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PubMed1997

Kinetic analysis of the intestinal iron absorption process in situ. The potential of vascularly autoperfused intestinal loops.

1 Blood sampling from mesenteric venules during absorption in situ is a useful tool to analyse intestinal absorption kinetics and prehepatic metabolism in different sections of the rat small intestine. By use of a micromanipulator, the method can be applied to the duodenum. This part of the small intestine shows the strongest adaptation of non-haem iron absorption to the demand for iron. 2 Iron absorption kinetics was linear in duodenal and jejunal segments. In iron-deficient animals, intestinal iron absorption capacity was increased in the duodenum, while simultaneously determined galactose absorption showed no change. 3 In situ perfusion and cannulation of mesenteric venules in duodenal segments are described. The use of a micromanipulator permits varying the blood volume collected by changing the vertical angle between the cannula and the mesenteric vessel. 4 Intestinal iron absorption rates remained close to constant when blood flow rates were varied by a factor of about ten. Plasma concentrations of absorbed iron vs mesenteric blood flow rates followed a hyperbolic function, as the plasma concentration of absorbed iron in mesenteric venules increased to the same extent as the blood flow decreased. 5 As the plasma transferrin concentration did not change over the experimental period, the concentration of absorbed iron in the mesenteric plasma exceeded the iron-binding capacity of plasma transferrin at low blood flow rates. This observation shows that enhancement of intestinal iron absorption does not require a corresponding increase in plasma iron-binding capacity in the intestinal tissue. 6 Vascularly perfused gut loops were also used to measure prehepatic metabolism, which may influence organotropism of carcinogenic metabolites. Therefore, this type of preparation is likely to find a variety of toxicological applications.

Animals↗

PubMed1999

[Magnetic resonance angiography (MRA) of the abdominal aorta and its branches].

Technical aspects of 3D contrast-enhanced magnetic resonance angiography are exposed, detailing more particularly the pulse sequence used and the mode of injection of contrast agent. Then, various vascular territories are analyzed, and illustrated using various examples of main pathologies observed in routine clinical practice: abdominal aorta, renal arteries, pelvic and mesenteric vessels, and peripheral arteries.

Aneurysm↗

PubMed2002

Preserved endothelium-dependent but impaired beta-adrenergic relaxation of the resistance vessels in experimental renal failure.

Chronic renal failure is associated with increased cardiovascular morbidity and reduced arterial elasticity. Only little information is available on the functional effects of uraemia on resistance arteries. Therefore, we studied the influence of renal failure on rat small mesenteric vessels. The responses of arterial rings were investigated in a Mulvany myograph 6 weeks after 5/6 nephrectomy or sham operation. The subtotal nephrectomy resulted in a 1.9-fold elevation of plasma urea nitrogen but was without significant effect on blood pressure. Endothelium-dependent relaxations, largely mediated via arterial K(+) channels, were preserved in the resistance vessels of uraemic rats. Endothelium-independent vasorelaxations, mediated via exogenous nitric oxide and the opening of ATP-sensitive K(+) channels, were also unchanged. However, the responses induced by isoprenaline were slightly reduced, indicating impaired relaxation via beta-adrenoceptors in experimental renal failure.

Animals↗

PubMedDate not supplied

Contraction of small mesenteric arteries induced by micromolar concentrations of ATP released from caged ATP.

The concentration dependence of ATP-induced contractions in isolated resistance arteries was estimated using photolysis of caged ATP. Rat mesenteric vessels were isolated and mounted for force registration in a small chamber allowing illumination from a xenon-flash lamp. Photolysis of 100 microM caged ATP, which released about 20 microM ATP within a few milliseconds in the vessel, induced a transient contraction with an amplitude approximately 40-50% of the response induced by 10 microM noradrenaline. The responses could neither be induced by the light flash as such nor by caged ATP alone nor by photolysis of caged phosphate. The amplitude of the contractions was dependent on the concentration of caged ATP, and the effective concentration for ATP was estimated to be in the range of 1-10 microM. In contrast, when ATP was introduced by diffusion, about a 100-fold higher concentration was required. Thus photolytic release of ATP minimizes metabolism before its action on receptors and reveals action of ATP in a concentration range consistent with a role of ATP as a transmitter in nervous regulation of the tone of resistance vessels.

Adenosine Triphosphate↗

PubMed1975

A case of carcinoid.

