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In the resection of mesenteric tumors or primary malignant lesions of the small bowel, exposure of the superior mesenteric vessels is important. This is the necessary criterion of resectability and the condition of obtaining maximal margins in the lymphatic drainage area. It also helps avoid unnecessary sacrifice of branches and tributaries to the superior mesenteric vessels from uninvolved portions of the bowel.
BACKGROUND/AIMS: To investigate treatment outcome and patterns of failure of sequential chemotherapy (CHT) and/or concurrent hypofractionated radiotherapy (RT) and CHT followed by surgery in locally advanced non-metastatic pancreatic adenocarcinoma. METHODOLOGY: Seven patients with locally advanced but marginal resectable tumors (close contact but no signs of infiltration of the mesenteric vessels and/or vena portae) were treated with hypofractionated RT (5x3 Gy per week) and concurrent continuous infusion (300 mg/sqm/24 h, 7 days per week) of 5-fluorouracil (FU). Ten patients with locally advanced disease with radiologically suspected infiltration of the mesenteric vessels and/or v. portae were treated with 2 cycles of Cisplatin (75 mg/sqm) and Gemcitabine (2x1250 mg/sqm), and patients without tumor progression received the same concurrent RT/CHT as group 1. Four weeks after RT/CHT radical pancreatectomy was planned for patients with stable disease or remission. RESULTS: Toxicity was low in both groups, with no CTC grade 4 toxicity. In group 1, RT/CHT was completed in all patients. There was no radiological remission, but stable disease in 5 out of 7 patients. All 5 patients underwent resection of the primary tumor with a R0-resection in 3 patients. In group 2, 8 patients completed CHT and RT/CHT treatment as planned. There were 3 with partial remission. Operation was done in 4 patients, but only one R0 resection was achieved. The median survival time for all 17 patients is 13 months, with 1- and 2-year survival being 53% and 18%, respectively. Local progression was observed in 9, peritoneal seeding in 7 and distant metastasis (mostly liver and lung) in 8 patients. CONCLUSIONS: The neoadjuvant therapy could be administered with low toxicity. Results of this study warrant further investigation aiming at optimal tailoring in of this treatment approach in these two subgroups of patients.
Duodenal obstruction caused by ileocolic intussusception in the absence of intestinal malrotation is extremely rare. We present and discuss the imaging findings in an infant with an intussusception secondary to a duplication cyst in whom sonography also showed inversion of the orientation of the mesenteric vessels and a distended stomach. A contrast medium study revealed a proximal duodenal obstruction with a beak appearance suggestive of midgut volvulus. At surgery, an ileocolic intussusception causing duodenal obstruction without concomitant malrotation or volvulus was found. The combination of duodenal obstruction and abnormal relationship of the mesenteric vessels as a result of ileocolic intussusception has not previously been reported in the literature.
In order to verify whether the migration of Schistosoma mansoni from mesenteric vessels towards the liver under the action of general anesthetics (althesin, ether, enflurane, halothane, propanidid and thiopental sodium) is reversible, 65 mice were submitted to an anaesthetic and then perfused after dissection 24 hours later. The Schistosoma counts from porto-mesenteric vessels of the mice from control groups (60 mice) were compared with those of the mice under experiment. The counts from the hepatic area of the groups were also compared. No significant difference in the counts in the mice under experiment and those of control groups was noted.
The outstanding angiographic features of small intestinal intussusception are: (a) abrupt disappearance of mesenteric vessels at the neck of the intussusception with crowding of the vasa recta; (b) appearance of long collateral channels at the neck of intussusception; (c) angulation and retraction of major intestinal branches; (d) reversal of the course and angulation of the invaginated mesenteric vessels; (e) overlapping of the mesentery vessels by branches of the intussuscipiens; (f) abrupt change in the appearance of the vasa rectae of the distended intussuscipiens and the distal nondistended small intestines.
