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Autoregulatory patterns in the arteriolar network of cat mesentery.

The purpose of this study was to examine the distribution and extent of autoregulatory behavior among arterioles in the arcade network of the cat mesentery. We found that 71% of 169 arterioles studied dilated and 63% showed blood flow autoregulation with arterial pressure reduction to 55-60 mm Hg. There appeared to be a direct relation between the degree of dilation and the degree of autoregulation when individual vessels were compared (r = 0.71). The dilation of individual arterioles was also correlated with the degree of autoregulation of other vessels in the same field (r = 0.51). To a lesser extent, the degree of dilation of individual arterioles was correlated with the degree of dilation of other vessels in the same field (r = 0.30). In comparing vessels which dilated, the largest average response was found in preparations where all vessels dilated. On a percentage basis the small arterioles located distally in the network dilated more than the large arterioles located proximally. In preparations having both reactive and nonreactive arterioles to pressure reduction, the nonreactive vessels were usually located geographically in proximity to each other. The flow distribution in the arteriolar network remained relatively stable on pressure reduction; the total tissue area perfused by a first-order arteriole shifting by 3% on the average.

Animals↗

Symptomatic mesentery Castleman disease mimicking a pancreatic tumor.

Castleman disease (CD) is an uncommon lymphoproliferative disorder of unknown etiology. It can be localized or multicentric. There are two major histological variants. The hyaline-vascular type predominates in the thorax and the mesenteric disease is usually of the plasma cell type. Hyaline-vascular CD of the mesentery is very rare. We report such a neoplasm of mesenteric root in a 38-year-old woman who presented with abdominal discomfort. Dynamic magnetic resonance imaging (MRI) of CD has rarely been reported previously. The imaging findings of CD on computed tomograms, MR images and angiograms were described.

Adult↗

Replanting the inferior mesentery artery during infrarenal aortic aneurysm repair: influence on postoperative colon ischemia.

BACKGROUND: Replanting the inferior mesentery artery (IMA) to prevent ischemic colitis (IC) has been discussed for many years; yet, to our knowledge, no prospective studies have been conducted to compare the incidence of histologically proven IC in patients with and without IMA revascularization. The aim of this prospective study, with histologic evaluation of the sigmoid colon mucosa, was to assess the influence of replanting the IMA on IC and mortality. METHODS: From January 1999 to December 2003, 160 consecutive patients who were operated on for a symptomatic (n = 21) or asymptomatic (n = 139) infrarenal aortic aneurysm were prospectively assessed and randomly assigned either to replanting or ligating the IMA. Sigmoidoscopy with biopsy was performed on day 4 or 5 after surgery; an autopsy was performed on patients not surviving to day 5 after surgery. All patients gave written informed consent. RESULTS: Of the 160 randomized patients, 128 had a confirmed patent IMA and formed the basis of this study. Their age was 70 +/- 8 years (men, 70 +/- 8 years; women, 73 +/- 7 years). The IMA was replanted in 67 patients (52%) and ligated in 61 (48%) intraoperatively. IC developed in six patients with a replanted IMA and in 10 with a ligated IMA (relative risk [RR], 0.55; 95% confidence interval [CI], 0.21 to 1.41; chi2 = 1.62; P = .203). Blood loss in the two cohorts did not differ significantly (P = .788); however, patients with IC had a significantly higher blood loss compared with the cohort without IC (P = .012) and were older (P = .017). Age, sex distribution, clamping time, the use of tube or bifurcated grafts, and intraoperative hypotension did not differ between patients with ligated or replanted IMA. CONCLUSION: Although replanting the IMA did not confer a statistically significant reduction of perioperative morbidity or mortality in this study, it appears that older patients and patients with increased intraoperative blood loss might benefit from IMA replantation, because this maneuver does not increase perioperative morbidity or substantially increase operation time.

Aged↗

Polysplenia and jejunal atresia with agenesis of the dorsal mesentery.

Polysplenia syndrome has been well described. It is associated with gastrointestinal atresia in patients with situs inversus abdominus; however, it appears that this case represents the first occurrence of polysplenia with jejunal atresia having agenesis of the dorsal mesentery and partial situs inversus abdominus.