A patient is described with a malignant carcinoid tumour of the ileum with nodal secondaries causing mesenteric vessel occlusion and ileal infarction.

Aged↗

PubMed2003

Pregnancy-induced alterations of vascular function in mouse mesenteric and uterine arteries.

Normal pregnancy involves dramatic changes to maternal vascular function, while abnormal vascular adaptations may contribute to pregnancy-associated diseases such as preeclampsia. Many genetic mouse models have recently emerged to study vascular pathologies of pregnancy. However, vascular adaptations to pregnancy in normal mice are not fully understood. Thus, we studied changes in vascular reactivity during normal mouse pregnancy. We hypothesized that pregnant mice will have enhanced endothelial-dependent vasodilation compared with nonpregnant mice, via an enhancement of the nitric oxide synthase (NOS) prostaglandin H synthase (PGHS), and other endothelial-derived hyperpolarizing pathways. Late pregnant (Day 17-18) C57BL/6J mice (n = 10) were compared with nonpregnant mice (n = 7). Uterine and mesenteric arteries were mounted on a wire myograph system and assessed for endothelium-dependent (methacholine) and -independent (sodium nitroprusside; SNP) relaxation responses. Endothelial-dependent relaxation was enhanced in pregnant uterine and mesenteric arteries, which was blunted after the addition of inhibitors of the PGHS or NOS pathways. In nonpregnant mice, these pathways had no effect in modulating relaxation in uterine arteries, whereas vasodilation in mesenteric arteries was reduced only by NOS inhibition. Both uterine and mesenteric vessels had nonnitric oxide- and nonprostaglandin-mediated relaxation, but this relaxation was not enhanced during pregnancy. Endothelial-independent relaxation was also enhanced in pregnant uterine but not mesenteric arteries. Our data indicate that uterine and mesenteric arteries from pregnant mice have enhanced vasodilation. Understanding vascular adaptations to normal mouse pregnancy is crucial for interpreting changes that may occur in genetic mouse models.

Animals↗

PubMed2003

Mechanisms of vasorelaxation to 17beta-oestradiol in rat arteries.

We have investigated the involvement of the endothelium, K+ channels, oestradiol receptors, and Ca2+ influx in 17beta-oestradiol-induced vasorelaxation in rat mesenteric arterial beds and aortae. 17beta-Oestradiol (10 pM-1 mM) caused acute vasorelaxations in mesenteric arterial beds and aortae from male and female rats. In male rat mesenteric vessels and aortae, the vasorelaxations were mostly independent of the endothelium and nitric oxide (NO). However, indomethacin (10 microM) enhanced the relaxant responses to 17beta-oestradiol. In male rat mesenteric beds, 60 mM KCl, tetrabutylammonium chloride (300 microM), 4-aminopyridine (1 mM), and barium chloride (30 microM), charybdotoxin (100 nM), but not glibenclamide (10 microM) and tamoxifen (10 microM), inhibited vasorelaxation to 17beta-oestradiol. In male rat aortae, 60 mM KCl did not affect vasorelaxation to 17beta-oestradiol. However, in the presence of indomethacin, vasorelaxation to 17beta-oestradiol was enhanced but this was sensitive to 60 mM KCl. Pre-treatment with 17beta-oestradiol (100 microM) inhibited CaCl2-induced contraction. The present findings indicate that, in rat mesenteric beds and aortae, 17beta-oestradiol causes acute and potent vasorelaxation which may be enhanced in the presence of a cyclooxygenase inhibitor. In mesenteric arterial bed, 17beta-oestradiol-induced vasorelaxation occurs primarily via activation of K+ channels. In the aorta, vasorelaxations involved activation of K+ efflux when the cyclooxygenase pathway was inhibited, and also inhibition of Ca2+ influx.

Animals↗

PubMed1988

[Action of adenosine on intestinal motility after experimental mesenteric ischemia in dogs].

