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PubMedDate not supplied

Limitations of angiography for mesenteric ischemia caused by midgut carcinoid tumors.

Mesenteric ischemia associated with carcinoid tumors often presents with nonspecific abdominal pain and is usually due to mesenteric branch artery occlusion caused by elastic vascular sclerosis. Mesenteric ischemia was defined by the operative findings of cyanosis or infarction. Eleven patients with intraabdominal metastatic carcinoid tumor were evaluated by angiography. Angiographic narrowing and occlusion of multiple peripheral jejunal and ileal intramesenteric branch arteries was present in 3 patients with mesenteric ischemia, but also occurred in 5 of 8 patients without mesenteric ischemia. Other angiographic abnormalities included staining of the primary tumor (5) or metastases (6), tenting of small mesenteric vessels (5), and occlusion of draining mesenteric veins (2). We conclude that in patients with midgut carcinoid tumors, angiographic narrowing and occlusion of peripheral mesenteric arteries most likely represents elastic vascular sclerosis, is indicative of mesenteric invasion of tumor, but correlates poorly with the presence of ischemia in the subtended bowel. Alternatively, a normal selective arteriogram should exclude mesenteric ischemia as the cause of abnormal pain.

Adult↗
PubMedDate not supplied

[The action of noradrenaline, vasopressin and deoxycorticosterone acetate on the activity of the Na+,K+ pump in the veins and arteries of different vascular regions].

Noradrenaline and vasopressin were shown to stimulate the Na+/K(+)-pump activity both in veins and in arteries, whereas desoxycorticosteronacetate did not increase it in pulmonary and mesenteric vessels and even depressed it in the mesenteric vein. There is different potentiation exerted by noradrenaline and vasopressin upon the Na+/K(+)-pump activity in veins and in arteries. The data obtained suggest the regional heterogeneity in the Na+/K(+)-pump activity in neurohormone activated blood vessels.

Animals↗
PubMed1998

Mesenteric and skeletal muscle microvascular responsiveness in subacute sepsis.

This study was performed to assess the effects of subacute sepsis in rats on the in vitro reactivity of arterioles (internal diameter, 100-150 microm) to alpha1- and alpha2-adrenergic stimulation and to angiotensin II. Male Sprague-Dawley rats were rendered septic by intraperitoneal implantation of a gelatin capsule containing sterile rat feces and 1 x 10(6) viable colony forming units of Escherichia coli. Control rats underwent sham laparotomy and implantation of a gelatin capsule containing only sterile feces. In vitro reactivity of arterioles from mesentery and skeletal muscle were studied 48 h later in a pressurized (50 mmHg) no flow state using videomicroscopy. Subacute sepsis decreased the contractile response of nonprecontracted microvessels from both anatomical sites to phenylephrine (both p < .01 versus control) and blunted the relaxation response to staurosporine (both p < .01), an inhibitor of protein kinase C. The small contraction to angiotensin II of mesenteric vessels was inhibited by sepsis (p < .05) but was unaltered in the skeletal muscle microcirculation. In the precontracted mesenteric microvessels from septic rats, endothelium-dependent relaxation to clonidine and to adenosine 5'-diphosphate were decreased (both p < .01 versus control), whereas in skeletal muscle microvessels, clonidine and adenosine 5'-diphosphate elicited constriction (both p < .01). Relaxation to the endothelium independent vasodilators sodium nitroprusside and pinacidil was preserved across all vessels. In conclusion, mesenteric and skeletal muscle microvascular responses to angiotensin II and alpha1- and alpha2-adrenergic stimulation are altered in subacute sepsis. This may in part lead to systemic hypotension and altered organ perfusion during states of chronic sepsis.

Angiotensin II↗
PubMed1988

Small bowel disease in children: diagnosis with CT.

The computed tomographic (CT) scans of 22 children with small bowel disease and those of 110 children with no small bowel disease were analyzed by two observers who were blinded with respect to clinical history and final diagnoses in order to determine which CT findings reliably indicated neoplastic, inflammatory, or noninflammatory processes. Bowel-wall thickening was the most reliable sign of disease. Five of six patients (83%) with bowel-wall thickness greater than 1 cm had neoplastic disease. Nine of ten patients (90%) with bowel-wall thickness between 3 mm and 1 cm had inflammatory disease, while four of six patients (66%) with wall thickness less than 1 cm and increased attenuation of mesenteric fat or an increase in the number of mesenteric vessels had noninflammatory edema. The presence of mesenteric masses was not a helpful sign for differentiating various disease processes. The results of this retrospective study suggest that the identification and classification of small bowel disease in children is possible from the objective analysis of CT findings.

