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At least 235 records · Page 13Linked to original sources
PubMed1986

[Effect of interstitial factors on parameters regulating fluid transport through the walls of the mesenteric vessels of the cat].

With the aid of microocclusion technique, hydraulic conductivity and effective pressure were studied in different blood vessels of capillary type in the cat mesenterium. The fluid permeability of the microvessel walls depended on their segmentary type, vector of transmural flux and protein content of surrounding tissue. The greatest value of the hydraulic conductivity was found in the postcapillary venules. The anisotrophic distribution of fluid in the interstitial spece seems to depend on topography of the microvessels with different transport characteristics.

Animals↗
PubMed2004

Multidetector-row CT angiography of the aorta and visceral arteries.

Within recent years, technical developments of multidetector-row CT (MDCT) have dramatically changed the application of CT angiography in the assessment of abdominal vascular pathologies. The simultaneous acquisition of multiple thin collimated slices in combination with enhanced gantry rotation speed offers thin slice coverage of extended volumes without any loss in spatial resolution. Using 4 detector-row CT scanners, the scan volume still has to be restricted and focused on dedicated abdominal vessel territories in order to provide high spatial resolution (1-2 mm), while 16 detector-row technology now enables full abdominal coverage from the diaphragm to the groin with full spatial resolution. Therefore, comprehensive CT angiography of the abdomen can be performed without the necessity of focusing on any vascular territory. This technique enables the evaluation of the whole arterial visceral vasculature (e.g., hepatic vessels, mesenteric vessels, renal arteries) and the aortic-iliac axis in a single data acquisition.

Angiography↗
PubMed1982

Endoscopic bipolar electrocoagulation: development of a new bipolar coagulator for stopping gastrointestinal bleeding.

We have developed an endoscopically deliverable bipolar coagulator with a pair of active bipolar electrodes and tested its efficacy and safety in canine gastric bleeding models. Hemostasis was achieved with a few applications in all "ulcer maker", gastric serosal vessel, mesenteric vessel and endoscopic "hot biopsy" models. Histologically the mean muscular injury was 10.1% in ulcer maker models and 17.1% in hot biopsy models, significantly less than monopolar electrodes. No full thickness injury resulted. Initial clinical trials in 32 patients with upper gastrointestinal bleeding revealed 100% immediate hemostasis; it could stop spurting arterial bleeding. Our bipolar coagulator is a promising addition to the endoscopic hemostatic methods.

Adolescent↗
PubMed1994

Pharmacological characterization of presynaptic calcitonin gene-related peptide (CGRP) receptors on CGRP-containing vasodilator nerves in rat mesenteric resistance vessels.

Rat mesenteric arteries are innervated by calcitonin gene-related peptide (CGRP)-containing vasodilator nerves (CGRP nerves). This study investigated the presence of presynaptic CGRP receptors on CGRP nerves and the receptors' role in the regulation of CGRP release from these nerves. The rat mesenteric vascular bed was perfused with Krebs' solution containing 7 microM methoxamine plus 5 microM guanethidine to produce active tone and block adrenergic neurotransmission. In this preparation, periarterial nerve stimulation (PNS;2 Hz) and bolus infusion of CGRP (50 pmol) caused a decrease in perfusion pressure caused by vasodilation. Vasodilator response to PNS was abolished by 0.3 microM tetrodotoxin and by 1 microM human CGRP[8-37] (CGRP[8-37]), a CGRP receptor antagonist, which also abolished the response to bolus infusion of CGRP. Perfusion of CGRP (0.03-0.5 nM) dose-dependently inhibited vasodilator response to PNS, whereas it did not affect the response to bolus infusion of CGRP. The inhibitory effect of CGRP (0.3 nM) was antagonized by CGRP[8-37] (3 and 10 nM). Lower concentrations of CGRP[8-37] (1-10 nM) potentiated the vasodilator response to PNS, but higher concentrations (100 nM-1 microM) inhibited the response. The vasodilator response to bolus infusion of CGRP was dose-dependently inhibited by CGRP[8-37]. Eel calcitonin (5 and 50 microM), forskolin (0.01 and 0.1 microM), 3-isobutyl-1-methylxanthine (0.3 and 1 microM) and cyclic 8-bromo-adenosine 3':5'-monophosphate (10 and 100 microM) had no effect on the PNS-induced vasodilation. These results suggest that CGRP nerves are endowed with presynaptic CGRP receptors, which regulate CGRP release from the nerves via a negative feedback mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Angiotensin converting enzyme inhibition reduces the expression of transforming growth factor-beta1 and type IV collagen in diabetic vasculopathy.