The purpose of the present work was to demonstrate beneficial action of adenosine on intestinal motility in the dog after experimental ischemia and to establish the role of A1- and A2-purinergic receptors. Adenosine was compared to an A1-agonist (N6-cyclohexyl-adenosine or CHA), an A2-agonist (5'-(N-ethyl) carboxamido-adenosine or NECA) and an inhibitor of adenosine cellular uptake (dipyridamole). Motility was analyzed by recording the electromyogram with intraparietal electrodes. Experimental ischemia was obtained by clamping the superior mesenteric artery during two hours. Under physiologic conditions, adenosine (1 mg.kg-1.i.v.) increased myoelectric complexes frequency by 49 p. 100 and the jejunal motility index by 46 p. 100. CHA (1 microgram.kg-1.i.v.) and dipyridamole (0.5 mg.kg-1.i.v.) increased myoelectric complexes frequency by 42 p. 100 and 67 p. 100 while NECA (1 microgram.kg-1.i.v.), increased the motility index by 30 p. 100. Adenosine and NECA increased mesenteric arterial blood flow by 35 p. 100 and 57 p. 100 respectively. After a two hours ischemia the return to normal electromyogram was 10.1 +/- 5.7 h. Adenosine (administered 10 min after the end of ischemia) reduced this recovery period to 3.3 +/- 0.8 h, NECA to 1.3 +/- 0.8 h and dipyridamole to 5.0 +/- 2.6 h. We conclude that, under physiological conditions, adenosine modifies jejunal motility directly via A1-receptors of smooth muscle and indirectly via A2-receptors of mesenteric vessels. On the other hand, after experimental ischemia, adenosine improves the post-ischemic restoration via vessels A2-receptors only.

Adenosine↗

PubMed2005

Role of PGI2 and effects of ACE inhibition on the bradykinin potentiation by angiotensin-(1-7) in resistance vessels of SHR.

The present study determined the participation of PGI2 in the angiotensin-(1-7) [Ang-(1-7)]/bradykinin (BK) interaction, in the presence and absence of Angiotensin Converting Enzyme (ACE) inhibition, trying to correlate it with tissue levels of both peptides. The isolated mesenteric arteriolar bed of Spontaneously Hypertensive Rats (SHR) was perfused with Krebs or Krebs plus enalaprilat (10 nM), and drugs were injected alone or in association. BK (10 ng)-induced relaxation was potentiated by Ang-(1-7) (2.2 microg) in the presence or absence of enalaprilat. Ang-(1-7) receptor blockade [A-779 (4.8 microg)] did not interfere with the BK effect in preparations perfused with normal Krebs, but reversed the increased BK relaxation observed after ACE inhibition. PGI2 release by mesenteric vessels was not altered by BK or Ang-(1-7) alone, but was increased when both peptides were injected in association, in the absence or in the presence of enalaprilat. ACE inhibition caused a 2-fold increase in the BK tissue levels, and a significant decrease in the Ang-(1-7) values. We conclude that endogenous Ang-(1-7) has an important contribution to the effect of ACE inhibitors participating in the enhancement of BK response. The mechanism of Ang-(1-7) potentiating effect probably involves an increased production of PGI2. Our results suggest that a different enzymatic pathway (non-related to ACE) is involved in the local Ang-(1-7) metabolism.

Angiotensin I↗

PubMed1976

Isolated mesenteric injury due to blunt abdominal trauma.

Isolated injuries of the small bowel mesentery or mesocolon with subsequent bowel infarction due to blunt abdominal trauma are rare. Two cases are described: 1 involving the mesentery to the terminal ileum and 1 involving the transverse mesocolon and middle colic artery, both with bowel infarction. The modes of clinical presentation and management of patients with injuries to the mesentery, mesocolon and mesenteric vessels following blunt trauma are described.

Abdominal Injuries↗

PubMed1988

Evidence that dopaminergic innervation is not involved in the vasodilatation of cat superior mesenteric arterial bed: the role of beta-adrenoceptors and circulating catecholamines.

In the presence of phentolamine, stimulation of the cat splanchnic nerve decreased the resistance of the superior mesenteric arterial bed. This effect was not significantly influenced by sulpiride. Sulpiride, in the presence of phentolamine, did not inhibit the decrease in resistance in animals pretreated with guanethidine but propranolol or ablation of the adrenal glands prevented the effect of stimulation. These results are not compatible with the assumption that dopamine released from dopaminergic nerves is involved in the vasodilatation but do provide evidence for the role of beta-adrenoceptors and circulating catecholamines in the vasodilatation of mesenteric vessels.

Adrenalectomy↗

PubMed2005

Vascular reactivity of mesenteric arteries and veins to endothelin-1 in a murine model of high blood pressure.

