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PubMed1978

The influence of prostaglandins on noradrenaline-induced vasoconstriction isolated perfused mesenteric blood vessels of the rat.

1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E(2) (PGE(2)) and PGE(1) in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the alpha-adrenoceptor in this tissue was also studied.2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration-dependent flattening of the noradrenaline concentration-effect curve.3 A concentration-dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin-depressed responses to noradrenaline was: PGE(2), PGE(1), PGA(1), PGF(2alpha), PGA(2).4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE(2) and PGE(1) restored responses towards the control level whereas PGA(1), PGA(2) and PGF(2alpha) increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed.5 At concentrations equi-effective in restoring depressed responses to control levels PGA(1) but not PGE(2), caused a parallel shift of the noradrenaline concentration-effect curve to the left and a small, gradual rise in the basal perfusion pressure.6 The reason for the differing effects remains obscure but does not seem to involve a change in the alpha-adrenoceptor as indicated by the pA(2) of phentolamine. Furthermore, the restorative and potentiating effect of PGA(1) is not mediated by blockade of neuronal uptake of noradrenaline.7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug-receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.

Animals↗

PubMed1990

Age-related decrease of calcitonin gene-related peptide-containing vasodilator innervation in the mesenteric resistance vessel of the spontaneously hypertensive rat.

We previously demonstrated that the mesenteric resistance blood vessels have nonadrenergic, noncholinergic vasodilator innervation in which calcitonin gene-related peptide (CGRP) is a possible neurotransmitter. The role of CGRP-containing vasodilator nerves in hypertension was investigated in perfused mesenteric vascular beds isolated from spontaneously hypertensive rats (SHR). The adrenergic vasoconstrictor responses to perivascular nerve stimulation in both SHR (8-, 15-, and 30-week-old) and age-matched Wistar-Kyoto (WKY) rat preparations increased with aging, but the response was greater in SHR than in WKY rats at all ages. The preparation isolated from SHR and WKY rats was precontracted by continuous perfusion of Krebs' solution containing 7 x 10(-6) M methoxamine plus 5 x 10(-6) M guanethidine. In both SHR and WKY rats, perivascular nerve stimulation (1-8 Hz) produced frequency-dependent vasodilation, which was blocked by 1 x 10(-7) M tetrodotoxin, pretreatment with 5 x 10(-7) M capsaicin, and denervation by cold storage (4 degrees C for 72 hours). The vasodilation induced by perivascular nerve stimulation in SHR greatly decreased with age, whereas a slight decrease in the response with age was found in WKY rats. The neurogenic vasodilation in the young SHR preparation was similar in magnitude to the vasodilation in age-matched WKY rats, whereas the vasodilation in 15- and 30-week-old SHR was significantly smaller than that in age-matched WKY rats. In both SHR and WKY rats, perfusion of rat CGRP (1 x 10(-10) to 3 x 10(-8) M) produced marked vasodilation in a concentration-dependent manner. The CGRP-induced vasodilation in SHR increased with age, whereas an age-related decrease in vasodilation was found in WKY rats. Perivascular nerve stimulation (4 and 8 Hz) of the perfused mesenteric vascular bed evoked an increased release of CGRP-like immunoreactive substance in the perfusate, which was significantly less in 15-week-old SHR than in age-matched WKY rats. Immunohistochemical studies showed an age-related decrease in CGRP-like immunoreactive fibers in SHR but not in WKY rats. These results suggest that CGRP-containing vasodilator innervation is greatly decreased when SHR develop and maintain hypertension. It is also suggested that the decreased vasodilator mechanism by CGRP-containing nerves contributes to the development and maintenance of hypertension.

Aging↗

PubMed1988

Release of [3H]-noradrenaline from the sympathetic nerves to bovine mesenteric lymphatic vessels and its modification by alpha-agonists and antagonists.

