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At least 37 records · Page 2Linked to original sources
PubMed1992

Effects of long-term laxative treatment on neuropeptides in rat mesenteric vessels and caecum.

In order to investigate the toxic effects of long-term treatment with anthraquinone laxatives, rats were fed either chocolate alone, or chocolate adulterated with senna or danthron (1,8-dihydroxyanthraquinone) for 5 months. Mesenteric blood vessels and the outer muscle layers of the caecum, together with the myenteric plexus, were examined using ultrastructural, histochemical, immunohistochemical and immunoassay techniques. There was no ultrastructural evidence of degeneration in either the mesenteric vessels or the caecum. In the mesenteric vessels, levels of neuropeptide Y were significantly reduced in the danthron-fed rats, but levels of substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were unaffected by all treatments. In the caecum, VIP-, SP- and CGRP-immunoreactivity and catecholamine-fluorescence were unchanged by the laxative treatments.

Animals↗
PubMed1975

Intestinal atresia in fetal dogs produced by localized ligation of mesenteric vessels.

Experimental ileal atresia and stenosis were produced by a localized ligation of the mesenteric vessels in fetuses from 13 pregnant mongrel dogs having gestational ages of 45-55 days. The intestinal infarct in the fetus was characterized by an aseptic coagulation necrosis selectively limited to the mucosa and submucosa, and also by intense hyperemia and minimal cellular reaction in the adjacent tissue. Eleven days after the devascularization, type 2 intestinal atresia, in which there is a long cord between the blunt ends microscopically similar to that seen in humans.

Animals↗
PubMed1989

[Acute obstruction of the mesenteric vessels--a diagnostic and therapeutic problem].

Analysis was made of 175 patients treated for acute obstruction of the mesenteric vessels. The incidence was higher in males (male/female ratio = 2.5/l) and in winter--62 per cent of the cases. An the basis of thorough analysis of the most common diseases responsible for thrombus formation and thromboembolism and the basic symptoms in the clinical picture, ad ot table was elaborated for early diagnosis of acute obstruction of mesenterial vessels, enabling to take quick decision even without angiography. The level of obstruction in 57 per cent of the patients was in the stem of the mesenterial arteries; conclusion is hence made that, when possible, only reconstructive vascular operation associated or not with intestinal resection, will lead to permanent cure. Of all 175 patients in this series, 81 (46.5 per cent) were operated and 68 of them (83.9 per cent) died; only 13 survived (16 per cent). All of the unoperated 94 patients (53.5 per cent) died. Hence, a total of 162 patients died (92.6 per cent) and 13 survived (7.4 per cent).

Acute Disease↗
PubMed1987

[Inhibition of the formation of platelet thrombus by molsidomine and SIN-1 in the mesenteric vessels rats].

Molsidomine and SIN-1 were tested in a thrombosis model in which thrombi are produced in small mesenteric vessels. An interference contrast system based on a Leitz Orthoplan microscope was used to visualize thrombus formation. Vascular lesions were produced with a Coherent CR-Z supergraphite ion laser (Argon laser) in vessel of 20-30 micron diameter. Molsidomine and SIN-1 i.v. at doses of 0.1 and 0.5 mg/kg had a marked and significant antithrombotic effect in arterioles and in venules. Molsidomine at doses of 0.1 and 0.5 mg/kg had no antithrombotic effect 90 min following intravenous injection.

Animals↗
PubMed1981

Effects of vasopressin on smooth muscle cells of guinea-pig mesenteric vessels.