We characterized vascular reactivity to endothelin-1 (ET-1) in mesenteric vessels from DOCA-salt hypertensive and SHAM control mice and assessed the effect that endothelial-derived vasodilators have on ET-1-induced vasoconstriction. Changes in the diameter of unpressurized small mesenteric arteries and veins (100- to 300-microm outside diameter) were measured in vitro using computer-assisted video microscopy. Veins were more sensitive than arteries to the contractile effects of ET-1. There was a decrease in arterial maximal responses (E(max)) compared to veins, this effect was larger in DOCA-salt arteries. The selective ET(B) receptor agonist, sarafotoxin 6c (S6c), contracted DOCA-salt and SHAM veins but did not contract arteries. The ET(B) receptor antagonist, BQ-788 (100 nM), but not the ET(A) receptor antagonist, BQ-610 (100 nM), blocked S6c responses. BQ-610 partially inhibited responses to ET-1 in mesenteric veins from DOCA-salt and SHAM mice while BQ-788 did not affect responses to ET-1. Co-administration of both antagonists inhibited responses to ET-1 to a greater extent than BQ-610 alone suggesting a possible functional interaction between ET(A) and ET(B) receptors. Responses to ET-1 in mesenteric arteries were completely inhibited by BQ-610 while BQ-788 did not affect arterial responses. Nitric oxide synthase inhibition potentiated ET-1 responses in veins from SHAM but not DOCA-salt mice. There was a prominent role for ET-mediated nitric oxide release in DOCA-salt but not SHAM arteries. In summary, these studies showed a differential regulation of ET-1 contractile mechanisms between murine mesenteric arteries and veins.

Algorithms↗

PubMed1993

Mesenteric involvement of thromboangiitis obliterans (Buerger's disease) in a woman.

Although patients with peripheral arterial occlusive disease due to thromboangiitis obliterans (TAO) have been well characterized and the relationship of this disease to tobacco is stressed, little attention has been focused on its ability to involve the mesenteric vasculature and its ability to affect women. We report a rare case of a known TAO female patient who presented with abdominal pain due to inflammatory changes of the mesenteric vessels. The resulting small bowel ischemic changes and formation of intramural gas were demonstrated on a small bowel follow-through and a plain abdominal film. An angiography finally showed a superior mesenteric artery occlusion.

Adult↗

PubMed1992

Direct vascular actions of hydrochlorothiazide and indapamide in isolated small vessels.

The mechanism by which thiazides lower peripheral resistance is unresolved. The aim of this study was to investigate the mechanisms of the acute vasodilator action of hydrochlorothiazide and the 'thiazide-like' diuretic indapamide on human, guinea pig and rat small arteries. Vessels were mounted on a myograph and the relaxation profile of both drugs and interactions with K+ channels and the vascular eicosanoid system were studied. Neither drug had any relaxant effect in rat mesenteric vessels and indapamide did not relax human arteries. Hydrochlorothiazide in both human and guinea pig vessels produced significantly more relaxation of noradrenaline than K(+)-constricted vessels (P less than 0.001). Relaxation to hydrochlorothiazide was reduced in the presence of charybdotoxin. Maximal-induced hydrochlorothiazide relaxation was reduced by 64% in human arteries (P less than 0.001) and by 91% in guinea pig vessels (P less than 0.001). Incubation with glibenclamide and indomethacin had no effect on the relaxant activity of hydrochlorothiazide and indapamide. Indapamide-induced relaxation was unaffected in the presence of charybdotoxin. These results show marked differences in the acute vasodilator action of hydrochlorothiazide and indapamide. There appears to be involvement of Ca(2+)-activated K+ channels in the acute vasorelaxant activity of hydrochlorothiazide.

Animals↗

PubMed1988

Vasodilator responses to alpha-human-atrial natriuretic peptide in isolated omental and pulmonary arteries from rabbit and man.

In isolated vessels from the pulmonary and mesenteric/omental arterial circulations of rabbit and man, the effects of synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were investigated. The vessels had an outer diameter of 0.6-1.2 mm and were contracted by noradrenaline (NA) and prostaglandin (PG) F2 alpha (mesenteric/omental arteries) or by 5-hydroxytryptamine (5-HT) and PGF2 alpha (pulmonary arteries). It was found that in rabbits, mesenteric vessels contracted by NA and PGF2 alpha were not significantly relaxed by alpha-hANP. Rabbit pulmonary vessels contracted by PGF2 alpha or 5-HT were concentration-dependently relaxed by alpha-hANP (maximum 70%). Human omental vessels contracted by NA and PGF2 alpha showed a moderate (30%) relaxation after addition of the peptide. Human pulmonary arteries contracted by 5-HT were relaxed by alpha-hANP almost to baseline, while PGF2 alpha-contracted vessels showed a maximum relaxation of 65%. It is concluded that alpha-hANP has a relatively selective effect on pulmonary arterial vessels from rabbit as well as man. The results suggest that the peptide may be involved in the regulation of pulmonary vascular tone.