PURPOSE: To evaluate the performance of radiologists in the diagnosis of internal hernia with specific computed tomographic (CT) findings. MATERIALS AND METHODS: Abdominal CT scans obtained in 42 patients were retrospectively reviewed by three radiologists. The case group consisted of 18 patients with internal hernias (two paraduodenal, 16 transmesenteric); the comparison group was 24 patients with no internal hernia. Images were reviewed in a random and blinded fashion. Individual and group performance was evaluated with receiver operating characteristic (ROC) analysis, and interobserver agreement was measured with Cronbach coefficient alpha. Individual CT signs relevant as predictors of transmesenteric hernia were identified with logistic regression analysis and ranked by their odds ratio and P values. RESULTS: Both paraduodenal hernias were diagnosed by all readers on the basis of CT signs, including a retrogastric saclike mass of small-bowel loops. Diagnosis of transmesenteric hernia was more difficult and variable, with an average accuracy of area under the ROC curve (A(z)) of 77%, sensitivity of 63%, and specificity of 76%. CT signs of transmesenteric hernia were recognized consistently (Cronbach coefficient alpha >or= 0.80) and included a cluster of dilated small-bowel segments and stretching and displacement of mesenteric vessels. Coexisting volvulus and ischemia were diagnosed with low sensitivity (46% and 43%, respectively) but high specificity (96% and 98%, respectively). CONCLUSION: Diagnosis of internal hernia with CT remains difficult. Special attention should be given to the clustering of bowel loops, the mesenteric vessels, and signs of small-bowel obstruction.
Physiological and histochemical studies have clearly demonstrated the control and innervation of the sympathetic nerve on the splanchnic veins. However, the origins of postganglionic fibers remain to be determined. In this study, we used the retrograde transport of horseradish peroxidase (HRP) technique to trace the origins of postganglionic neurons in pre- and paravertebral sympathetic ganglia that innervate the mesenteric vein. A segment (6-8 mm) of mesenteric vein close to the duodeno-jejunal junction was isolated. HRP was applied externally on the vein segment to allow uptake into the nerve endings. In 10 cats, there was a total of 9275 HRP-labeled neurons in the pre- and paravertebral ganglia. The neuron distribution (mean +/- S.E.M.) was as follows: 452 +/- 77 (49%) in the superior mesenteric ganglion (SMG), 248 +/- 62 (27%) in the right celiac ganglion (RCG), 111 +/- 23 (12%) in the left celiac ganglion (LCG) and 58 +/- 16 (6%) in the splanchnic ganglia. Although the appearance of HRP neurons in the paravertebral ganglia (T10-L3) was relatively sparse, there were still significant numbers in L1 (26 +/- 13, 3%), T13 (15 +/- 5, 2%) and other ganglia. The results indicate that more than 90% of the presynaptic sympathetic neurons innervating the mesenteric vein make their synaptic connections in the prevertebral ganglia, mostly SMG and then RCG as well as LCG. Postsynaptic neurons arising directly from the paravertebral ganglia (mostly L1 and T13) constitute to about 6% of the total.
In the present study we characterized the effects of and receptors for endothelins (ETs) in the guinea pig mesenteric arterial and venous vasculatures. Endothelin-1 (ET-1) (10-500 pmol) induced a dose-dependent increase of perfusion pressure of the arterial and venous beds. ET-2 (10-500 pmol) also induced a dose-dependent vasoconstriction on both sides of the mesenteric circulation but was less potent than ET-1. In contrast, ET-3 (10-1,000 pmol) and the selective ETB agonist IRL 1620 (1,000 pmol) were inactive. A nitric oxide (NO) synthase inhibitor, L-NAME (200 microM), markedly potentiated the vasoconstrictor response to ET-1 (100 pmol arterial side; 1,000 pmol venous side) on both sides of the mesenteric vasculature. In precontracted mesenteric vessels, ET-1 (0.1-5 pmol) and IRL-1620 (1,000 pmol) induced a small yet significant vasodilation only on the arterial side. Furthermore, BQ-123 (1 microM), an ETA receptor antagonist, significantly reduced the ET-1-induced venoconstriction and completely blocked the vasoconstriction on the arterial side. Hence, the arterial and venous mesenteric vessels of the guinea pig respond to ETs by activation of ETA receptors. Furthermore, the endothelium may act as a physiologic barrier to the constrictor effects of ETs by basally releasing NO.