1. Isolated segments of bovine mesenteric lymphatic vessels were loaded with [3H]-noradrenaline and its efflux in response to field stimulation examined. Vessels were attached to an isometric force transducer for the simultaneous recording of mechanical activity. 2. Field stimulation at 1, 4 and 8 Hz (0.3 ms pulses, 1 min train) increased spontaneous contraction rate and evoked 3H release up to a maximum of 4.5% of total tissue 3H at 8 Hz. Output per pulse was maximal at 4 Hz. 3. Tetrodotoxin (3 x 10(-6) M) blocked the release of 3H in response to field stimulation although the drug did not attenuate release evoked by high K+ (65 mM) solution. Field-evoked release of 3H was also absent in Ca2+ -free solution containing EGTA (1 mM). 4. When vessels were preincubated with labelled transmitter plus cocaine (5 x 10(-5) M) evoked release of 3H was absent. After preloading with [3H]-noradrenaline, cocaine (10(-6) M) potentiated both the mechanical response to field stimulation and evoked 3H release. 5. The relatively non selective alpha-adrenoceptor antagonist phentolamine (3 x 10(-6) M) and the alpha 2-antagonists yohimbine (10(-8) M) and rauwolscine (10(-6) M) significantly increased evoked 3H release at both of the frequencies examined (1 and 4 Hz). In contrast, the selective alpha 1-antagonist prazosin (10(-6) M) failed to alter 3H release to 4 Hz stimulation although release at 1 Hz was potentiated in the presence of the drug. 6. The postsynaptic excitatory response to field stimulation remained in the presence of prazosin (10(-6) M), but was converted to an inhibitory effect in the presence of phentolamine (3 x 10(-6) M), yohimbine (10(-6) M) or rauwolscine (10(-6) M). 7. Evoked 3H efflux was significantly reduced by clonidine (10(-6) M), xylazine (10(-6) M) and exogenous noradrenaline (5 x 10(-7) M), although phenylephrine (10(-6) M) reduced release only at the lower of the two frequencies tested (1 Hz). 8. These findings suggest that release of 3H by field stimulation reflects endogenous transmitter release and that this is subject to autoinhibition via feedback onto inhibitory prejunctional alpha 2-adrenoceptors. The postjunctional excitatory response is mediated via postjunctional alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.

Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The animals were treated with dexamethasone or its vehicle (sesame oil) for 1 day (1.8 mg/kg) and for 14 days (1.8 mg/kg/wk). The superior mesenteric artery with its branches was isolated and perfused with Tyrode's solution at a constant flow rate of 5 ml/min. Administration of norepinephrine (1-10 nmol), arginine vasopressin (0.03-0.3 nmol), or angiotensin II (0.1-1 nmol) produced vasoconstriction and increased the output of 6-keto-prostaglandin F1 alpha and prostaglandin E2 in a dose-related manner in mesenteric vessels. Administration of 10 nmol bradykinin or 19 nmol A23187 enhanced the output of prostaglandins without altering vascular tone. The vasoconstrictor response to arginine vasopressin, but not norepinephrine or angiotensin II, was enhanced in mesenteric vessels from rats treated with dexamethasone for 14 days but not for 1 day. In contrast, the output of basal as well as norepinephrine, arginine vasopressin, angiotensin II, bradykinin, or A23187-induced prostaglandin output was significantly reduced in mesenteric vessels from rats treated with dexamethasone for 1 or 14 days. Prostaglandin output in mesenteric arteries from rats treated with dexamethasone for 1 and 14 days was not different. These data indicate that dexamethasone treatment for longer but not for shorter periods results in a selective increase in vascular reactivity of mesenteric vessels to arginine vasopressin that is independent of prostaglandin synthesis. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension.

Animals↗

PubMed2005

A major role for AT1b receptor in mouse mesenteric resistance vessels and its distribution in heart and neuroendocrine tissues.

In mice, angiotensin (Ang) II type-1 (AT(1)) receptors exist as AT1a, and AT(1b) subtypes. In an effort to understand the role of AT(1b) in regulating vascular function, AT(1) subtype mRNA and its functional relevance in the mesenteric resistance vessels were determined using wildtype (WT) and AT(1a) knockout (AT(1a)(-/-) mice) mice. With RT-PCR followed by restriction-enzyme digestion, we found that AT(1b) accounted for almost all (98%) of AT(1) receptors in the mesenteric resistance vessels of WT mice. Also, the Ang II response in the vessels of AT(1a)(-/-) mice was comparable to that of WT mice, suggesting an important role for AT(1b) in regulating vasoreactivity. To further characterize AT(1b) receptor distribution, several other tissues were examined. Among them, AT(1b) is only predominantly expressed in hypothalamus, whereas AT(1a) exists exclusively or as a major subtype in heart, pituitary, adrenal glands and brainstem. These results further underscore a tissue-specific role for AT(1b) receptor in mice.