Abnormalities, Multiple↗

Characterization of alpha-adrenoceptor activity in the preterm piglet mesentery.

To characterize neonatal mesenteric alpha-adrenoceptor populations, an extracorporeal perfusion circuit was established to control intestinal blood flow in prematurely delivered (by cesarean section at 90% of gestational age) piglets. Activation of alpha 1-adrenoceptors was documented by observing dose-dependent increases in mesenteric perfusion pressure after intramesenteric arterial injection of methoxamine; alpha 2-adrenoceptor activity was confirmed by finding similar increases in mesenteric perfusion pressure after intramesenteric arterial injections of BHT 933. Peripheral intravenous injections of WB 4101 (a competitive alpha 1A-adrenoceptor antagonist), but not clorethylclonidine (CEC, an alpha 1B-adrenoceptor antagonist), significantly blunted (P < .05, ANOVA) the mesenteric vasoconstrictor responses to methoxamine. The mesenteric vasoconstrictor response to BHT 933 (an alpha 2-adrenoceptor agonist) also was blunted by WB 4101, but not by CEC. These data suggest that alpha 1A- and alpha 2-adrenoceptors can be activated in the small intestinal mesentery of piglets well before they reach full-term maturation, although receptor specificity has not been fully established.

Adrenergic alpha-Agonists↗

Vasomotion in rat mesentery during hemorrhagic hypotension.

Although vasomotion has been considered a feature of the microvascular bed under physiological conditions, it has also been observed following hypotension in several tissues. In this work, 158 mesenteric microvessels of 36 rats were investigated quantitatively in normovolemic and hemorrhaged animals, focussing on diameter changes, particularly vasomotion incidence and characteristics. The femoral arteries of Wistar rats (body weight BW = 188 +/- 23 g, mean +/- SD) anesthetized with pentobarbital were cannulated for arterial pressure (AP) monitoring and blood withdrawal. The protocol consisted of 15 min control and 30 min of hemorrhagic hypotension (AP = 52 +/- 5 mmHg, hemorrhaged vol. = 17 +/- 4 ml/kg BW). During control normovolemic conditions, analysis of mesenteric microcirculation using intravital videomicroscopy revealed neither arteriolar nor venular vasomotion. During hemorrhagic hypotension (HH) microvascular blood flow reduced to 25% of control. While venules did not show diameter changes during HH, arterioles contracted to 85 +/- 20% of control and arteriolar vasomotion appeared in 42% of the animals and 27% of the arterioles. The amplitude of arteriolar diameter change during HH relative to mean diameter and to control diameter averaged 65 +/- 24% (range: 32-129%) and 41 +/- 10% (range: 25-62%), respectively. Vasomotion analysis showed two major frequency components: 1.7 +/- 0.8 and 7.0 +/- 5.2 cycles/min. Arterioles showing vasomotion had a mean control diameter larger than the remaining arterioles and showed the largest constriction during HH. We conclude that hemorrhagic hypotension does not change venular diameter but induces arteriolar constriction and vasomotion in rat mesentery. This activity is expressed as slow waves with high amplitude and fast waves with low amplitude, and is dependent on vessel size.

Animals↗

Multiple angiitis of mesenterial arteries in guinea pigs induced by intraperitoneal administration of high doses of Na2 EDTA. II. Electron microscopic study.

By application of high doses of EDTA we could induce angiitis-like lesions in the mesenterial arteries. In this paper we report the findings of electronmicroscopic investigations of these lesions. They consist of dissociation of the smooth muscle cells by scanty intermuscular spaces, probably by loosening of the basal laminae and matrix. Both endothelial cells and smooth muscle cells show minimal changes. The elastic lamellae were partially interrupted.

Animals↗

Experimentally induced aneurysms of mesenterial arteries. Studies on the histogenesis of acquired aneurysm.

In previous studies (YAMAGUCHI et al. 1981 a, b) we administered vast amounts of Na2EDTA into the peritoneal cavity of guinea pigs and demonstrated multiple angiolytic changes of mesenterial arteries. In this experiment, with the same procedures, aneurysm formation of these arteries was encountered based on the above angiolysis. The vascular changes described may be induced by the same mechanisms which provoked angiolysis followed by loosening of elasticity, raised blood pressure and lack of surrounding support.

