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At least 1,387 records · Page 77Linked to original sources
PubMed1961

The effect of morphine on the adrenergic nerves of the isolated guinea-pig jejunum.

Nerves accompanying the mesenteric blood-vessels of the isolated guinea-pig jejunum were stimulated and changes in the longitudinal muscle coat were recorded. Stimulation of the nerves led to a rapid relaxation if the intestine was contracted by a previous administration of histamine. The relaxation was inhibited by morphine and partially restored by nalorphine. Bretylium and atropine also inhibited the relaxation and cocaine increased it somewhat. Morphine, atropine, and bretylium had no significant effect on the depressant action of noradrenaline on histamine contractions, whereas cocaine slightly enhanced the action of noradrenaline. Morphine, but not the other drugs, prevented the inhibitory action of dopamine.

Adrenergic Agents↗
PubMed1990

The distribution of substance P-containing nerves to the rat small intestine.

The concentrations of substance P-like immunoreactivity (SPLI) were measured in mesenteric nerves and vessels of control rats and rats treated with capsaicin during the second day of life. The results showed that there was a significantly higher concentration of SPLI in the jejunum than in the terminal ileum, and that there was a loss of SPLI from these tissues following neonatal treatment with capsaicin. The results suggest that the substance P-containing afferent innervation of the upper small intestine is greater than in the terminal ileum. The significance of these results to the Intensity or Summation hypothesis of visceral pain, and to the thresholds of visceral reflexes from different areas of the small intestine is discussed.

Animals↗
PubMed1983

The effect of intravenous adrenaline and noradrenaline infusion of peripheral lymph flow in the sheep.

Pressure fluctuations and lymph flow were measured in popliteal, prefemoral and mesenteric efferent lymphatic vessels in conscious sheep. Intravenous adrenaline infusion increased frequency of lymphatic contraction and lymph flow in all three vessels. In the case of the prefemoral vessels flow remained high after the infusion had stopped. Intravenous noradrenaline infusion also increased frequency of contraction and lymph flow in all three vessels but prefemoral flow was depressed after the infusion had stopped. Lymphatic frequency of contraction and lymph flow increased when the animals were started. Anaesthetizing the animals with pentobarbitone did not abolish lymphatic contractions, nor did it prevent the response to adrenaline and noradrenaline infusion. The most obvious interpretation of these results is that adrenaline and noradrenaline act by increasing frequency and force of pumping of lymphatic vessels.

Anesthesia, General↗
PubMed1995

Chyloabdomen in a neonatal foal.

A 12-hour-old female standardbred foal developed signs of abdominal pain, tachycardia, tachypnoea and fever associated with chylous ascites. Small intestinal obstruction was due to segmental, mid-jejunal lymphangiectasia. Post mortem examination revealed a lack of communication between afferent and efferent lymphatic vessels in the mesenteric lymphocentre, a defect which was suspected to be congenital.

Abdominal Pain↗
PubMed1992

Temperature and hydrostatic pressure-dependent pathways of low-density lipoprotein transport across microvascular barrier.

To further investigate the chemical and physical nature of low-density lipoprotein (LDL) transport pathways across intact microvessels, the effect of changes in temperature and microvessel hydrostatic pressure were measured in individually perfused postcapillary vessels within frog mesenteric vascular beds. LDL microvessel transport was measured at two microvessel temperature ranges (18-21 degrees C and 4-6 degrees C) and compared with transport of fluorescein, a small solute. Also, LDL transport was measured at a series of hydrostatic pressures (3-20 cmH2O) at microvessel temperatures of 18-21 degrees C and 4-6 degrees C to determine whether LDL transport was coupled to water flow, which would be evidence for hydraulic pathways of solute transport across the microvascular barrier. Quantitative fluorescence microscopy was employed to determine apparent solute permeability coefficients (Ps) under the various temperature and hydrostatic pressure conditions studied. The ratio of Ps fluorescein 18-21 degrees C/4-6 degrees C [1.6 +/- 0.3 (SD)] indicated that fluorescein was freely diffusible across the microvascular barrier through water-filled pathways as transport was inversely proportional to temperature-dependent changes in viscosity. The larger ratio for LDL (Ps LDL 18-21/4-6 degrees C = 9.5 +/- 8.1) than for fluorescein cannot be explained by LDL transport through fixed hydraulic pathways alone and suggests additional or alternate LDL transport mechanisms. In addition, Ps LDL increased as microvessel hydrostatic pressure increased at microvessel temperatures of 18-21 degrees C but not at 4-6 degrees C. Coupling of LDL transport to water flow at the high microvessel temperature range, but not at the low range, indicated the presence of a hydraulic transport pathway that was effectively absent when the microvessel was cooled. These results demonstrated a highly temperature and hydrostatic pressure-dependent LDL pathway that is consistent with a dynamic porous extracellular or transcellular mechanism of LDL transport.