1. In previous studies we have shown that, after the administration of adriamycin, hypertension developed in rats who became pregnant (adriamycin-pregnant rats), whereas virgin animals remained normotensive. Subsequently, we showed that this hypertension was prevented by administration of L-arginine, suggesting that deficient synthesis of nitric oxide may be pathogenetic in this model. 2. To further assess the role of nitric oxide in this model, we measured mean arterial blood pressure after administration of L-arginine to adriamycin-pregnant rats or of NG-nitro-L-arginine-methyl ester (L-NAME) to normal pregnant rats. In other experiments, we assessed the response of isolated perfused arterial mesenteric vessels, precontracted with noradrenaline, to acetylcholine, L-arginine or L-NAME. 3. Blood pressure was decreased in normal pregnant rats, whereas it was elevated in adriamycin-pregnant rats. L-NAME treatment increased blood pressure in normal pregnant rats and L-arginine decreased it in adriamycin-pregnant rats. 4. Mesenteric vessels of adriamycin-pregnant rats exhibited an exaggerated vasoconstrictory response to noradrenaline, when compared with the blunted response observed in normal pregnancy. The addition of L-NAME in vitro induced a further contraction, significantly greater in normal pregnant rats. The vasodilatory response to acetylcholine and L-arginine was greater in vessels from adriamycin-pregnant rats. In contrast, responses to either nitroprusside or diazoxide were similar in all groups. 5. The results suggest a state of reduced nitric oxide synthesis in rats with adriamycin nephropathy, leading to vascular maladaption and hypertension in pregnancy.
UNLABELLED: Previously, we reported that propofol hyperpolarizes vascular smooth muscle (VSM) cells of small arteries and veins. The current study was designed to determine whether propofol-mediated hyperpolarization is the result of specific effects on potassium channels known to exist in VSM and on steps in the intracellular nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and cyclic adenosine monophosphate (cAMP) second messenger pathways. VSM transmembrane potentials (E(m)) were measured in situ in sympathetically denervated, small mesenteric arteries and veins of Sprague-Dawley rats. Effects of propofol on VSM E(m) were determined before and during superfusion with specific inhibitors of VSM calcium-activated (K(Ca)), adenosine triphosphate-sensitive (K(ATP)), voltage-dependent (K(v)), and inward rectifying (K(IR)) potassium channels and with endogenous mediators of vasodilation. Propofol significantly hyperpolarized VSM in small mesenteric vessels. This hyperpolarization was abolished on inhibition of K(Ca) and K(ATP) channel activity and on inhibition of NO and cGMP (but not cAMP). Assuming a close inverse correlation between the magnitude of VSM E(m) and contractile force, these results suggest that propofol induces hyperpolarization and relaxation in denervated, small mesenteric vessels by activation of K(Ca) and K(ATP) channels. Such channel activation may be mediated by activation of NO and cGMP, but not cAMP, second messenger pathways. IMPLICATIONS: The results of this study indicate that propofol-mediated hyperpolarization in vascular smooth muscle can be attributed to the activation of calcium-activated, adenosine triphosphate-sensitive potassium channels, the nitric oxide, and cyclic guanosine monophosphate pathways.