Angiotensin I↗

PubMed1987

45Ca fluxes in rat mesenteric resistance vessels.

In order to evaluate previously utilized 45Ca influx measurements in Wistar-Kyoto (WKY) rat mesenteric resistance vessels, 45Ca compartments obtained under steady-state conditions have been determined. Curve fitting of 45Ca efflux curves resulting from a 50 min washout of 45Ca from vessels incubated in 45Ca-labeled physiological saline solution (PSS) for 1.5 h yields a biexponential as the best fit. The rapidly exchanging compartment has a t1/2 of 58 +/- 5 s, while the slowly exchanging compartment has a t1/2 of 10.5 +/- 1.5 min. A two-compartment model is proposed, with the rapidly exchanging compartment hypothesized to be extracellularly bound Ca2+, and the more slowly exchanging compartment to be intracellular Ca2+. This model is supported by the observation that high K+ increases the 45Ca content of the slowly exchanging fraction, while decreasing that of the rapidly exchanging fraction. Two components of 45Ca efflux can be further distinguished by washout in ice-cold Ca2+-free PSS containing 2 mM EGTA. Under these conditions, the rapidly lost fraction has a t1/2 of 70 +/- 7 s, while the more slowly lost fraction has a t1/2 of 28.9 +/- 5 min. High K+ also increases the 45Ca content of this fraction. The curve relating the steady-state uptake of 45Ca into this fraction to time can best be fitted to a single exponential, for which the t1/2 and 45Ca content are not different from those determined from steady-state 45Ca efflux data.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

[Positive predictive value and negative predictive value of spiral CT in the diagnosis of closed loop obstruction complicated by intestinal ischemia].

PURPOSE: To assess the positive predictive value and the negative predictive value of spiral CT in the diagnosis of "closed-loop" obstruction complicated by intestinal ischaemia. MATERIALS AND METHODS: Between January 1999 and January 2002, 120 patients with small intestine closed-loop obstruction who had undergone surgical laparotomy within 2-6 hours from abdominal and pelvic spiral CT were retrospectively reviewed. The CT scans were performed using 5-mm slice thickness, 1 s scan delay, 5 x 5-mm collimation and 1.5 pitch after administering i.v. iodinated contrast material (120 ml volume, 60 s scan delay, 2.5-3 ml/s rate) with an automatic injector. For the diagnosis of closed-loop obstruction the following CT findings were examined: identification of the transitional area, 'C', 'U' or 'beak' shape of the obstructed loops, radial distribution of the involved mesenteric vessels. For the diagnosis of loop ischaemia, the following findings were evaluated in addition to the CT signs described above: submucosal oedema, increased, reduced, or no enhancement of the loop walls, oedema of the mesenteric vessels, fluid within the loops or in the intraperitoneal spaces. RESULTS: 'U', 'C', 'beak' loop configuration with poor or no contrast enhancement of the obstructed loop walls, ascites, rotation and engorgement of mesenteric vessels enabled the diagnosis of 26 cases of closed-loop obstruction complicated by ischaemia, infarction. U- or C-shaped loops with radial distribution and/or rotation of mesenteric vessels towards the obstruction site suggested the correct diagnosis in 94 cases, but did not allow identification of ischaemia in 25 cases. The positive predictive value of spiral CT related to ischaemic loop complications was 100%; the negative predictive value was 73%. CONCLUSIONS: Spiral CT is a reliable imaging technique enabling the diagnosis of closed-loop obstruction with or without intestinal ischaemic complications. Any alterations detected in the trophic status of the loops or mesentery imply ischaemic complications requiring emergency surgery. On the contrary, if only CT signs of closed-loop obstruction are detected, the existence and/or development of ischaemia cannot be ruled out.

Adult↗

PubMed1998

Pressure-volume relationships in sheep mesenteric lymphatic vessels in situ: response to hypovolemia.