1 The effects of vasopressin on the membrane and contractile properties of smooth muscle cells of guinea-pig mesenteric arteries, and mesenteric and portal veins were investigated in various ionic environments by means of a micro-electrode technique and an isometric tension recording method. The results were compared with those obtained with oxytocin and noradrenaline (NA).2 In the mesenteric jejunal artery, the mean membrane potential was -56.6 +/- 2.3 mV, s.d, and the membrane was electrically quiescent. Application of outward current pulses generated small graded responses, and the current voltage relationship was linear with application of an inward current pulse.3 Vasopressin and NA depolarized the membrane and increased the membrane resistance. Vasopressin was a 1000 times more potent than oxytocin in depolarizing the membrane. In high concentrations, vasopressin (1 x 10(-3) or 1 x 10(-2) iu/ml) or NA (5.9 x 10(-5) M) generated slow oscillatory membrane potential changes (slow waves) and spikes during the depolarization. The excitatory actions of vasopressin and NA were not suppressed by tetrodotoxin (3.1 x 10(-7) M) or ouabain (1.3 x 10(-6) M) and the actions of vasopressin were not suppressed by adrenoceptor blocking agents (3.9 x 10(-7) M phentolamine or 3.6 x 10(-7) M propranolol).4 The depolarization induced by vasopressin or NA is mainly due to a decrease in the K-permeability of the membrane. However, the contribution of other ionic species to the depolarization induced by vasopressin or NA differed, e.g. in low concentrations of [Na](o), the NA-induced depolarization was suppressed to a greater extent than that due to vasopressin. In low concentrations of [Ca](o), the vasopressin-induced depolarization was suppressed to a greater extent than with NA.5 In low concentrations of [Ca](o) and in the presence of vasopressin or NA, spike generation was inhibited but slow waves were not. In low concentrations of [Na](o), the vasopressin-induced slow waves and spikes were for the great part preserved, but with a high concentration of [Ca](o), vasopressing-induced slow waves were suppressed.6 Both vasopressin and NA produced contractions in the jejunal mesenteric artery. However, the maximum contraction in response to vasopressin was larger than that to NA, although both induced similar membrane depolarization. In a low concentration of [Na](o), vasopressin but not NA produced a contraction.7 In the cranial mesenteric artery, NA (5.9 x 10(-5) M) depolarized the membrane and produced a contraction, while vasopressin (1 x 10(-1) iu/ml) and oxytocin (1 x 10(-1) iu/ml) neither depolarized the member nor produced a contraction. In the mesenteric vein, NA (5.9 x 10(-5) M) slightly depolarized the membrane and produced a small contraction. On the other hand, in the portal vein, NA (5.9 x 10(-7) M) produced a marked depolarization and a contraction. Vasopressin (1 x 10(-1) iu/ml) and oxytocin (1 x 10(-1) iu/ml) produced neither excitatory nor inhibitory actions in these veins.8 It is concluded that vasopressin acts on only small muscular arteries, while NA acts on all mesenteric vessels, particularly the portal vein. Therefore, the hepatic portal vascular resistance may be increased by NA and reduced by vasopressin.

Animals↗
PubMed1988

N-acetyl-leukotriene E4 is a potent constrictor of rat mesenteric vessels.

N-Acetyl-leukotriene E4 administered to conscious freely moving rats produced a dose-dependent vasoconstriction in the mesenteric vessels which led to profound reduction of blood flow to the gut. Renal and hindquarter blood flow and vascular resistance were not affected even by high doses of N-Acetyl-leukotriene E4. N-Acetyl-leukotriene E4 was 10-fold more potent than the thromboxane analog U-46619 and 1000-fold more potent than prostaglandin F2 alpha but 2-5-fold less potent than leukotriene D4/E4 to induce mesenteric vasoconstriction. These data indicate that N-acetyl-leukotriene E4 is a biologically active metabolite of peptide leukotrienes, and might play a role in cardiovascular derangements mediated by leukotrienes.

Animals↗
PubMedDate not supplied

Effect of troxerutin on laser-induced thrombus formation in rat mesenteric vessels, coagulation parameters and platelet function.