OBJECTIVE: The purpose of this study was to assess the role of transforming growth factor (TGF)-beta1 in the development of diabetes-associated mesenteric vascular hypertrophy and in the antitrophic effect of angiotensin converting enzyme inhibitors. DESIGN AND METHODS: Streptozotocin-induced diabetic and control Sprague-Dawley rats were randomly allocated to treatment with the angiotensin converting enzyme inhibitor ramipril or to no treatment and were killed 1 or 3 weeks after the streptozotocin injection. Blood was collected and mesenteric vessels removed. Mesenteric vascular weight was measured and TGF-beta1 and alpha1 (type IV) collagen messenger (m)RNA levels were analysed by Northern analysis. Immunohistochemical analyses for TGF-beta1 and type IV collagen were also performed. RESULTS: The diabetic rats had increased mesenteric vessel weight at 3 weeks but not at 1 week and a concomitant rise in mesenteric TGF-beta1 and in alpha1 (type IV) collagen mRNA levels. Ramipril treatment attenuated mesenteric vessel hypertrophy and prevented the increase in TGF-beta1 and alpha1 (type IV) collagen mRNA levels after 3 weeks of diabetes. The immunohistochemical analysis revealed that diabetes was associated with increased TGF-beta1 and type IV collagen protein and extracellular matrix accumulation in mesenteric vessels, and this increase was reduced by ramipril treatment. CONCLUSIONS: These results support the concept that TGF-beta is involved in the changes associated with diabetic vascular disease, and suggest a mechanism by which angiotensin converting enzyme inhibitors exert their antitrophic effects.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Measurement of flow characteristics during individual contractions in bovine mesenteric lymphatic vessels.

We developed a novel technique for measuring flow characteristics during individual contractions in lymph vessels. Bovine mesenteric lymph vessel segments (n = 15) were mounted in organ baths and allowed to equilibrate for 1 hr. Transmural pressure was subsequently increased by 2 cm H2O increments at 15 min intervals and vessel outputs were collected during the final 10 min of each period and measured. Flow also was continuously recorded with an in-line Doppler transducer connected to a flow analyzer, and flow characteristics were analyzed. The two methods of flow measurement correlated well (r2 = 0.92). Mean flow increased with increasing transmural pressure and reached a maximum of 0.5 +/- 0.1 ml/min at a transmural pressure of 8 cm H2O. The rate of spontaneous contractions, the peak flow during a contraction-induced wave, and the total volume of flow during a wave also increased with increasing transmural pressure and reached maximums of 12.4 +/- 1.0 min-1, 8.2 +/- 1.6 ml/min, and 0.21 +/- 0.06 ml, respectively. Wave duration changed little in response to changes in transmural pressure. Continuous in-line flow measurement is an accurate technique for assessing flow characteristics during individual contractions in lymph vessels in vitro. Transmural pressure regulates flow by influencing spontaneous contraction frequency and total and peak flows during contraction-induced waves.

Animals↗
PubMed2000

Method for dissection of mesenteric metastases in mid-gut carcinoid tumors.