We applied the principles of cardiac mechanics to study the contraction cycles of postnodal sheep mesenteric lymphatic vessels in an in situ preparation. A segment of intestinal lymphatic was isolated from lymph input and provided with Krebs solution from a reservoir. Pressure-volume relationships were assessed under various transmural pressure conditions using videomicroscopic techniques to measure diameter changes and a miniature catheter pressure transducer to monitor intralymphangion pressure. The contraction cycles were quite variable but, on average, exhibited three phases of systole and three phases of diastole with periods of isovolumetric contraction and relaxation. Elevations of transmural pressure up to 4 cm H2O resulted in significant increases in stroke volume, ejection fraction, pulse pressure, and output/minute but not contraction frequency. Regression analysis of the end systolic (ESPVR) and end diastolic pressure-volume relations (EDPVR) revealed a linear ESPVR (r2 = 0.83 +/- 0.03) and exponential EDPVR (r2 = 0.83 +/- 0.02), a result that is similar to that observed in cardiac contraction cycles. Following a 25% whole blood volume bleed (a stimulus known to enhance lymphatic pumping), significant increases in stroke volume, ejection fraction, and output/minute were observed up to transmural pressures of 4 cm H2O. While an index used to assess cardiac contractility (end systolic elastance-Ees) was not observed to change after the bleed, a shift to the left of the end-systolic pressure-volume relations compared with the sham-bled group (significant shift of regression lines for ESPVR) suggested that hemorrhage exerted a positive inotropic effect on mesenteric lymphatics.

Animals↗

PubMed1991

Characterization of beta-adrenoceptor subtypes and indications for two cell populations in isolated bovine mesenteric lymphatic vessels.

The pharmacological characterization of beta-adrenoceptor subtypes and the identification of two cell populations were investigated in isolated bovine mesenteric lymphatic vessels. The beta-adrenoceptor agonists isoprenaline, dobutamine and salbutamol concentration dependently decreased the amplitude and the frequency of spontaneous contractions and the amplitude of electrically induced contractions. The order of potency was isoprenaline greater than salbutamol greater than dobutamine. These effects were competitively antagonized by atenolol with pA2 values close to 7 with isoprenaline and dobutamine as agonists, and near 5.5 with salbutamol as the agonist. Noradrenaline concentration dependently reduced electrically induced contractions, an effect which was reversed to a slight enhancement after blockade of beta-adrenoceptors with propranolol (10(-6) M). These results confirmed the presence of postjunctional beta 1- and beta 2-adrenoceptor subtypes in lymphatic vessels and provide the first indication of the existence of two pharmacologically and functionally distinct cell populations, one of which exhibits pacemaker activity.

Adrenergic beta-Agonists↗

PubMed1992

Indomethacin administration after temporary ischemia causes bowel necrosis in mice.

Several reports have suggested indomethacin administration causes necrotizing enterocolitis (NEC) in infants. Few experimental studies have addressed this relationship. We studied the effects of indomethacin after temporary intestinal ischemia in CD-1 mice, using a previously reported method of simulating NEC in mice. This involved occlusion of both superior mesenteric vessels for 15 minutes. Three groups were studied. In group 1, 12 mice had superior mesenteric vessels occluded for 15 minutes, followed by intravenous (IV) administration of saline for three doses over 3 days. In group 2, 12 mice had sham laparotomy, without occlusion of vessels, followed by IV administration of indomethacin for three doses over 3 days. In group 3, 36 mice had mesenteric vessel occlusion for 15 minutes, followed by IV administration of indomethacin for three doses over 3 days. The results were as follows: group 1, bowel necrosis developed in 1 of 12 animals (8%); group 2, all 12 animals survived without bowel damage (0%); and group 3, 22 of 36 animals developed bowel necrosis (61%) (Fisher's Exact Test: occlusion alone v occlusion and indomethacin, P = .002; indomethacin alone v occlusion and indomethacin, P = .00015.) We conclude that whereas occlusion alone or indomethacin alone does not cause bowel necrosis, temporary intestinal occlusion followed by indomethacin causes bowel necrosis in over 60% of animals studied. In the shocked preterm infant who may have suffered temporary intestinal ischemia, administration of indomethacin may be the second step to development of NEC.