The antithrombotic effect of Troxerutin have been studied in an experimental model of thrombosis in which rat mesenteric vessels (arterioles and venules) 25-30 microns in diameter were injured by well defined argon laser lesions. Furthermore in vitro effect of this agent on coagulation parameters (IIa, Xa inhibition, TT, heptest), and platelet function (platelet adhesion to the siliconised glass and extracellular matrix, platelet spreading) has been investigated 2 h after oral drug administration. Troxerutin at a dose of 10 mg/kg markedly inhibited thrombus formation in venules. Higher dose (50 mg/kg) was needed to obtain the same antithrombotic effect when arterioles were studied. After application of a single dose of Troxerutin (100 mg/kg) antithrombotic effect lasted for 6 h to 7.5 h when venules were studied, and for 4.5 h to 6 h when arterioles were investigated. In in vitro study we did not observe any effect of Troxerutin on coagulation parameters. In concentrations of 100 micrograms/ml in platelet rich plasma Troxerutin significantly inhibited platelet adhesion to the extracellular matrix and siliconised glass as well as platelet spreading. It is likely that this drug possesses antithrombotic effect evaluated by inhibition of platelet function and protection of endothelial cells.

Animals↗
PubMed1984

[Changes in gastric mucosa, liver and mesenteric vessels following bipolar electrocoagulation].

The implications of bipolar electrocoagulation with a modified probe (BICAP) were tested in rat gastric mucosa, liver tissue and mesenteric vessels. This was done during the coagulation and at different intervals, up to 14 days later, by intravital microscopy of the exposed organs. A histological treatment of the respective tissues ensued at the closing of each experiment. Applying a current of 25 watt and contact times lasting for 5 secs and longer, perfect tissue necrosis develops which has clean and straight edges. The extensions on the surface and into the depth of gastric mucosa match precisely the contact area with the instrument. In the deeper mucosal layers there is a fungiform spread of necrosis while in the liver it remains uniform and shows the same diameter as on the surface. As a late result and notwithstanding the confinement of the coagulation to the mucous membrane, a local peritonitis may develop. Within contractile vessels the action of bipolar coagulation stops the blood flow which is only irreversible, when the current and contact times are extended to bring about necrosis in neighbouring tissue. Within the microcirculation of the liver the blood flow is preserved up to the very boundary of the necrosis.

Animals↗
PubMed2001

Lead-cadmium interaction effect on the responsiveness of rat mesenteric vessels to norepinephrine and angiotensin II.

The comparison of the reactivity to norepinephrine (NE) and angiotensin II (A II) of isolated mesenteric blood vessels obtained from rats simultaneously poisoned with lead and cadmium to those responses of rats treated singly with lead or cadmium was performed. Male Buffalo rats aged 6-8 weeks were administered intragastrically with lead (35 mg Pb/kg body wt.) and/or cadmium (5 mg Cd/body wt.), once a week for a period of 7 weeks. Control rats were given equimolar amounts of sodium acetate and/or sodium chloride. Changes in mesenteric vascular resistance due to NE and A II injections were measured ex vivo as an increase in perfusion pressure in vessels prepared by McGregor's method. The dose-response curve for NE (0.01-5.0 microg) determined for vessels of rats poisoned simultaneously with lead and cadmium was shifted to the left in comparison to controls (not poisoned rats), similarly to these determined for rats poisoned with lead or cadmium. ED(50) NE pointed out in the control group (0.83+/-0.5 microg) was significantly greater than in metal treated groups (0.44+/-0.09; 0.45+/-0.26 and 0.5+/-0.11 microg in lead, cadmium, lead and cadmium-treated rats, respectively). This study indicated a tachyphylaxis in responses of isolated mesenteric vessels to A II injected in increasing doses, and the weaker, in comparison to controls, response of vessels of rats poisoned with lead and/or cadmium to A II at a dose of 0.4 microg. The decreasing response to A II could result from changes in calcium ions transport through L-type channels in vascular smooth muscle cells, because verapamil (2.0 microM) inhibited the A II-induced vasoconstriction more weakly in rats poisoned with metals than in controls. Inhibitor of prostaglandins synthesis, ketoprofen (200 microg/ml per min.) attenuated the pressor effect of NE in blood vessels obtained from all rats, but this effect was less potent in arteries of cadmium poisoned rats. Ketoprofen also inhibited the vasoconstrictory action of A II in all groups, but this effect was lower in vessels of rats poisoned simultaneously with lead and cadmium. We suggest that the release of vasoactive prostaglandins as a consequence of endothelial angiotensin receptor stimulation changes more under the influence of metals administered to rats simultaneously than under the influence or lead or cadmium administered singly. Treatment with a nitric oxide synthase inhibitor (L-NOARG; 22 microg/ml per min.) potentiated a NE-induced pressor response in all groups. However, the increase in perfusion pressure was greater in rats poisoned with cadmium in comparison to controls. L-NOARG potentiated the A II induced vasoconstriction only in cadmium poisoned rats, also indicating a greater influence of nitric oxide in cadmium treated rat vasculature. Two-way ANOVA showed the existence of lead-cadmium interactions effects on the reactivity of rat isolated mesenteric vessels to NE, A II and papaverine.