Child↗
PubMed2002

Recurrent nonocclusive mesenteric ischemia after resection of iliac artery aneurysm.

A case of recurrent nonocclusive mesenteric ischemia in a patient with isolated internal iliac artery aneurysm penetrating the sigmoid colon is described. On the day after the aneurysm and the sigmoid colon had been resected, the patient developed necrosis of the left hemicolon. Fourteen and nineteen days after left hemicolectomy, massive intestinal bleedings occurred, requiring ileectomy. On the basis of operative findings of good pulsation of visceral arterial branches; angiography showing patent mesenteric vessels with some spasms; and pathological findings suggesting mesenteric ischemia, these ischemic events were diagnosed as nonocclusive mesenteric ischemia. Low-output syndrome induced by massive intestinal bleeding and atrial fibrillation and sepsis were responsible for the establishment of the nonocclusive mesenteric ischemia. Development of disseminated intravascular coagulation and continuous administration of diuretics for acute renal failure seemed to have further perturbed the mesenteric circulation. The patient died of subsequent multiple organ failure 4 months after the first operation. We should pay more attention to nonocclusive mesenteric ischemia in patients with mesenteric ischemia, and strict circulatory management during the perioperative period is essential in these patients.

Aged↗
PubMed1996

MR angiography of abdominal ischemia.

Advances during the past decade in MRI have made this modality increasingly suitable for evaluating abdominal vascular diseases. Preliminary results in canine models and humans suggest that MRI has the potential of becoming a definitive, noninvasive test for the diagnosis of both acute and chronic mesenteric ischemia. MRI can provide both morphological information about the patency or degree of stenosis in mesenteric vessels as well as quantitative functional information such as blood flow and blood oxygen saturation in these vessels. The MR techniques developed for studying the mesenteric circulation also can be used for improving the diagnosis and posttreatment evaluation of vascular diseases in other abdominal organ systems.

Acute Disease↗
PubMed1995

Region of epidural blockade determines sympathetic and mesenteric capacitance effects in rabbits.

BACKGROUND: The mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. The role of capacitance changes in the splanchnic venous bed can be clarified by comparing blocks of differing segmental distributions. Specifically, we speculated that blocks that include the innervation to the mesenteric circulation alter hemodynamics, sympathetic activity, and venous capacitance to a greater extent than blocks without blockade of sympathetic nerves to this critical vascular bed. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric vein diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Responses were compared after administration of epidural lidocaine using a dose and catheter level that limited anesthetic to lumbar levels (lumbar group) or thoracic levels (thoracic group). In addition, hemodynamic responses were recorded after thoracolumbar block in animals receiving alpha-chloralose but breathing spontaneously (spontaneous ventilation group) and in awake animals (awake group). RESULTS: Mean arterial pressure decreased 38.3 +/- 5.8% in the thoracic group but only 16.5 +/- 2.8 in the lumbar group. Sympathetic efferent nerve activity decreased in the thoracic group but increased in the lumbar group. An increase in vein diameter followed thoracic epidural anesthesia, but venoconstriction was observed after lumbar epidural block. The addition of intravenous sedation with alpha-chloralose did not increase the hypotensive effect of epidural anesthesia in this model. CONCLUSIONS: Block of sympathetic fibers to the splanchnic circulation with thoracic epidural lidocaine produces mesenteric venodilatation that contributes to hypotension in rabbits. A lesser decrease in blood pressure follows blocks limited to lower segments, because baroreceptor stimulation produces increased splanchnic sympathetic activity and mesenteric venoconstriction. Responses in this model are comparable with and without general anesthesia and mechanical ventilation. To minimize hemodynamic consequences, epidural blockade should ideally be confined to the fewest necessary segments, avoiding splanchnic innervation if possible.

Anesthesia, Epidural↗
PubMed1996

Sympathetic and mesenteric venous responses to baroreceptor or chemoreceptor stimulation during epidural anesthesia in rabbits.