Aneurysm↗

Heterogeneity in mechanisms underlying vasodilatory responses in small arteries of the rat hepatic mesentery.

We have characterised nerve-mediated vasodilations in small arteries of the rat hepatic mesentery. Stimulation of sympathetic nerves (10 Hz, 10 s) produced a vasodilation which was abolished by the beta-adrenoceptor antagonist, propranolol (2 x 10(-6) M), but was unaffected by NG-nitro-L-arginine methyl ester (L-NAME, 10(-5) M). Stimulation of sensory nerves produced a large vasodilation that was abolished by capsaicin (10(-6) M). This vasodilation was unaffected by L-NAME (10(-5) M), but significantly reduced by the calcitonin gene related peptide (CGRP) antagonist, CGRP8-37 (10(-6) M), or inhibition of adenylate cyclase (SQ22356, 2 x 10(-5) M; 2',5'-dideoxyadenosine, 2 x 10(-4) M). Stimulation of cholinergic nerves produced a small vasodilation which was significantly reduced by scopolamine (10(-6) M). Expression of mRNA for CGRP1 receptors, muscarinic m2, m3 and m5 receptors and neurokinin1 (NK1) and NK3, receptors was detected. Perivascular nerves were immunoreactive for CGRP and substance P. No role was found for substance P, neuronal NO, ATP or adenosine in nerve-mediated responses. L-NAME (10(-5) M) potentiated vasoconstrictions following sympathetic nerve stimulation. This effect was reversed by L-arginine (10(-3) M) and cromakalim (10(-6) M) and mimicked by glybenclamide (10(-5) M), thus implicating KATP channels. Vasodilation in response to sensory nerve stimulation was directly proportional to the level of preconstriction, while vasodilation in response to neurogenic or applied acetylcholine was inhibited at high levels of preconstriction. We hypothesize that, under conditions of intensive vasoconstriction, some endothelial-dependent vasodilations may be less important than vasodilations activated directly through the smooth muscle.

Adenylyl Cyclase Inhibitors↗

Receptors involved in nerve-mediated vasoconstriction in small arteries of the rat hepatic mesentery.

1. We have investigated the neurotransmitters and receptor subtypes involved in nerve-mediated vasoconstriction in small arteries of the rat hepatic mesentery. 2. A dense sympathetic innervation was demonstrated using catecholamine histochemistry and antibodies against the synaptic vesicle protein synaptophysin. 3. Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated very strong expression of the alpha1A-adrenergic, neuropeptide Y (NPY) Y1, P2X1- and P2X4-purinergic receptors, moderate expression of the alpha2B-adrenergic receptor and the purinergic P2X5- and P2X7-receptors and weak expression of the alpha1B-, alpha1D-, alpha2A- and alpha2C-adrenergic receptors and the P2X2- and P2X3-purinergic receptors. NPY2 and P2X6 receptor expression was absent. 4. Electrical field stimulation (10 Hz, 10 s) produced contractions which were abolished by tetrodotoxin (10(-6) M) and/or guanethidine (GE, 5 x 10(-6) M) and a combination of benextramine (10(-5) M) and alpha,beta-methylene ATP, (alpha,beta-mATP, 3 x 10(-6) M) or PPADS (10(-5) M). Selective alpah1-adrenergic receptor antagonists showed the potency order of prazosin > WB-4101 > 5-methyl-urapidil > BMY 7378. Yohimbine (10(-8) M, 10(-7) M), alpha,beta-mATP (3 x 10(-6) M) and PPADS (10(-5) M) each enhanced the response to nerve stimulation. 5. Some experiments demonstrated a slow neurogenic contraction which was abolished by GE or the selective NPY1 receptor antagonist 1229U91 (6 x 10(-7) M). 6. We conclude that nerve-mediated vasoconstriction results from the activation of postsynaptic alpha,beta-adrenergic and P2X-purinergic receptors and under some conditions, NPY1 receptors. Neurotransmitter release is modulated by presynaptic alpha2-adrenergic receptors and possibly also P2X-purinoceptors. The major postsynaptic subtypes involved were well predicted by mRNA expression as measured by RT-PCR, suggesting that this technique may be a useful adjunct to studies aimed at identifying functional receptor subtypes.