Analysis of Variance↗
PubMed2003

MDCT of renal and mesenteric vessels.

Computed tomography angiography (CTA) with multiple detector-row CT (MDCT) has evolved into an established technique for non-invasive imaging of renal and mesenteric vessels. With adequate selection of acquisition parameters (thin collimation) high spatial-resolution volumetric data sets for subsequent 2D and 3D reformation can be acquired. Contrast medium (CM) injection parameters need to be adjusted to the acquisition speed of the scanners. Whereas fast acquisitions allow a reduction of total CM volume in the setting of CTA, this is not the case when CTA is combined with a second-phase abdominal MDCT acquisition for parenchymal (e.g., hepatic) imaging. Renal CTA is an accurate and reliable test for visualizing vascular anatomy and renal artery stenosis, and therefore a viable alternative to MRA in the assessment of patients with renovascular hypertension and in potential living related renal donors. CTA, combined with abdominal/parenchymal MDCT is a first-line diagnostic test in patients with suspected abdominal vascular emergencies, such as acute mesenteric ischemia, and an excellent tool to assess a wide variety of vascular abnormalities of the abdominal viscera.

Acute Disease↗
PubMed1997

Effect of angiotensin II on the reactivity of isolated mesenteric vessels to norepinephrine in rats poisoned with cadmium.

This study was designed to investigate the effect of cadmium on vascular response to norepinephrine (NE) administered before and during infusion of angiotensin II. The experiments were performed on isolated mesenteric vessels obtained from rats administered cadmium chloride intragastrically in doses of 20 mg Cd/kg body wt. once a week for 7 weeks. Changes in mesenteric vascular resistance due to NE were measured in the constant flow system as an increase in perfusion pressure. There was significant difference in the 50% effective doses (ED50) for NE between the two groups of rats when the dose-response curves were normalized to their respective maximal responses: ED50 NE for cadmium-exposed rats was lower and the dose-response curve was shifted to the left. Another change indicating an increased vasoconstrictor action of NE due to cadmium is more effective potentiation of exogenous NE responses produced by angiotensin II infused in dose of 5 mg/ml. In contrast to the controls in cadmium poisoned rats, propranolol in a dose of 300 ng/ml did not change significantly the vasoconstrictor response to NE and diminished the difference between angiotensin effect in vessels. Nifedipine (100 ng/ml), infused together with angiotensin II, inhibited pressor response to norepinephrine in preparation from both control and cadmium treated rats, to 60.5% and 69.3%, respectively. These results suggest an increase in the postsynaptic alpha adrenergic response and show a stronger potentiation of exogenous NE responses produced by angiotensin II, probably due to its influence on the calcium homeostasis in vessels of cadmium poisoned rats.

Analysis of Variance↗
PubMed1977

Midgut volvulus with secondary thrombosis of superior mesenteric vessels in a pregnant woman.

An anomaly of the position of the midgut in a pregnant woman predisposes to volvulus. Vascular repair, despite the abdominal catastrophe, sometimes allows parts of the intestine to be saved. A case of volvulus in a pregnant woman is described. At operation, 18 hours after onset, two anomalies were found: reverse rotation of the midgut and an anomaly of the collecting system of the superior mesenteric vein. Most of the midgut was infarcted. Thrombi were removed from the superior mesenteric vessels, and a portion of the anamalous superior mesenteric vein was reconstructed. All but 3 M. of the small bowel and the entire right colon were resected. Prolonged treatment with parenteral hyperalimentation enabled us to control the appearance of a moderate degree of malabsorption. To our knowledge, no similar case has been reported previously in the literature.