BACKGROUND: Baroreceptor and chemoreceptor reflexes maintain homeostasis through mechanisms that involve sympathetic activation. Because sympathetic control of the mesenteric veins plays a central role in hemodynamic responses to stress, the effects of epidural blockade on reflex responses to hypoxia and bilateral carotid occlusion (BCO) were examined by monitoring direct measures of splanchnic sympathetic neural traffic and mesenteric venous capacitance. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric venous diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Intraluminal venous pressure was monitored by a servo-null micropressure technique. Responses were recorded during repeated administration of three different stresses, F1O2 = 0% for 40 s, F1O2 = 11% for 2.5 min, and BCO for 60 s. Animals received either thoracolumbar epidural blockade (0.4 ml/kg lidocaine 1.5%; n = 7) or 15 mg/kg intramuscular lidocaine (n = 7). RESULTS: Hypoxia and BCO produced sympathetic stimulation and active constriction of mesenteric veins. Epidural anesthesia accentuated the mean arterial pressure decrease from F1O2 of 0%, caused the 11% response to F1O2 to become depressor instead of pressor, and decreased the pressor effect BCO. Sympathetic efferent nerve activity and venous diameter responses to hypoxia and BCO were attenuated or eliminated. CONCLUSIONS: The hemodynamic effects of hypoxia result from a combination of direct depression and reflex activation. Thoracolumbar epidural anesthesia in rabbits impairs compensatory reflexes invoked by chemoreceptor stimulation and eliminates response to baroreceptor stimulation. Loss of splanchnic control of mesenteric capacitance contributes to the inhibition of the hemodynamic response to hypoxia or BCO during epidural anesthesia in rabbits.

Anesthesia, Epidural↗
PubMed1991

[Non-occlusive mesenteric infarction following cardiovascular surgery].

In the majority of patients with intestinal infarction, it is generally agreed that the occlusion of mesenteric arteries or vein is the primary etiologic factor; however, some showed no evidence of thrombosis, embolization or vasculitis as the causative factor. In many patients, this particular type of infarction is the terminal event of the episode. From October 1977 to December 1986, 24 patients with mesenteric infarction were investigated following cardiovascular surgery in our institute. Among them, 15 were diagnosed with organic vascular occlusion; however, the other 9 showed no evidence of thromboembolism or any other organic vascular occlusive lesion of mesenteric vessels and were diagnosed as non-occlusive mesenteric infarctions. All of these patients were in severe cardiac failure (LOS) postoperatively. There was no typical symptom, although abdominal fullness and diarrhea were the major and consistent findings. In blood chemical analysis, the enzymatic levels such as serum GOT, LDH and CPK were significantly elevated and discrepancy between serum GOT and serum GPT was observed. In this clinical situation, it was difficult to establish a correct diagnosis mainly because of the few signs and symptoms present relating to the mesenteric infarction. On the other hand, when the correct diagnosis was made, these patients were too critically ill to be treated conservatively. The outcome of these patients was grave and all of them died which showed 100% of mortality rate. The conservative management did not produce favorable progress, which accelerated LOS and prevented patients from recovering from cardiac failure. The aggressive surgical approach to this particular type of acute mesenteric ischemia might have offered an improved prognosis from these catastrophic events.

Adult↗
PubMed1997

[Intramural blood vessels of the large intestine of the horse (Equus przewalskii f. caballus)].

The vascular system of the large intestine of 12 horses was examined by means of vascular corrosion casts, histology and transmission electron microscopy providing the following results. The Aa. et Vv. breves et longae leave the mesenteric vessels, respectively the subserously on the teniae lying cecal vessels to reach the tela subserosa at the mesenteric margin. The short vessels enter the deeper layers of the wall instantly, whereas the Aa. et Vv. longae move towards the submucosa by penetrating the muscular layers after a variable subserous course. The tela submucosa contains an arterial and a venous vascular plexus. In broader areas of the submucosa a three-dimensional vascular network can be found. This consists of a deep and a superficial vascular plexus, which are closely interconnected. The deep plexus is applied to the inner circular muscles, whereas the superficial plexus is adjacent to the muscularis mucosae. The (deep) arterial plexus receives its afflux from the Aa. breves et longae and supplies parts of the circular muscle layer with recurrent muscle branches. The vascularisation of the mucosa also originates from the submucosal (superficial) plexus. In the basal tunica mucosa, the ascending arteries form a transversal network from which arterioles branch into periglandular capillaries around each Lieberkühn crypt. Close to the lumen, a polygonal subepithelial capillary system is formed. The capillaries turn into postcapillary venules immediately below the epithelium of the mucosal surface. Veins move vertically through the submucosa to enter the submucosal plexus after few inflowing side branches. Branches of the subserous-submucosal connections form an intermuscular plexus between the circular and longitudinal muscular layer. This plexus supplies the capillaries of the tunica muscularis. The subepithelial capillaries are predominantly lined with a fenestrated endothelium, whereas the capillaries of the pericryptal mucosa mainly show a continuous endothelial lining. The latter contain multiple vesicles, which may fuse in order to form transcytoplasmic channels. Sphincter-like muscle bundles at the transition points from capillaries to venules may provide hemodynamic regulatory structures in the submucosa of the horse. Veins with circumferential cushions of smooth muscle fibres, so-called 'throttle veins', are also found.