With adequate medical management the midgut carcinoid tumor generally is an indolent malignancy associated with substantial life expectancy and appreciable life quality, even in the presence of liver metastases and significant tumor burden. Abdominal complications may occur in this entity of carcinoids owing to entrapment of intestines and encasement of mesenteric vessels by mesenteric metastases and associated marked mesenteric fibrosis. This may be the cause of abdominal pain, disabling diarrhea, weight loss to the extent of malnutrition, and eventually the risk of death with acute or chronic intestinal obstruction or intestinal gangrene. Operative removal of the mesentericointestinal lesion is often indicated to prevent or treat these complications but may be technically difficult when mesenteric metastases extend in the vicinity of major vessels in the mesenteric root. At laparotomy 56 patients with advanced midgut carcinoids underwent removal of the mesenteric tumor with a method for preserving the mesenteric vessels. This was feasible by mobilizing and releasing the right colon and mesenteric root from posterior adhesions, identifying the mesenteric artery below the pancreas, and free-dissecting this artery on the tumor capsule in the mobilized mesentery. Dissection was successful even with tumors initially judged inoperable unless tumor growth completely surrounded the mesenteric vessels or extended retroperitoneally. One patient was subjected to distal intestinal artery bypass. Symptom relief was been substantial and often of long duration after mesenteric tumor removal in patients who prior to surgery often had threatening intestinal ischemia. Patients with advanced midgut carcinoids may benefit markedly from dissectional removal of mesenteric tumors, which (conceivably better than conventional wedge resection) preserves the length of the remaining intestine.

Angiography↗
PubMed1975

Degeneration and regeneration of adrenergic nerves in mesenteric blood vessels, iris and atrium of the rat after 6-hydroxydopamine injection.

Degeneration of adrenergic axons after 6-hydroxydopamine (6-OH-DA), 2 times 68 mg kg-1 i.v. within 6h, and the subsequent regeneration process over the following 205 days were studied in rat mesenteric vessels, wight atria and irides, using the histochemical fluorescence method of Falck and Hillarp. The objective of the study was to determine why noradrenaline is less depleted and recovers much more rapidly in the mesentery than in other tissues after 6-OH-DA (Finch et al., 1973). The mesentery was further studied by electron microscopy and noradrenaline content analyses, until day 29 after 6-OH-DA treatment. Virtually all adrenergic terminal axons in these tissues were destroyed one day after 6-OH-DA. The large nonterminal axon bundles which occur along the mesenteric vessels and rarely in the heart survived and revealed an intensified catecholamine fluorescence; correspondingly, the mesenteric noradrenaline content was only reduced to 29% of control values. In contrast, such large nonterminal axon bundles were not observed in control iris preparations, and no adrenergic fibres survived in the irides, as suggested by fluorescence microscopy. Regenerating axons were observed in all organs after 3-8 days. The number of nerve terminals along the circumference of the external elastic lamina, as observed in ultrathin cross sections of mesenteric vessels, appeared virtually normal 4 weeks after treatment. Meanwhile, the noradrenaline content of the mesentery returned to approximately 85% of control values. As suggested by fluorescence microscopy, complete adrenergic regeneration occurred in mesenteric vessels between days 46 and 105, while regeneration in atrium and iris was incomplete even at day 205; The density of adrenergic axons in the iris, morphometrically determined, was only 76% and 88% of controls on days 160 and 205, respectively. The survival of the many large nonterminal axon bundles in the mesentery with increased NA content explains the relatively small NA depletion of the mesentery; The rapid recovery of the mesenteric NA content is due to faster regeneration of adrenergic terminal axons in the mesentery as compared with iris and atrium. This is tentatively explained in terms of sprouting from the large axon bundles surviving close to the destroyed terminal axons of the mesenteric vessels, whereas in the other tissues no (iris) or only a few (atrium) large nonterminal axon bundles occur and persist to act as a source of quickly regenerated terminal axons.

Animals↗
PubMed1988

The origin and distribution of 5-hydroxytryptamine-like immunoreactive nerve fibres to major mesenteric blood vessels of the rat.