Adult↗
PubMed1985

Zinc and vascular reactivity in rat mesenteric vessels: possible altered dihomo-gamma-linolenic acid metabolism in spontaneously hypertensive rats.

Zinc at a concentration of 0.4 microgram/ml potentiated pressor responses to norepinephrine in isolated perfused mesenteric vessels of SHR and WKY. At a higher concentration, 3.2 micrograms/ml, it inhibited responses to norepinephrine in WKY but produced no such inhibition in SHR. However, a transient potentiation was observed in SHR with the higher concentration. Pressor responses to potassium in WKY were not affected by zinc at either concentration. In SHR, however, the higher dose of zinc inhibited pressor responses to potassium. The low dose had no effect. Since effects of zinc may be mediated by release of DGLA, we suggest that in SHR DGLA release may be impaired.

8,11,14-Eicosatrienoic Acid↗
PubMed1989

A PAF-acether antagonist (N 48740 RP/Rhône-Poulenc) and laser-induced thrombi in rat mesenteric vessels.

N 48740 RP, a pyrrolo(1,2-c)thiazole derivative and platelet-activating factor inhibitor, was tested in a thrombosis model, in which thrombi are produced in small rat mesenteric vessels. A phase contrast system, based on a Leitz Orthoplan microscope, was used to visualize thrombus formation. Vascular lesions were produced with a Coherent CR-2 supergraphite ion laser (argon laser) in vessels of 25-35 microns diameter. The results show a dose-dependent (5-20 mg/kg i.v.) antithrombotic effect of N 48740 RP which reaches its maximum between 30 min and 2 h after the injection and slowly decreases during the following 24-48 h.

Animals↗
PubMed1990

Alpha-adrenoceptors in dog mesenteric vessels--subcellular distribution and number of [3H]prazosin and [3H]rauwolscine binding sites.

Binding of the alpha-adrenergic antagonists [3H]prazosin and [3H]rauwolscine to well-characterized subcellular membrane fractions isolated from dog mesenteric arteries and veins was studied. Binding of both ligands was saturable with Kd values of 0.5 +/- 0.1 nM for [3H]prazosin and 5.85 +/- 0.85 nM for [3H]rauwolscine in arteries, and 0.87 +/- 0.4 nM for [3H]prazosin and 6.6 +/- 1.5 nM for [3H]rauwolscine in veins. In veins, the maximum number of binding sites for [3H]rauwolscine was higher than that for [3H]prazosin, whereas in arteries the maximum number of binding sites for each ligand was similar. In microsomes from dog aorta, the maximum number of bindings sites for [3H]prazosin was higher than that for [3H]rauwolscine. Neuronal membrane contamination in these studies was minimized by dissection procedures and evaluated by the comparison of [3H]saxitoxin binding in various preparations. Only mesenteric veins responded functionally to agonists acting on alpha 2 adrenoceptors. This study thus identified two distinct populations of [3H]prazosin and [3H]rauwolscine binding sites in the plasma membranes of dog mesenteric vessels and suggests that a much higher density of alpha 2-compared to alpha 1-adrenoceptor binding sites is required for a contractile response.

Animals↗
PubMed1985

[Effect of the chronic use of propranolol on the specific binding of 3H-WB-4101 with the membranes of the mesenteric vessels in rats].

It has been shown that the 15-bay use of dl-propranolol (100 mg/kg a day) leads to a significant increase in the dissociation constant (CD) of the sites of specific binding of 3H-WB-4101 with membranes of rat mesenteric vessels. The concentration (Bmax) of the binding sites does not significantly change. Propranolol and other adrenoblockers do not possess any affinity for alpha-adrenoreceptors of rat brain synaptic membranes, i.e. changes in the properties of these receptors in vascular membranes cannot be accounted for by the direct action of propranolol in vivo or by the influence of the drug left in the membranes in vitro. It is concluded that desensitization of alpha1-adrenoreceptors of the peripheral vessels may be an essential element in the mechanism of the hypotensive action under the chronic use of beta-adrenoblockers.

Adrenergic alpha-Antagonists↗