Animals↗

PubMed1990

Effects of long-term laxative treatment on rat mesenteric resistance vessel responses in vitro.

The effects of long-term treatment with the laxatives senna and 1,8-dihydroxyanthraquinone (danthron) were investigated in isolated mesenteric vascular beds of rats. The senna was administrated as ground senna pods mixed with milk chocolate. Danthron was also administered in this way. Chocolate-fed, senna-fed, and danthron-fed rats were supplied with usual feed, supplemented with chocolate, chocolate adulterated with ground senna pods, and chocolate adulterated with danthron, respectively. A group of control rats had no supplement. Perivascular nerve stimulation elicited frequency-dependent vasoconstriction of the mesenteric bed. There were no significant differences in responsiveness to perivascular nerve stimulation among mesenteric beds from the four groups. During two separate consecutive applications of capsaicin, a sensory neurotoxin, pressor responses to nerve stimulation of vascular beds from the control and chocolate-fed rats were inhibited on both occasions. However, in mesenteric beds from the senna-fed and danthron-fed groups, inhibition of pressor responses was the same on the first application of capsaicin as in the control and chocolate-fed groups, but the effect of the second application of capsaicin was greatly reduced. Calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine mimicked the inhibitory action of capsaicin on nerve stimulation in all groups, while substance P was without effect. There was no significant difference in responsiveness to these agents among the four groups. These results suggest that senna or its metabolites may cause a sensory neuropathy of mesenteric resistance vessels and that calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine, but not substance P, are possible candidates as mediators of the inhibitory effects induced by capsaicin.

Adenosine↗

PubMed1994

In vitro studies on responses to pentoxifylline and aminophylline of rat mesenteric resistance vessels.

Pentoxifylline (1-(5-oxohexyl)-3,7-dimethylxanthine) is a metylxanthine derivative used in the treatment of peripheral arterial disease. In isolated rat mesenteric resistance vessels mounted on an isometric myograph and precontracted with noradrenaline (5 microM), pentoxifylline (0.1 microM-10 mM) and aminophylline (0.1 microM-10 mM) evoked concentration-dependent relaxations. The resistance vessels were more sensitive to pentoxifylline, i.e., the concentration of the agonist evoking 50% relaxation (EC50 value) was 105 +/- 15 microM for pentoxifylline vs. 200 +/- 20 microM for aminophylline (P < 0.01). The vasorelaxant response to pentoxifylline was attenuated by mechanical removal of the endothelium, or by inhibition of the endothelial production of nitric oxide with NG-nitro-L-arginine. Inhibition of cyclooxygenase metabolism with indomethacin did not influence the response to pentoxifylline significantly, but was associated with an increased sensitivity to aminophylline. Furthermore, the vasorelaxation of resistance vessels elicited by pentoxifylline was diminished after incubation with tetraethylammonium, a nonselective K+ channel blocker, and pertussis toxin, an inhibitor of certain G-proteins. In contrast, the vasorelaxation elicited by aminophylline was generally enhanced by these experimental manipulations. The results indicate that the vasorelaxant properties of pentoxifylline and aminophylline in resistance vessels are mediated primarily at the level of the vascular smooth muscle cell, but that the mechanisms of the two agonists partly differ. Endothelial-derived factors (e.g., nitric oxide) contribute to the response to pentoxifylline, and may, through other mechanisms, attenuate the vasorelaxation elicited by aminophylline.

Aminophylline↗

PubMed1980

Prostaglandin action, release and inactivation by rat isolated perfused mesenteric blood vessels.