The pathophysiology of hypertension in chronic renal failure is complex, but sodium retention and volume expansion play an important role. High salt intake may aggravate hypertension in chronic renal failure, but the mechanisms of this action are not well established. In this study, we have tested the hypothesis that high salt intake aggravates hypertension in rats with chronic renal failure by decreasing nitric oxide synthase (NOS) expression and by increasing sympathetic nervous system activity. Sprague-Dawley rats were subjected to 5/6 nephrectomy (CRF) or sham-operation and fed a regular rat chow. Half of the rats were allowed to drink distilled water and half water containing 1% NaCl. Blood pressure was measured weekly by tail-cuff. Four weeks after nephrectomy or sham-surgery, animals were sacrificed and brains immediately separated and frozen. Norepinephrine (NE) content and NOS-mRNA gene expression were measured in the posterior hypothalamic (PH) nuclei, the locus coeruleus (LC), the paraventricular nuclei (PVN), and in the mesenteric vessels. The endogenous concentration of NE was greater in the PH, LC, and PVN of CRF rats than it was in control animals both during a normal and a high dietary salt intake. In control and CRF rats, the concentration of NE was greater (p < 0.01) during a high than during a normal salt intake in the PH, LC, PVN, and in the mesenteric vessels. A high salt intake reduced the nNOS-mRNA gene expression in the PH (from 100 +/- 2.4 to 46 +/- 1.0;p < 0.01), LC (from 92 +/- 1.9 to 69 +/- 1.2; p < 0.01) and PVN (from 63 +/- 0.8 to 46 +/- 1.3) of CRF rats. A similar reduction occurred in the PH (from 36 +/- 0.8 to 23.6 +/- 1.2), LC (from 33 +/- 1.4 to 24 +/- 1.1) and PVN (from 37 +/- 1. to 27 +/- 1.0) of control rats. High salt intake significantly reduced the nNOS-mRNA gene expression in the mesenteric arteries of control rats, but not in those of CRF rats. In conclusion, these studies provide evidence that in control and CRF rats, high salt intake inhibits nNOS-mRNA expression in the brain, resulting in activation of the sympathetic nervous system and higher blood pressure.
1. The pH-sensitive dye 2',7'-bis-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in segments of rat resistance vessels (internal diameter about 200 microns) with the vessels mounted in a myograph for simultaneous measurements of isometric contraction. 2. BCECF loaded slowly into the vessels over 1 h and did not affect the maximal contractility of the vessels. There was a loss of dye with time which, however, was very slow when the segments were only excited for 2 s/min, suggesting that the loss was mainly due to dye bleaching with only a very slow leak. 3. The ratio of the emissions (at 540 nm) with excitation at 495 and 450 nm was calibrated in terms of pH using the K+-H+ ionophore nigericin. This calibration gave a pHi value of 7.15 +/- 0.02 (n = 20), suggesting that hydrogen ions are not in electrochemical equilibrium in these vascular smooth muscles which have a membrane potential of about -60 mV. 4. Addition of 10 mM-NH4Cl caused a transient alkalinization and wash-out of 10 mM-NH4Cl a transient acidification. Increasing CO2 with maintained bicarbonate caused a rapid acidification followed by an incomplete recovery. Removal of CO2 and bicarbonate (HEPES-buffered solution) with constant extracellular pH caused a transient alkalinization but steady-state pHi was not significantly altered. 5. In bicarbonate-free buffer the Na+-H+ exchange blocker 5-(N-ethyl-N-isopropyl) amiloride (EIPA) and sodium-free conditions caused a slow acidification. In bicarbonate buffer (PSS) EIPA had no detectable effect after 10 min but the anion exchange blocker diisothio-cyanatostilbenedisulphonic acid (DIDS) caused a small acidification over that time course. 6. The rate of recovery after an acid load was about 50% lower in HEPES buffer compared to PSS and it was inhibited by EIPA. In PSS amiloride and EIPA each had a small inhibitory effect on the pH recovery after an acid load. DIDS also inhibited the recovery from an acid load in PSS and this effect was additive to that of EIPA. DIDS and EIPA also had additive inhibitory effects on the 22Na+ influx stimulated by the acid loading, while in HEPES buffer DIDS had no effect on either pH recovery or 22Na+ influx. These results suggest that a Na+-H+ exchange and an influx of bicarbonate coupled to sodium influx are of importance for pHi control in these vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
OBJECTIVE: Earlier, we reported that high insulin incubation in vitro leads to increased ETA receptor expression in cultured rat aortic smooth muscle cells (Diabetes 1998, 47: 934-944). Our later observation of enhanced endothelin-1 evoked vasoconstriction in aorta from the hyperinsulinemic obese Zucker rat indicated that this interaction might also be relevant in vivo. To further examine the relationship between insulinemia and endothelin, we characterized endothelin receptor expression and endothelin-1 peptide levels in vascular tissues and plasma from young and old obese Zucker rats. METHODS: 12 and 40-week-old Zucker obese and lean rats were used. Plasma endothelin-1 levels and endothelin-1 peptide content in the mesenteric artery and in the thoracic aorta were examined by radioimmunoassay. Messenger RNA levels of endothelin-1 peptide and ETA and ETB receptors were examined in the aortic and mesenteric vessels using RT-PCR. RESULTS: Obese rats from both age groups had significantly higher plasma levels of insulin (4-10 fold), total cholesterol (2-3 fold), triglycerides (10-fold), and glucose (approximately 1.5 fold) than their lean counterparts. There was a trend toward worsening lipoproteinemia and glycemia, but improved insulinemia with age in the obese rats. In association with these changes, obese rats exhibited attenuated endothelin-1 peptide and preproET-1 mRNA levels, but conversely elevated ETA and ETB receptor mRNA levels in both aortic and mesenteric vessels. CONCLUSION: These data suggest that vascular tissue from the metabolically dysregulated obese Zucker rat exhibits attenuated endothelin-1 peptide production and elevated endothelin receptor levels. Since elevated insulin levels have been linked to increased endothelin receptor expression, it is plausible that hyperinsulinemia upregulates endothelin receptors contributing to elevated vasoconstrictor responses to endothelin-1 in this model of obesity and hypertension.