Animals↗

Ascorbate blocks endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation in the bovine ciliary vascular bed and rat mesentery.

1. The effects of ascorbate were assessed on vasodilatation mediated by endothelium-derived hyperpolarizing factor (EDHF) in the ciliary vascular bed of the bovine isolated perfused eye and in the rat isolated perfused mesenteric arterial bed. 2. In the bovine eye, EDHF-mediated vasodilator responses induced by acetylcholine or bradykinin were powerfully blocked when ascorbate (50 microM) was included in the perfusion medium for at least 120 min; with acetylcholine a normally-masked muscarinic vasoconstrictor response was also uncovered. 3. The blockade of EDHF-mediated vasodilatation by ascorbate was time-dependent (maximum blockade at 120 min) and concentration-dependent (10 - 150 microM). 4. Ascorbate (50 microM) also blocked acetylcholine-induced, EDHF-mediated vasodilator responses in the rat mesenteric arterial bed in a time-dependent manner (maximum blockade at 180 min). 5. The ability of ascorbate to block EDHF-mediated vasodilatation is likely to result from its reducing properties, since this action was mimicked in the bovine eye by two other reducing agents, namely, N-acetyl-L-cysteine (1 mM) and dithiothreitol (100 microM), but not by the redox-inactive analogue, dehydroascorbate (50 microM). 6. In conclusion, concentrations of ascorbate present in normal plasma block EDHF-mediated vasodilator responses in the bovine eye and rat mesentery. The mechanism and physiological consequences of this blockade remain to be determined.

Acetylcholine↗

Effects of AQA-39 on granulocytes in the microcirculation of rat mesentery.

Recent evidence suggests that granulocytes play a key role in perfusion of the microcirculation. In this regard two phenomena are of specific importance: pseudopod formation and adhesion to the endothelium. Thus we studied the influence of AQA-39 on leukocyte adhesion to the endothelium in rat mesentery venules and on pseudopod formation in human granulocytes. Direct intravital estimates of granulocyte fracture stress were obtained by measurement of the ratio of leukocyte and midstream velocity. The marginating and circulating cell flux and the areal density of stationary granulocytes on the intraluminal side of the endothelium were measured simultaneously in the same venular segments. During administration of 10 mg kg-1 AQA-39 the fracture stress is significantly reduced resulting in decreased areal density of marginating cells and also washout of strongly adhering stationary leukocytes found frequently on the endothelium of such vessels. Furthermore it was observed on single granulocytes that AQA-39 leads to transient obliteration of pseudopod formation. These results suggest that the effect of AQA-39 on flow may be mediated in part by reduction in granulocyte adhesion to the endothelium and suppression of pseudopod formation.

Animals↗

Effects of idarubicin and idarubicinol on rat coronary resistance and vasoconstrictor responsiveness of isolated aorta and mesentery.

It has been hypothesized that coronary vasoconstriction is involved in the cardiotoxic action of anthracyclines. The purpose of this study was to determine whether an increase in coronary resistance induced by idarubicin (IDA) or its primary circulating metabolite idarubicinol (IDOL) is correlated with a decrease in vascular sensitivity to vasoconstrictor agonists. Coronary vasoconstriction was studied in single-pass perfused rat hearts after a 10-min infusion of 0.5 mg IDA or IDOL. In the endothelium-intact rat thoracic aorta and mesentery we measured the inhibition of phenylephrine (PE)- and KCl-induced contraction in the presence of IDA and IDOL, respectively. The increase in coronary vascular resistance evoked by IDOL (121%) exceeded that of IDA (75%). IDA (10-100 micromol/l) concentration-dependently diminished vascular sensitivity to PE and KCl due to a reduction in maximal contractile response (Emax), i.e. the antagonism by IDA of PE- or KCl-induced vasoconstriction was non-competitive, indicating a post-receptor cellular mechanism. These reductions of PE or KCl efficacy elicited by IDOL were significantly larger than those elicited by the corresponding doses of IDA. The decrease in efficacy of PE in the presence of IDA and IDOL was characterized by IC50 estimates of 44.3 and 30.7 mumol/l, respectively. With a 10-fold lower IC50, IDA inhibited the reactivity of small mesenteric arteries to noradrenaline with 10-fold higher potency. The correlation between the increase in coronary resistance and the decrease in vasoconstrictor responsiveness may suggest that these anthracyclines act through a common cellular mechanism.