1 The following experiments were undertaken to confirm that prostaglandin is necessary for noradrenaline to exert its full vasoconstrictor effect in rat mesenteric blood vessels. Prostaglandin release and inactivation were also studied. 2 The cyclo-oxygenase inhibitor, 5, 8, 11, 14-eicosatetraynoic acid caused a significant depression of the concentration-effect curve to noradrenaline. As with indomethacin, responses were restored to control levels by prostaglandin E2 (PGE2) but PGE2 did not restore responses to noradrenaline depressed by papaverine. 3 PGE2-like activity was released from tissues at rest, equivalent to 50 +/- 20 pg PGE2/min. The substance was probably a stable prostaglandin since activity remained on acidifying and extracting into chloroform. The increase in release stimulated by noradrenaline was reduced below resting values by indomethacin. 4 There was a net loss of 7 +/- 1 and 1 +/- 0.2 ng PGE2/min from tissues perfused with 40 and 4 ng/min PGE2 respectively. No uptake occurred at lower PGE2 perfusion rates. 5 When indomethacin was used to depress responses to noradrenaline 15(S)-15-methyl PGE2 methyl ester was 12 times more potent than PGE2 in restoring responses to control values. The cyclic endoperoxide analogue U-46619 caused only partial restoration of indomethacin-depressed responses to noradrenaline but increased perfusion pressure at 2 ng/ml and above. 6 The results confirm that endogenous prostaglandin release, possible of PGE2, is obligatory to the full vasoconstrictor effect of noradrenaline. Noradrenaline increases the amount of prostaglandin released which may be taken up and inactivated by 15-hydroxy prostaglandin dehydrogenase or beta-oxidase. U-46619 may mimic both PGE2 and thromboxane A2.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1988

Pinacidil opens K+-selective channels causing hyperpolarization and relaxation of noradrenaline contractions in rat mesenteric resistance vessels.

1. The effects of pinacidil on noradrenaline-induced tone, smooth muscle membrane potential and 42K- and 86Rb-efflux from isolated mesenteric resistance vessels (internal diameter 200 microns) of the rat have been studied. 2. Pinacidil (0.3-10 microM) produced concentration-dependent suppression of noradrenaline-induced tone. 3. Pinacidil (0.3-10 microM) caused concentration-dependent hyperpolarization of the smooth muscle. 4. In rat resistance vessels loaded with 42K, pinacidil (1-10 microM) significantly increased the 42K-efflux rate constant. 5. With the use of 86Rb as a marker for K+, 1 microM pinacidil did not affect the 86Rb-efflux rate constant, while 10 microM pinacidil transiently increased the 86Rb rate constant. 6. The results indicate that the relaxant action of pinacidil in these vessels is due to the opening of K+-channels and consequent hyperpolarization. The K+-channels opened are selective for 42K over 86Rb.

Animals↗

PubMed1995

Evidence that the L-arginine pathway plays a role in the regulation of pumping activity in bovine mesenteric lymphatic vessels.

The objective of this study was to investigate the role of the L-arginine pathway in the regulation of lymphatic pumping. Bovine mesenteric lymphatic vessels (8 to 12 cm in length containing four to six lymphangions) were immersed in an organ bath with input provided by a reservoir filled with Krebs solution. The vessels were stimulated to pump by applying a 6 cm H2O transmural pressure. The addition of 10(-7)-10(-4) M oxyhemoglobin, NG-monomethyl-L-arginine (L-NMMA), or methylene blue to the reservoir resulted in a reduction in lymphatic pumping. L-Arginine (10(-7)-10(-4) M) had no effect on spontaneous pumping activity. However, L-arginine reversed the inhibition caused by oxyhemoglobin and L-NMMA. When tested between 10(-7) and 10(-6) M, sodium nitroprusside (sNP) had variable effects on lymphatics. sNP depressed pumping in approximately 2/3 of the vessels and increased pumping in the remaining 1/3 of ducts. When the results were meaned, sNP caused a significant depression in activity. However, the lower concentration of sNP (10(-7) M) was able to reverse the inhibitory effects of oxyhemoglobin, L-NMMA, and methylene blue whereas the higher concentration (10(-6) M) caused further reductions in pumping activity. These results suggest that bovine lymphatic vessels produce nitric oxide or a related compound. L-Arginine metabolites appear to facilitate the pumping response by an as yet undefined mechanism.

Animals↗

PubMed2004

Blunt trauma to the gastrointestinal tract and mesentery: is there a role for helical CT in the decision-making process?