We have investigated the role of cytochrome P450 (CYP-450) metabolites of arachidonic acid in the modulation of vascular reactivity to angiotensin II in vivo using an in situ blood-perfused mesenteric preparation in anaesthetized spontaneously hypertensive rats (SHR). Miconazole, a non-selective inhibitor of CYP-450 that inhibits both hydroxylation and epoxidation, substantially suppressed mesenteric vasoconstrictor responses to angiotensin II in SHR, but had no effect on responses to noradrenaline or sympathetic nerve stimulation. In normotensive Wistar-Kyoto (WKY) rats, miconazole caused only a modest suppression of vasoconstrictor responses to angiotensin II. N-Methylsulphonyl-12, 12-dibromododec-11-enamide (DDMS), a new selective inhibitor of CYP-450 omega-hydroxylase activity, decreased mean intra-arterial blood pressure and significantly attenuated mesenteric angiotensin II-induced vasoconstrictor responses in SHR. Isolated mesenteric vessels were able to metabolize (14)C-labelled arachidonic acid to hydroxyeicosatetraenoic acids (HETEs) in vitro, and this was substantially inhibited by DDMS. The results from the present studies combined with the existing evidence that angiotensin II stimulates the release of 20-HETE, a CYP-450 metabolite of arachidonic acid, suggest that CYP-450-derived HETEs may be important mediators in angiotensin II-induced vasoconstriction. However, the development of more sensitive assays for the detection in vivo of 20-HETE in mesenteric vessels would be required to confirm these findings.
BACKGROUND: The therapeutic efficacy of interleukin-2 (IL-2) has been limited by a dose-dependent vascular leak syndrome. This may be related to neutrophil-mediated endothelial injury. Taurine has been shown to decrease this injury in vitro. This study investigates the role of taurine in preventing IL-2-induced lung injury, and the role of neutrophil-endothelial interactions in mediating this injury. METHODS: Study 1: Sprague-Dawley rats (n = 12/groups) were randomised to controls, IL-2-treated (1 x 10(6) units), and IL-2-treated with taurine (4% solution, orally for 48 h prior to IL-2 therapy). Lung injury was measured by extravascular lung water (wet/dry weight) and bronchoalveolar lavage protein concentration. Neutrophil infiltration was evaluated by measuring myeloperoxidase activity and bronchoalveolar lavage neutrophil concentration. Study 2: Rats (n = 10/group) were randomised into the same groups as study 1. Neutrophil-endothelial interactions in mesenteric vessels were assessed by intravital microscopy at half-hourly intervals. RESULTS: Taurine reduced IL-2-induced acute lung injury as reflected by a decrease in wet-to-dry lung weight ratio from 7.2 +/- 0.5 in the IL-2 group to 4.7 +/- 0.3 in the taurine group (p < 0.05), and a decrease in bronchoalveolar neutrophil concentration from 823 +/- 19.5 in the IL-2 group to 538 +/- 18 in the taurine group (p < 0.05). Intravital microscopy demonstrated that IL-2 increased leucocyte adhesion and migration in mesenteric vessels, and that this was significantly reduced by taurine. CONCLUSION: These data suggest that taurine prevents IL-2-induced tissue injury in part by decreasing neutrophil-endothelial interactions.