Animals↗

Frusemide inhibition of sympathetic vasoconstriction in the rat in situ blood perfused mesentery.

Mesenteric perfusion pressure was measured in the in situ blood-perfused mesentery of anaesthetized rats. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation at 3, 6 and 10 Hz before and after the administration of frusemide 5 mg/kg intravenously (i.v.) or vehicle. Loss of volume due to diuresis was prevented by replacement with intravenous saline. Frusemide did not cause any changes in blood pressure or baseline perfusion pressure. Responses to electrical stimulation were inhibited by frusemide (P less than 0.05) but unchanged by vehicle administration. Acute bilateral nephrectomy or treatment with indomethacin (2 mg/kg i.v.) prevented the inhibitory effect of frusemide on responses to sympathetic nerve stimulation. Responses to sympathetic nerve stimulation were potentiated by an infusion of angiotensin II (12 ng/min) into the mesenteric artery. This infusion did not alter either blood pressure or baseline perfusion pressure. Administration of frusemide 5 mg/kg i.v. attenuated the potentiating effect of angiotensin II on vasoconstrictor responses to electrical nerve stimulation. Frusemide may lead to the release of a prostanoid or prostanoid precursor which inhibits vascular constrictor responses.

Angiotensin II↗

Inhibition of vasoconstriction by platelet activating factor in the in situ blood perfused rat mesentery.

1. Perfusion pressure was measured in the in situ mesentery of anaesthetized rats perfused with blood at a constant 2 mL/min. 2. Increases in perfusion pressure were produced by mesenteric peri-arterial nerve stimulation at 10 Hz for 5 s at 2 min intervals and by bolus intra-arterial injections of the vasoconstrictors noradrenaline, angiotensin II and 5-hydroxytryptamine. 3. The intra-arterial infusion of platelet-activating factor (PAF) to produce a blood concentration of 3 X 10(-10) mol/L inhibited all responses to a similar extent. Intra-arterial prazosin (1-5 X 10(-9) mol/L), however, preferentially reduced responses to nerve stimulation and noradrenaline. 4. PAF at concentrations from 3 X 10(-11) to 10(-9) mol/L produced increasing inhibition of vasoconstrictor responses to nerve stimulation. The dose-response to PAF was shifted to the right by the concomitant intra-arterial infusion of the PAF antagonist SRI 63-441. 5. PAF at very low concentrations in vivo inhibits mesenteric vasoconstriction, produced by sympathetic nerve stimulation or various agonists, by a PAF-receptor mediated vasodilatation of the mesenteric vasculature.

Angiotensin II↗

Effects of chronic administration of atenolol on the in situ perfused mesentery of normotensive and hypertensive rats.

1. Atenolol 50 mg kg-1 was administered daily for 7 to 21 days to male normotensive Wistar rats and to Okamoto spontaneously hypertensive rats. Blood pressure and heart rate were monitored daily. 2. Following atenolol treatment the response to exogenous noradrenaline and to periarterial nerve stimulation was measured in the in situ blood perfused mesentery. 3. In normotensive animals, treatment with atenolol for 7 days had little effect on the responses of the mesenteric vasculature to either exogenous noradrenaline or to periarterial nerve stimulation. After 21 days, the response to noradrenaline was little changed, but there was a statistically significant decrease in the response to periarterial nerve stimulation at the higher stimulation frequencies (16 and 35 Hz). 4. In spontaneously hypertensive animals, treatment with atenolol for 7 days did not significantly affect the response of the mesenteric vasculature to either noradrenaline or periarterial nerve stimulation; however, after treatment for 21 days, responses to exogenous noradrenaline were reduced, while responses to periarterial nerve stimulation were even more markedly reduced, particularly at the lower stimulus frequencies. 5. The time course of the observed effects suggests that, over time, atenolol induces changes other than the simple blockade of beta-adrenoceptors which can be demonstrated to be present immediately. The decreased responses to periarterial nerve stimulation in normotensive and hypertensive animals suggest that the changes induced affect presynaptic mechanisms of noradrenaline release (either directly or indirectly), rather than changes in postsynaptic receptor sensitivity or vascular reactivity. The observation that the changes are more evident in hypertensive animals indicates that they may play an important role in the antihypertensive action of atenolol.