The CT diagnosis of bowel and mesenteric injuries is difficult and warrants optimal technique and skilled interpretation. We retrospectively reviewed 36 consecutive patients with blunt traumatic injuries to the bowel and mesentery at our regional level I trauma center during the past 3 years. Physical examination, laboratory, Computed tomographic (CT), and intraoperative findings were compared. Surgically proven bowel injuries (13 cases) occurred in the duodenum (three cases), ileum (two cases), jejunum (two cases), colon (three cases), and stomach (three cases). CT findings considered specific of bowel rupture were observed in 5/13 patients including: extraluminal oral contrast or luminal content extravasation (four cases) and discontinuity of hollow viscus wall (one case). In the remaining 8/13 CT findings considered suggestive of bowel injury consisted of: pneumoperitoneum (six), gas bubbles close to the injured hollow viscus (three), thickened (>4-5mm) bowel wall (five), bowel wall hematoma (three), intraperitoneal fluid of unknown source (three). Mesenteric injury (23 cases) were surgically observed at the level of the mesenteric vessels (17 cases), legament of Treitz (two cases), gastro-duodenal artery (one case), transverse (one case) and sigmoid mesocolon (one case). CT finding considered specific of mesenteric laceration was active extravasation of contrast material from the mesenteric vessels (10 cases). CT findings suggestive of mesenteric injury (13 cases) consisted of: mesenteric hematoma (five) and/or high attenuation fluid collections, within the mesenteric root (eight) and folds (four). Helical CT is sensitive in the identification of bowel and mesenteric injury after blunt trauma providing a wide spectrum of findings. However, CT cannot be used as the sole indicator in cases with isolated thichened bowel wall, mesenteric hematoma, bowel hematoma, pneumoperitoneum or gas bubbles. Persistent, active extravasation of intravenous constrast medium from the mesenteric vessels, in isolation or associated with further injuries, requires immediate exploration and repair; disruption of bowel wall and extravasation of oral contrast are definite signs of bowel rupture. Close clinical observation, monitoring, and surgical expertise are mandatory for appropriate management.

Contrast Media↗

PubMed2000

Experimental model of anorectal transplantation.

BACKGROUND: Anorectal transplantation with pudendal nerve anastomosis after rectal excision is a possible strategy that would avoid a colostomy and recreate potentially normal anorectal function. This study investigates the technical feasibility of anorectal transplantation with pudendal nerve and inferior mesenteric artery and vein anastomosis in a porcine model. METHODS: Four female pigs (22-42 kg) provided donor anorectum for four male recipients (29-39 kg) under standard general anaesthesia. The donor operation involved abdominoperineal excision of rectum (APR) taking the anal sphincter, pudendal neurovascular bundle and inferior mesenteric vessels. The recipient underwent APR, transperineal introduction of the donor graft, anastomoses of the rectum, inferior mesenteric vessels and pudendal neurovascular bundle, and perineal closure. Recorded variables were duration of each step of transplantation, ischaemic time, dimensions of anastomosed structures and postoperative graft viability. Animals were killed at 24 h, the state of the graft was noted and tissue was taken for confirmatory histology. RESULTS: Mean operation time was 372 (range 303-435)min. Mean ischaemic time was 118 (100-130)min. Before death, observation at laparotomy revealed two pink grafts, one slightly dusky but healthy graft and one outright failure, reflecting the state of the mesenteric vessels, which were patent in three and thrombosed in one. Histological examination showed no difference between control biopsies and the three cases with satisfactory mesenteric flow. Gross ischaemia was present histologically in the failed case. CONCLUSION: Anorectal transplantation is technically feasible in a pig model. Longer-term studies are now needed to assess return of function and overcome rejection issues.

Anal Canal↗

PubMed1970

Elastic vascular sclerosis of mesenteric blood vessels in argentaffin carcinoma.

Argentaffin carcinoma (carcinoid tumour) of the ileum has been found to be associated with ischaemic ileal necrosis due to elastic sclerosis of the mesenteric blood vessels. This vascular change was present in 17 out of 25 ileal tumours, all of them invasive, but was absent in 75 appendicular, rectal, and other carcinoids. The pathology is described and essential points of difference are noted from the cardiovascular changes in the carcinoid syndrome. This elastic vascular sclerosis may be due to a product of the tumour and constitute an additional component of the complex range of changes that makes up ;the carcinoid spectrum'.

Adolescent↗