Animals↗
PubMed1975

Exocoelomic internal hernia: elucidation of Papez's concept.

Two internal herinias of the intestines were found in adult males. One was a large translucent avascular membranous sac contining the small intestine from the duodenojejunal flexure to a point 6 in. proximal to the ileocaecal junction. The other was a peritoneal sac enclosing the small intestine, appendix, caecum and 6 in. of the ascending colon. The mesenteric and colic vessels were normal. Both hernias conformed to PAPEZ's concept of the so-called paraduodenal hernia that the hernial sac is derived from the umbilical coelom. The authors suggest that most of the so-called paraduodenal hernias are derived from the embryonic umbilical peritoneal diverticulum rather than from the peritoneal recesses or mesentery of the colon.

Adult↗
PubMed1999

Regulation of smooth muscle alpha-actin expression in vivo is dependent on CArG elements within the 5' and first intron promoter regions.

The aims of the present studies were to define sufficient promoter sequences required to drive endogenous expression of smooth muscle (SM) alpha-actin and to determine whether regulation of SM alpha-actin expression in vivo is dependent on CArG (CC(A/T)6GG) cis elements. Promoter deletions and site directed mutagenesis techniques were used to study gene regulation in transgenic mice as well as in smooth muscle cell (SMC) cultures. Results demonstrated that a Lac Z transgene that contained 547 bp of the 5' rat SM alpha-actin promoter was sufficient to drive embryonic expression of SM alpha-actin in the heart and in skeletal muscle but not in SMCs. Transient transfections into SMC cultures demonstrated that the conserved CArG element in the first intron had significant positive activity, and gel shift analyses demonstrated that the intronic CArG bound serum response factor. A transgene construct from -2600 through the first intron (p2600Int/Lac Z) was expressed in embryos and adults in a pattern that closely mimicked endogenous SM alpha-actin expression. Expression in adult mice was completely restricted to SMCs and was detected in esophagus, stomach, intestine, lung, and nearly all blood vessels, including coronary, mesenteric, and renal vascular beds. Mutation of CArG B completely inhibited expression in all cell types, whereas mutation of the intronic CArG selectively abolished expression in SMCs, which suggests that it may act as an SMC-specific enhancer-like element. Taken together, these results provide the first in vivo evidence for the importance of multiple CArG cis elements in the regulation of SM alpha-actin expression.

Actins↗
PubMed1978

Arteriolar nephrosclerosis in the Syrian hamster.

Syrian hamsters developed spontaneous renal lesions that resembled those of arteriolar nephrosclerosis in man, and differed from other spontaneously occurring or virus-induced renal diseases in other rodent species. Morphologic changes were mainly degenerative with little cellular exudation and were associated with histologic changes in the intrarenal vasculature. The renal lesions were progressive, often fatal and sometimes were complicated by glomerular amyloidosis with the nephrotic syndrome and uremia. Endstage kidneys often had fibrinoid necrosis of intrarenal arterioles and thus resembled lesions characteristic of the malignant phase of human essential hypertension. Fibrinoid necrosis of small arterioles was common in the uterus, ovaries or testes of affected animals; it was less frequent in mesenteric or coronary vessels. Cardiac thrombosis, often involving the left atrium or left atrioventricular valves, also was common. Changes occurred earlier and often were more severe in females than in males. This disease was a major cause of morbidity and mortality and hampered life-span studies.