Animals↗

Effects of hydroxyethyl rutosides upon the permeability of single capillaries in the frog mesentery.

1. We have investigated the effects of a standardised mixture of hydroxyethyl rutosides (HR) upon the permeability of the walls of single capillaries and venules of the frog mesentery. 2. In each experiment a single vessel was perfused via a micropipette with frog Ringer solutions containing bovine serum albumin (10 mg ml-1) and Ficoll 70 (40 mg ml-1) first in the absence of HR and then with HR added to the perfusate. The permeability of the vessel walls was assessed during each perfusion by using a development of the Landis micro-occlusion technique to estimate their hydraulic permeability (Lp) and the effective osmotic pressure (sigma delta pi) exerted across them by the perfusate macromolecules. 3. Measurements were made both in vessels which appeared to be healthy and in vessels showing signs of stasis or inflammation before perfusion. 4. HR at concentrations of 1.0, 0.1 and 0.01 mg ml-1 reduced hydraulic permeability to approximately half of its value in the absence of HR. It increased sigma delta pi to macromolecules at concentrations of 10, 1.0, 0.1, 0.01 and 0.001 mg ml-1. The effects of HR upon permeability were not reversed within 10 min of perfusion with an HR-free solution. 5. Ultrastructural examination of a number of vessels in which initial high values of permeability were reduced to values within the normal range of permeabilities by HR, showed clear signs of damage to the endothelium, with large gaps between adjacent endothelial cells. 6. These observations suggest that HR does reduce microvascular permeability both in healthy vessels and vessels showing of inflammation. The reduction in permeability of inflamed vessels does not appear to be the result of closure of the gaps between adjacent endothelial cells.

Animals↗

Vasodilator responses to dopamine in rat perfused mesentery are age-dependent.

1. Dose-dependent vasodilator responses to dopamine, isoprenaline, noradrenaline, 3-isobutyl-1-methylxanthine (IBMX) and sodium nitroprusside were obtained in isolated perfused mesentery preparations, taken from reserpine-treated rats of different ages. The preparations were pretreated with phenoxybenzamine (1 microM) and perfused with physiological salt solution containing cocaine (10 microM), additional KCl (20 mM) and vasopressin (0.1 microM). 2. Vasodilator responses to dopamine were abolished by the dopamine1 (DA1)-selective antagonist SCH 23390 (10 nM) and those to isoprenaline by propranolol (1 microM), but the vasodilator responses to noradrenaline were abolished only when SCH 23390 and propranolol were used together. This indicated that dopamine was acting via DA1-receptors, isoprenaline via beta-adrenoceptors and that noradrenaline could act via DA1-receptors and beta-adrenoceptors in this preparation. 3. Responses to all the vasodilator drugs decreased in magnitude between the ages of 1 and 2 months. Responses to dopamine declined further in 4 month-old rats and were negligible at 6 or 22-24 months of age. Responses to isoprenaline were well maintained up to 6 months of age, but were negligible at 22-24 months. 4. It is concluded that, in the rat mesenteric vasculature, there is a non-specific decline in responses to vasodilator drugs during development (1 to 2 months). Subsequently there is a specific decline in DA1-receptor-mediated and beta-adrenoceptor-mediated responses; the former are lost at an earlier age than the latter. This different time course suggests that age influences receptor numbers, or their coupling to adenylate cyclase, rather than a post-receptor event in the adenylate cyclase/cyclic AMP pathway.

Aging↗