Animals↗
PubMed1987

Supraceliac aortomesenteric bypass for intestinal ischemia.

The supraceliac aorta has received little attention as an inflow site of bypass graft origin for mesenteric arterial reconstruction; this article describes our experience with its use in 10 patients. Ten patients underwent bypass grafts (three vein and seven prosthetic grafts) from the supraceliac aorta incorporating the celiac axis to the superior mesenteric artery. All patients had two- or three-vessel mesenteric arterial occlusion. No operative deaths occurred. Nine patients were studied with postoperative arteriography. Nine of ten patients have had satisfactory results on follow-up from 5 to 99 months (mean 43 months), although two patients required operative revision to achieve this. The operative technique is described, including approach to the aorta in the lower mediastinum via upper abdominal exposure and pancreatic displacement to expose the superior mesenteric artery. This method permits avoidance of the infrarenal aorta, if desired because of atherosclerotic disease or previous operation. Antegrade supraceliac aortomesenteric grafts avoid turbulence and compression of conventional "retrograde" bypass beneath the mesentery. We conclude that supraceliac aortic grafts provide a useful visceral artery reconstruction technique.

Aorta, Abdominal↗
PubMed1996

[The blood vessel system of the large intestine of swine (Sus scrofa f. domestica)].

The circulatory system of the large intestine of 27 pigs was examined by means of corrosion anatomy (vascular casts), histology and electron microscopy. The results were as follows: The Aa. et Vv. breves et longae leave the mesenteric vessels and reach the wall of the intestine at the mesenteric margin. The short vessels enter the deeper layers of the wall, whereas the Aa. et Vv. longae, by taking a variable subserous course, reach the submucosa after penetrating the muscular layers. The tela submucosa contains an arterial and a venous vascular plexus. Where the submucosa is larger, there is a three-dimensional vascular network, a deep and superficial vascular plexus that are closely interconnected. The deep plexus is applied to the inner circular muscles, whereas the superficial plexus is adjacent to the muscularis mucosae. The deep arterial plexus receives its afflux from the Aa. breves et longae and provides part of the circular muscle layers with recurrent muscle branches. The vascularization of the mucosa is derived from the (superficial) submucosal plexus. The arteries that ascend the tunica mucosa ramify, in the form of a brush, into some arterioles. In the basal part of the mucosa, they turn into a periglandular capillary system, i.e. a network around each Lieberkühn crypt. Close to the lumen, a polygonal subepithelial capillary system is formed. Below the epithelium of the mucosal surface, the capillaries turn into postcapillary venules. These are running vertically through the submucosa, with few inflowing side branches, and finally enter the submucosal plexus An intermuscular plexus is formed by anastomoses between the circular and the longitudinal muscular layers from the branches of the subserous-submucosal connections. This intermuscular plexus provides the capillaries for the tunica muscularis. The subepithelial capillaries are, above all, furnished with a so-called fenestrated endothelium, whereas the capillaries of the pericryptal mucosa mainly show a continuous endothelium. The latter contains multiple vesicles that can fuse to form transcytoplasmic channels. In the wall of the large intestine of the pig, there are no sure indications as to the existence of either arterio-venous anastomoses or haemodynamic regulatory structures.

Animals↗
PubMed2004

Changes in mesenteric vascular reactivity and inflammatory response after cardiopulmonary bypass in a rat model.