Animals↗
PubMed1993

[Calcitonin gene-related peptide and neural control of vascular tone].

Rat mesenteric resistance blood vessels are innervated by nonadrenergic, noncholinergic (NANC) vasodilator nerves. In vitro pharmacological, biological and immunohistochemical studies have provided evidence that the calcitonin gene related peptide (CGRP), a 37 amino acid peptide translated by the calcitonin gene, has a potent vasodilator effect and acts as a vasodilator neurotransmitter for NANC vasodilator nerves. The CGRP-containing vasodilator nerves inhibit adrenergic nerve-mediated vasoconstriction through direct relaxation of vascular smooth muscle, while adrenergic nerves suppress the neurotransmision of CGRP-containing nerves by inhibiting CGRP release from the nerve. Thus, CGRP-containing nerves and adrenergic nerves control vascular tone with reciprocal interferences. In in vivo studies, spinal cord (T9-12) stimulation of pitched rats produced a NANC depressor response mediated by endogenous CGRP, suggesting that CGRP-containing nerves are regulated by the central nervous system. The malfunction of CGRP-containing vasodilator nerves may be involved in cardiovascular diseases such as essential hypertension, coronal vasospasm, cerebral vasospasm and Renaud's phenomenon. It is suggested that the CGRP-containing vasodilator nerves play an important role in the regulation of vascular tone.

Amino Acid Sequence↗
PubMedDate not supplied

Collateral blood flow in the distal ileum of neonatal piglets: a clue to the pathogenesis of necrotizing enterocolitis.

Normal blood flow was measured in two regions of the ileum (distal and proximal) of normal birth weight (NBW) and low birth weight (LBW) neonatal piglets. Compensatory collateral blood flow in response to occlusion of vessels in the mesenteric vascular arcades was also measured in distal and proximal ileum of NBW and LBW neonatal piglets. Under normal control conditions the blood flow in the distal ileum of NBW piglets is reduced (40% less than proximal) and in LBW animals this reduction is greater (55% less than proximal). Both proximal and distal ileum of NBW animals but the proximal ileum only of LBW animals could mount compensatory collateral flow, whereas the distal ileum of LBW animals was unable to do so. This decompensation in LBW distal ileum may explain the predilection of NEC lesions for the distal ileum and proximal colon.

Animals↗
PubMedDate not supplied

[Dopamine receptors of the smooth muscles].

It is shown that the interuption of sympathetic nerves in the smooth muscles of the deferent duct or ejejunum of rats achieved by a 4-day keeping of the duct in cold or by the reserpine treatment of the animals does not produce any essential effect on the dopamine action. The contraction of smooth muscles in the isolated deferent duct, mesenteric and renal vessels of rats is effectively eliminated by alpha-andrenolytics (dihydroergotoxin, phentolamine), while the inhibitory effects of dopamine (lowering of vasotonicity of the rats' jejunum tone) are suppressed with propranolol. Galoperidol and methylergometrin display in experiments with smooth muscle organs but a low degree of antagonism to dopamine. The activity of phentolamine as an antagonist of norepinephrine and dopamine in the deferent duct is identical.

Animals↗
PubMed1994

The effects of radiation on the contractile activity of guinea pig mesenteric lymphatics.

In order to assess the effects of irradiation on lymphatic function, the contraction frequency and maximum and minimum diameters of guinea pig mesenteric collecting lymphatic vessels were measured in vivo 4 hours after 1000 rads of abdominal irradiation. The mean contraction frequency for lymphatics from irradiated guinea pigs (7.6 +/- 0.7) was significantly higher than for normals (non-irradiated) (4.7 +/- 0.7) during an initial control observation period, but there was no difference in maximum or minimum diameter between the two groups during this period. Topical application of 10(-4) M noradrenaline (NA) significantly increased contraction frequency in both groups; lymph vessel diameter significantly decreased after NA in irradiated, but not in normal guinea pigs. Intravenous infusion of calcium dobesilate (200 mg/kg) caused a significant increase in the contraction frequency of lymphatic vessels in both normal (to 9.4 +/- 1.5) and irradiated (to 9.8 +/- 1.2) animals, but diameter was not significantly altered. Thus, lymphatic vessels from irradiated guinea pigs were still responsive to exogenous stimuli 4 hours post-irradiation and were initially pumping more actively than those from normal guinea pigs, presumably in response to radiation-induced edema. They also exhibited a supersensitivity to the vasoconstrictive effects of NA, perhaps due to an alteration of the pacemaker or smooth muscle cells by irradiation.