The synthesis of prostacyclin (PGI2) and thromboxane A2 (TXA2) by the mucosal and muscular portions of the duodenum, jejunum, ileum and ascending colon, as well as that by mesenteric vessels, was investigated in starved and semistarved rats. The jejunal mucosa and muscularis showed a marked increase in PGI2 synthesis after fasting for 48 h and 72 h or semistarvation for 9 days when compared with controls. Jejunal TXA2 synthesis did not alter. In contrast, PGI2 and TXA2 synthesis in ileal mucosa and muscularis was significantly reduced after fasting for 48 h, 72 h and semistarvation for 9 days. PGI2 and TXA2 synthesis by duodenal and colonic muscularis was unaffected by fasting or semistarvation. PGI2 synthesis in mesenteric vessels was significantly increased by fasting and semistarvation. No changes in PGI2 or TXA2 were detected at 24 h in fasted rats in any of the tissues studied when compared with controls. These selective changes in PGI2/TXA2 secretion may be important mediators of adaptive changes in the small intestine in response to starvation.
The cyclooxygenase inhibitors aspirin and indomethacin enhanced platelet aggregation in mesenteric vessels, suggesting that the normal mesentery produces an antiaggregatory prostaglandin. Testing of mesentery incubate in mouse platelet-rich plasma disclosed an antiaggregatory material with the properties of prostacyclin. Chromatography showed that mesentery made several radiolabeled products from [3H]arachidonic acid, including one that cochromatographed with 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable hydrolysis product of prostacyclin. Gas chromatography-mass spectrometric analysis of mesentery incubate showed the presence of 6-keto-PGF1 alpha, synthesized from the mesentery's endogenous arachidonic acid. The enhancement of platelet aggregation in mesenteric vessels contrasts with earlier data showing that in similarly injured mouse cerebral vessels aggregation was retarded by both aspirin and indomethacin. This divergent effect of cyclooxygenase inhibitors in different vascular beds may depend on the relative importance of prostacyclin in the different beds or on the capacity of cyclooxygenase inhibitors to influence this prostacyclin production in different beds. Caution is urged before acceptance of a central role for PGI2, however, because of the capability of microvasculatures and adjacent tissue to synthesize a number of other products whose interaction with platelets and with aspirin and indomethacin remains to be elucidated.
Surgical treatment of ductal adenocarcinoma of the pancreas is considerably influenced by the delicate retroperitoneal position of the gland with close contact to major mesenteric vessels, lymphatics and nerve structures as well as by the unfavourable tumor biology including high affinity towards nerve tissue and early systemic spread. Based on these preconditions, kind and extent of resective measures have to be discussed with special care. Total pancreatectomy to improve radicality has been abandoned because of exaggerated early and late mortality and morbidity. The principle of distal gastric resection as part of the classic Whipple operation was shown to be oncologically not effective. It seems to be justified only if the tumor reaches the duodenopancreatic angle. Resection of the mesenteric vein is technically feasible with acceptable mortality, but leads to unfavourable survival rates since the respective lesions mostly are in an advanced stage. Extensive tissue clearance around the mesenteric vessels did not improve survival, but led to intractable diarrhoea in up to 76% of the cases. Concerning 114 patients resected for pancreatic head cancer in the own department actuarial 5-year survival was 6%. There was no significant difference whether classic Whipple (3%) or pylorus preservation (8%) was applied. None of the node positive patients survived more than 4 years. In contrast, those with negative nodes achieved 29% 5-years survival (p = 0.0059). Following 26 resections of the left pancreas for ductal carcinoma non of the patients survived more than 2 years. Results of the recent literature and the own experience are suggestive to believe that node positive stages won't benefit from extensive surgery. Therefore anatomical resection including the peripancreatic lymph node compartment is sufficient to preserve the chance for cure in early stages. Nowadays preservation of the stomach is the standard technique during pancreatoduodenectomy, which is, provided a perioperative mortality of less than 5%, accepted also as best palliation in suitable patient of advanced stages.