5-Hydroxytryptamine-like immunoreactive nerve plexuses were demonstrated by indirect immunofluorescence histochemistry in whole-mount preparations and cryostat sections of blood vessels from the mesenteric vasculature of the adult rat. The major veins showed a density of innervation greater than that of the accompanying arteries. Removal of the coeliac-superior mesenteric ganglion complex resulted in almost total loss of 5-hydroxytryptamine-like immunoreactive nerves from superior mesenteric blood vessels. The results of crush lesions applied to distal vessels of the superior mesentery indicate that there were no 5-hydroxytryptamine-like immunoreactive nerve fibres extending from the enteric nervous system to these vessels. The administration of 6-hydroxydopamine resulted in a large reduction in the noradrenergic innervation, accompanied by a similar fall in the number of 5-hydroxytryptamine-like immunoreactive nerve fibres. It is suggested that the cell bodies of the 5-hydroxytryptamine-like immunoreactive nerve fibres demonstrated in the superior mesenteric vasculature are located within the sympathetic ganglia which supply the noradrenergic innervation to the same region and that the 5-hydroxytryptamine-like immunoreactivity may be co-localized with noradrenaline within sympathetic nerve fibres.

Animals↗
PubMed1988

Cellular hypertrophy in mesenteric resistance vessels from renal hypertensive rats.

To determine whether the increased thickness seen in media of mesenteric resistance vessels of Wistar-Kyoto rats made hypertensive by a Goldblatt procedure (one-kidney, one clip model) was due to hypertrophy or hyperplasia of smooth muscle cells, the cellular dimensions of these vessels were estimated using a new, unbiased stereological method (the disector). Furthermore, to investigate whether the changes seen could be secondary to the increased blood pressure, morphometric measurements were also made in renal arcuate arteries, which, due to the constricting silver clip, probably had not been exposed to the increased pressure load. Vessels were mounted on a myograph, and their media thickness, lumen diameter, and maximum active wall tension response were measured. In the mesenteric vessels media thickness had increased by 58%, whereas no changes were seen in the renal vessels. Vessels were then fixed, and serial sections were made in the mesenteric vessels. The disector was used to calculate the numerical cell density in each vessel. By combining the myograph measurements and the estimated numerical cell density, the number of cells per segment unit length was calculated (renal hypertensive rats, 6.8 micron-1; sham-operated Wistar-Kyoto rats, 6.3 micron-1; p greater than 0.40) and mean cell volume was determined (renal hypertensive rats, 1541 micron 3; sham-operated Wistar-Kyoto rats, 1256 micron 3; p less than 0.02). No morphometrical changes were found in single sections of the renal arteries. We conclude that the increased media thickness observed in mesenteric resistance vessels of one-kidney, one clip Goldblatt hypertensive rats mainly was caused by smooth muscle cell hypertrophy.

Animals↗
PubMed2000

SPARC gene expression is increased in diabetes-related mesenteric vascular hypertrophy.

The anti-adhesive extracellular matrix protein SPARC (secreted protein and rich in cysteine; osteonectin or BM-40) has been implicated in the regulation of matrix turnover, cell migration, and proliferation. The present study sought to examine whether modulation in the expression of this protein may play a role in diabetes-associated vascular remodeling. SPARC mRNA and protein were measured in mesenteric vessels of diabetic rats and controls. Hypertrophy of mesenteric vessels was noted after 3 and 32 weeks of diabetes as revealed by the increase in mesenteric vessel wet weight and an increased wall/lumen ratio. SPARC mRNA was sparsely present in intima and adventitia of control vessels. There was a marked increase in SPARC gene expression in the intima and adventitia of mesenteric vessels after 1, 3, and 32 weeks of diabetes. SPARC protein was demonstrated in the vessel wall in control animals and was increased in the mesenteric vessels of diabetic rats after 1 and 32 weeks of diabetes. Administration of the inhibitor of advanced glycation end-product formation, aminoguanidine, to diabetic rats attenuated both the hypertrophic response in mesenteric vessels and the overexpression of SPARC mRNA and protein without affecting glycemic control or food intake. In summary, diabetes-related mesenteric vascular hypertrophy is associated with an increase in SPARC expression in the vessel wall. The modulation of SPARC expression in mesenteric vessels of diabetic rats might be of pathogenetic significance in the development of vascular remodeling in diabetes.