Animals↗
PubMed1977

The roles on intraluminal oxygen and glucose in the protection of the rat intestinal mucosa from the effects of ischaemia.

Rat ileal loops were subjected to 15 minutes ischaemia by clamping both mesenteric and collateral vessels, after which the functional capacity of their mucosae was assessed according to their ability to accumulate phenylalanine "in vitro". Groups of intestines were rinsed before being subjected to ischaemia. Independent and additive protective effects were observed when the rinsing buffer was oxygenated and/or when it contained glucose. Indeed, an oxygenated, glucose-containing buffer afforded full protection to the mucosa, whereas a nitrogenated, glucose-free buffer had no action.

Animals↗
PubMed1998

Effect of magnesium on calcium responses to vasopressin in vascular smooth muscle cells of spontaneously hypertensive rats.

This study investigated the modulatory effect of magnesium (Mg++) on basal and agonist-stimulated intracellular free calcium (Ca++) concentration ([Ca++]i) in vascular smooth muscle cells from spontaneously hypertensive rats (SHR). Effects of increasing extracellular Mg++ concentration ([Mg++]e) on vasopressin (AVP)-induced [Ca++]i responses were determined in primary cultured unpassaged vascular smooth muscle cells from mesenteric and aortic vessels (representing resistance and conduit arteries, respectively) of Wistar Kyoto rats (WKY) and SHR. [Ca++]i was measured by fura-2 methodology. Underlying mechanisms for Mg++ actions were determined in Ca(++)-free buffer and in the presence of diltiazem (10(-6) M), an L-type Ca++ channel blocker. Basal and AVP-stimulated [Ca++]i responses were significantly increased (p < .05) in SHR (pD2 = 8.3 +/- 0.1, Emax = 532 +/- 14 nM for SHR; pD2 = 8.0 +/- 0.04, Emax = 480 +/- 15 nM for WKY). [Mg++]e dose-dependently reduced basal and agonist-induced [Ca++]i responses. High [Mg++]e (4.8 mM) attenuated [Ca++]i responses to AVP in WKY (Emax = 328 +/- 30 nM) and SHR (Emax = 265 +/- 27 nM) and normalized AVP-elicited hyper-responsiveness in SHR (pD2 in high [Mg++]e, 8.1 +/- 0.3 for SHR, 7.8 +/- 0.6 for WKY). Extracellular Ca++ withdrawal and diltiazem abolished the attenuating effects of high [Mg++]e in WKY but not in SHR. These findings demonstrate that Mg++ dose-dependently reduces [Ca++]i and that high [Mg++]e attenuates AVP-stimulated [Ca++]i responses and normalizes sensitivity to AVP in SHR. In WKY, Mg++ actions are dependent primarily on Ca++ influx through L-type Ca++ channels, whereas in SHR, the modulatory effects of [Mg++]e are mediated both by Ca++ influx through Ca++ channels and by intracellular Ca++ release.

Animals↗
PubMed1986

Action and metabolism of des(Arg)kinins in mesenteric arteries.

