abdominal cavity. We performed this procedure in four patients, two adult and two pediatric, who had extensive neoplasms of the root of the mesentery. Their underlying diseases were mesenteric fibroma, vascular dysplasia of the root of the mesentery, pancreatic cancer, and desmoid tumor. RESULTS: Local control of the lesions was achieved in all four cases, preserving at the same time enough small intestine to avoid short bowel syndrome. All patients survived the operation and live on enteral nutrition 6 to 49.5 months after the procedure. CONCLUSIONS: The procedure of partial abdominal exenteration, ex vivo resection, and autotransplantation is an extension of our experience with intestinal transplantation. In selected cases, this technique may be useful in the treatment of extensive, otherwise unresectable lesions of the root of the mesentery.

Abdominal Pain↗

PubMed1982

Pindolol--the pharmacology of a partial agonist.

1 Pindolol is a non-selective beta-adrenoceptor blocking agent; its affinity to adrenoceptors in guinea pig atria (beta 1) is not significantly different from that in guinea pig trachea (beta 1 + beta 2) and canine vascular smooth muscle (beta 2). 2 Pindolol displays a striking diversity of agonist activities in isolated tissues. Stimulant effects correspond to 40--50% of the maximum effects of isoprenaline in isolated kitten atria and guinea pig trachea and to only 10% in guinea pig atria. Effects in canine isolated mesenteric vessels are those of a full agonist, maximum responses equaling those of isoprenaline. These findings suggest that the stimulant effects of pindolol are exerted principally on beta 2-adrenoceptors. 3 Cardiac stimulation produced by pindolol in the dog is sufficient to compensate for the cardiac depression resulting from blockade of beta-adrenoceptors in the heart. Reductions in cardiac output and compensatory increases in total peripheral resistance do not occur or are much smaller than those produced by beta-adrenoceptor blocking agents lacking sympathomimetic activity. 4 Pindolol-induced relaxation of bronchial smooth muscle prevents or minimizes the bronchoconstrictor effects of injected spasmogens in the cat. 5 Pindolol has marked vasodilator activity, small doses reducing femoral and mesenteric vascular resistance by approximately 30%. Doses comparable to those used in hypertensive patients lower blood pressure by 20 mmHg in non-anaesthetized dogs.

Animals↗

PubMed1999

Effect of allopurinol on venous endothelial dysfunction after resuscitated hemorrhagic shock.

BACKGROUND: Blood flow deficits contribute to organ dysfunction in patients resuscitated from hemorrhage. AIM: To determine the contribution of xanthine oxidase mediated reperfusion injury to venous endothelial function after resuscitated hemorrhagic shock. METHODS: Rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50mg/kg bolus and a 25mg/kg/h infusion of the xanthine oxidase inhibitor allopurinol (allo) after shock but before resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group (Std) and a non-hemorrhage group (No HS) served as control. Endothelial function was quantified at baseline, 30 min (R30) and 90 min (R90) post resuscitation as a change in mesenteric vessel diameter after topical application of acetylcholine (Ach), an endothelial dependent vasodilator. RESULTS: Resuscitation restored cardiac output and blood pressure in both hemorrhage groups. First order venules (V1) demonstrated a 39% and a 36% reduction in ability to dilate to Ach at R30 and R90 after resuscitation with shed blood and Ringer's lactate (Std). Second order venules (V2) demonstrated a 20% and a 25% reduction in ability to dilate to Ach at R30 and R90 after resuscitation with shed blood and Ringer's lactate (Std). Addition of allopurinol to standard resuscitation attenuated this response resulting in the preservation of endothelial dependent venous vasodilation. CONCLUSIONS: These data suggest that xanthine oxidase mediated ischemia-reperfusion injury contributes to venous endothelial dysfunction in the mesenteric microcirculation after resuscitated hemorrhagic shock. Endothelial function can be preserved by the addition of the xanthine oxidase inhibitor allopurinol to standard resuscitation lending support for its inclusion as an adjunct to resuscitation after hemorrhagic shock.

Allopurinol↗