Adult↗

PubMed1992

Flow-induced release of adenosine 5'-triphosphate from endothelial cells of the rat mesenteric arterial bed.

Adenosine 5'-triphosphate (ATP) was released into the perfusate of rat isolated mesenteric arterial beds during each of two consecutive increases in flow. There was no significant difference between the amounts of ATP released on each occasion. Substance P was also released into the perfusate by increased flow, although its release was more variable. Removal of the endothelium of the mesenteric vessels with sodium deoxycholate led to a significant reduction (74%) in the amount of ATP released compared with the release before the endothelium had been removed. This suggests that the ATP released into the mesenteric arterial perfusate during increased flow arises from endothelial cells.

Adenosine Triphosphate↗

PubMed2001

[Superior mesenteric vein syndrome: a case of duodenal stenosis caused by atypical malposition of the superior mesenteric vein].

Cases in which mesenteric vessels lead to stenosis of the duodenum are very rare. Several cases have been reported of patients suffering from stenosis of the last third of the duodenum due to a malpositioning of the superior mesenteric artery or the left renal vein. We report a 78-year-old patient who was suffering from dyspepsia, pain in the upper abdominal region, nausea, and vomiting. The medical history revealed that the patient had undergone a subtotal gastrectomy according to Billroth II at the age of 19 because of similar complaints. In the last 20 years the patient had to be laparotomized several times for ileus of the small intestine. Now the patient presented abdominal complaints with nausea and pressure in the upper abdominal region. Assuming an efferent-loop syndrome and adhesions, the patient was laparotomized. We discovered malpositioning of the superior mesenteric vein, leading to stenosis of the superior part of the duodenum. In fact, 60 years ago surgeons performed a duodenojejunostomy, circumvening the stenosis of the duodenum. With a "delay of 60 years", we then performed a subtotal gastrectomy according to Billroth II. The postoperative course was uneventful; the patient had no complaints and increased in body weight. To our knowledge, this is the first time that a stenosis of the duodenum due to malpositioning of the superior mesenteric vein has been observed.

Aged↗

PubMed1999

Transvascular Imaging: Feasibility Study Using a Vector Phased Array Ultrasound Catheter.

BACKGROUND: Transvascular imaging is defined as the acquisition of anatomic and functional information of structures lying beyond the confines of a vascular conduit within which the imaging device resides. Interrogating structures surrounding the vascular conduit is the subject of this feasibility study using a novel underblood, phased array ultrasound-tipped catheter. METHODS: An intravascular catheter (10-F, 3.2-mm-diameter, four-way articulation) tipped with a 5.5- to 10-MHz frequency agile, vector phased array transducer with full Doppler capability (Sequoia, Acuson) was used. The imaging transducer has a wide range of tissue penetration (2 mm to >10 cm from the lens). The catheter was introduced via an 11-Fr femoral venous sheath into the inferior and superior vena cavae and right heart chambers. As the catheter was advanced, attention was directed to visualization of structures surrounding the vessel in which the catheter resided. RESULTS: From the cavae and femoral vein the thoracic, abdominal and femoral arteries could be easily imaged. Anatomy that was visualized included the liver, hepatic veins, gallbladder, and mesenteric vessels. Normal and pathological anatomy and Doppler physiology could be readily appreciated. Doppler (i.e., pulsed- and continuous-wave, color flow, and tissue Doppler) fostered unique transvascular physiological hemodynamic and flow assessment. CONCLUSION: Transvascular imaging is feasible in human subjects using this 10-Fr catheter tipped with a 5.5- to 10-MHz vector phased array transducer. Intravascular navigation to a desired location within the body and the performance of diagnostic or therapeutic procedures at a remote site under direct ultrasound visualization are possible. Full Doppler capability extends the concept of transvascular hemodynamic and physiological assessment.

Journal Article↗