Kallidin and bradykinin can be hydrolyzed at their C-termini to produce des(Arg10)kallidin and des(Arg9)bradykinin respectively. These des(Arg)kinins, previously thought to be biologically inactive, are now known to have potent effects on B1 receptors. Although stimulation of B1 receptors has been reported to produce peripheral vasodepressor responses in certain experimental states, only constriction has been reported in isolated vessels (i.e., rabbit aorta, basilar artery, mesenteric vein). In the present study, we have investigated the biologic activity of des(Arg) kinins on a peripheral resistance vessel (rabbit mesenteric artery). We found that des(Arg)bradykinin relaxes mesenteric arteries, and that its potency relative to kallidin and bradykinin is consistent with the presence of B1 receptors. Further, intact mesenteric arteries, and a plasma membrane fraction purified from these arteries, contained a carboxypeptidase activity which was capable of producing des(Arg)kinins from both kallidin and bradykinin. Thus, these data demonstrate that the vasculature has the enzymatic capacity to form B1 kinins, and that stimulation of B1 receptors in resistance vessels can be associated with peripheral vasodilation.

Animals↗
PubMed2004

Early vitamin E supplementation attenuates diabetes-associated vascular dysfunction and the rise in protein kinase C-beta in mesenteric artery and ameliorates wall stiffness in femoral artery of Wistar rats.

AIMS/HYPOTHESIS: The impact of early vitamin E supplementation on vascular function in diabetes remains unresolved. Therefore, we examined the effects of vitamin E on functional and structural parameters and on chemical markers that are disturbed in diabetes in mesenteric and femoral arteries. METHODS: Segments of both arteries, taken from control and 8-week-old streptozotocin diabetic Wistar rats that were treated or not with vitamin E, were mounted on wire and pressure myographs, after which endothelium-dependent and -independent vasodilation was assessed. Passive mechanical wall properties and the localisation and levels of protein kinase C (PKC)-beta(2) and AGE were evaluated in these vessels. RESULTS: Vitamin E supplementation was associated with improved endothelium-dependent and -independent vasodilatation in mesenteric arteries from diabetic rats. Impaired endothelium-dependent vasodilatation in diabetic mesenteric vessels was associated with PKC-beta(2) up-regulation and this was prevented by vitamin E supplementation. Increased AGE accumulation and plasma isoprostane levels in diabetic rats were not changed by vitamin E. In the femoral artery, vitamin E supplementation had no effect on endothelium-dependent or -independent vasodilatation, but did prevent the wall stiffening associated with diabetes. CONCLUSIONS/INTERPRETATION: Early vitamin E supplementation has a beneficial effect on diabetes-induced endothelial dysfunction in resistance arteries. This benefit may arise from a direct effect on smooth muscle function, as a result of inhibition of the PKC-beta(2) isoform by vitamin E.

Acetylcholine↗
PubMed1998

The clinical course of asymptomatic mesenteric arterial stenosis.

PURPOSE: The incidence of subsequent symptomatic mesenteric vascular disease is unknown for patients who have asymptomatic mesenteric arterial stenosis. The purpose of this study was to determine the risk of developing acute and chronic mesenteric ischemia in patients identified by lateral aortography to have significant mesenteric artery stenosis. METHODS: From 1989 through 1995, 980 consecutive aortograms with anteroposterior and lateral projections were reviewed within 1 week of arteriography to identify patients who had significant mesenteric stenosis but no symptoms of mesenteric ischemia. Eighty-two patients were found to have 50% stenosis of at least one mesenteric artery and were monitored by interview to determine if symptoms of acute or chronic mesenteric ischemia developed. RESULTS: Ten patients were lost to follow-up, and 12 patients were withdrawn from the study because of mild mesenteric arterial disease (1% to 49% stenosis) in combination with more significant disease of other vessels. Follow-up was 1 to 6 years. The overall mortality rate was 40%, and mesenteric ischemia developed in four patients. Each of these four patients had significant (>50%) stenosis or occlusion of the celiac artery, superior mesenteric artery, and inferior mesenteric artery. Eighty-six percent of the 15 patients with significant three-vessel arterial disease had mesenteric ischemia, had other vague abdominal symptoms, or died. CONCLUSIONS: Patients with significant three-vessel mesenteric arterial stenosis should be considered for prophylactic mesenteric arterial reconstruction. Mesenteric arterial reconstruction should be routine when these patients undergo aortic reconstruction for aneurysmal or occlusive disease.

Acute Disease↗