Animals↗
PubMed2004

Eplerenone blocks nongenomic effects of aldosterone on the Na+/H+ exchanger, intracellular Ca2+ levels, and vasoconstriction in mesenteric resistance vessels.

There is increasing evidence for rapid nongenomic effects of aldosterone. Aldosterone has been demonstrated to alter intracellular pH and calcium in isolated cells. However, few studies have correlated these effects with aldosterone-mediated physiological responses. Therefore, we studied rapid effects of aldosterone on vascular reactivity, intracellular Ca2+, and pH in resistance vessels. Furthermore, we explored whether the new antimineralocorticoid drug eplerenone could effectively block nongenomic aldosterone-mediated effects. The vasoconstrictor action of aldosterone was examined directly by determining the diameter of small resistance mesenteric vessels (160-200 microm resting diameter), simultaneously with intracellular pH or Ca2+. Aldosterone (10 nm) caused a rapid constriction of resistance vessels (8.1% +/- 1.0% reduction in the diameter below control conditions, P < 0.05). Aldosterone potentiated phenylephrine-mediated constriction in small and large mesenteric vessels. Aldosterone induced a rapid increase of intracellular Ca2+ and cellular alkalinization. Vasoconstrictor action of aldosterone and nongenomic effects on the sodium-proton exchanger (NHE1) activity or intracellular Ca2+ responses was abolished by eplerenone. The vasoconstrictor response of aldosterone was related to phosphatidylinositol 3-kinase (PI3-K): the hormone decreased protein kinase B phosphorylation; pharmacological inhibition of PI3-K (10 microm LY294002 or 1 microm wortmannin) increased arterial contractility. Inhibitors of ERK 1/2 phosphorylation (15 microm PD98059) had no effect on aldosterone-mediated vasoconstriction. Inhibition of protein kinase C with 1 microm bi-sindolylmaleimide I and/or inhibition of NHE1 with 100 microm amiloride abolished aldosterone vasoconstrictor action of resistance mesenteric arteries. We conclude that aldosterone-mediated increase in vascular tone is related to a nongenomic mechanism that involves protein kinase C, PI3-K, and NHE1 activity. Eplerenone is an effective blocker of nongenomic effects of aldosterone in vascular tissue.

Aldosterone↗
PubMed1985

Vascular changes at the prehypertensive phase in the mesenteric arteries from spontaneously hypertensive rats.

Morphometric measurements of three categories of mesenteric vessels (representing elastic, muscular and arteriolar vessels) from prehypertensive spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) were carried out at the light and electron microscope levels. Structural alterations of the blood vessels were already present in the SHR, even though the blood pressure was not yet elevated as compared with age-matched WKY. No change was found in the elastic vessels (superior mesenteric artery). Among the muscular arteries (i.e. large mesenteric arteries), the increase in vessel wall cross-sectional area was due to the increase in the intima, media and adventitia. Increase in media was due to hyperplasia of the smooth muscle cells. The smooth muscle cells were not hypertrophied. Nerve density was also higher in the large mesenteric arteries of SHR. In the arteriolar vessels (i.e. small mesenteric arteries), wall to lumen ratio, as well as media to lumen ratio, were increased in the SHR. The number of smooth muscle cell layers was also increased. In all these vessel types, the cross-sectional area of the lumen under maximal relaxation was similar between SHR and WKY, except in small mesenteric arteries where the lumen was smaller in the SHR. Our results suggest that structural alteration of the blood vessels at the prehypertensive phase may be one of the contributing factors leading to the development of hypertension in the SHR.

Age Factors↗