BACKGROUND: Mesenteric ischemia and acidosis leading to intestinal ischemia has been observed during cardiopulmonary bypass (CPB) despite normal flow in the mesenteric vessels. The aim of this study was to assess mesenteric endothelium-dependent reactivity and vasoconstrictor responses of small mesenteric arteries in a rat model of CPB without aortic cross-clamping. METHODS: After femoral cannulation a partial 90 minutes CPB was performed with hemodynamics and blood gas parameters monitoring. Blood samples and segments of small mesenteric arteries were obtained in rats sacrificed 2.5 hours (CPBH2.5) or 6 hours (CPBH6) after femoral cannulation. Sham surgery (sham H2.5, sham H6) was performed with femoral cannulation only. Segments of small mesenteric arteries were placed in a myograph in order to assess the contractile response to phenylephrine (with or without NO synthase inhibitor) or the endothelium-dependent relaxation to acetylcholine. Systemic inflammation was evaluated by measuring plasma concentrations of TNFalpha. Pulmonary and intestinal infiltration of activated leukocytes was assessed by immunohistochemistry. RESULTS: CPB induced increased contractile response to phenylephrine which persisted after blockade of NO synthesis as well as transient impairment of endothelium-dependent relaxations. CPB also led to early and marked release of TNFalpha. CONCLUSIONS: CPB was responsible for mesenteric endothelial dysfunction and direct increase in the contractile response to alpha1-adrenergic agonist with increased systemic inflammatory response. This phenomenon might contribute to an increase in the risk of mesenteric ischemic events during cardiac surgery especially when vasopressor agents are used.

Acetylcholine↗
PubMed2001

In vitro pharmacologic effect of two endothelin-1 antagonists on equine colonic arteries and veins.

OBJECTIVE: To evaluate the effectiveness of 2 potential endothelin (ET)-1 antagonists in blocking the contractile responses of equine colonic vessels to increasing concentrations of ET-1. SAMPLE POPULATION: Mesenteric vessels from 6 clinically healthy horses. PROCEDURE: Colonic vessels (arterial and venous rings) were placed in organ baths with oxygenated Tyrode solution at 37 C. Each was attached to a force transducer interfaced with a polygraph, and 2 g of tension was applied and equilibrated for 45 minutes. Then, B-1 (PD 142893) and B-2 (PD 145065) ET-1 antagonists were tested. One ring from each vessel type was used as a control for determining concentration-response relationships of ET-1 (10(-10) to 10(-6)M). Three rings of each vessel type were incubated with 3 concentrations of each antagonist (10(-7), 10(-6), and 10(-5) M) for 30 minutes before ET induced contractions were determined. The maximum contractile response and pA2 values were determined. RESULTS: Vessels contracted in a concentration-dependent manner to ET-1. Arteries responded slowly but reached greater contractions. Veins responded immediately with sustained contractions. Both antagonists inhibited contractions in a concentration-dependent manner with significant differences at 10(-6) and 10(-5)M for arteries and 10(-5) M for veins. Complete blockade of contractions was observed with B-2 (10(-5)M). The pA2 values for B-1 were 8.26 and 6.82 for arteries and veins, respectively, whereas they were 8.25 and 7.21 for B-2. CONCLUSION AND CLINICAL RELEVANCE: Both antagonists effectively blocked ET-1-induced contractions of equine colonic vessels. Because B-2 is water soluble and caused complete blockade at 10(-5) M, it appears to be the preferred antagonist.

Animals↗
PubMed2000

[Arg8]-vasopressin-induced responses on coronary and mesenteric arteries of rats with myocardial infarction: the effects of V1a- and V2-receptor antagonists.

After myocardial infarction, plasma levels of [Arg8]-vasopressin rise to recover hemodynamics. The vascular responses to [Arg8]-vasopressin were studied in vitro in isolated hearts and mesenteric artery segments of rats with 1-day and 3-week-old infarcts, in absence and presence of the V1a-receptor antagonist SR-49059 and the V2-receptor antagonist OPC-31260. Vascular responses of coronary arteries were similar in sham and infarcted hearts. On average, coronary flow was maximally decreased by 70 +/- 3% from baseline values of 11.1 +/- 0.3 ml/min, with pD2 values of 10.52 +/- 0.05. In mesenteric artery segments of sham and infarcted rats, maximal contractile forces, expressed as percentage of contraction to 125 mM KCl, were similar (232 +/- 23% and 239 +/- 8%, respectively). However, pD2 values from infarcted rats (9.22 +/- 0.07) were significantly lower compared with sham (9.55 +/- 0.07) rats. In coronary as well as mesenteric vessels, the vasoconstrictor responses, being more susceptible to SR-49059 (apparent pA2, between 9.12 and 9.82) than to OPC-31260 (apparent pA2, between 6.21 and 6.92), seemed mediated by the V1a receptor. These data indicate that in mesenteric but not in coronary vessels, an altered responsiveness to vasopressin could be observed. Responses are mediated mainly by the V1a receptor.

Animals↗
PubMed1984

Computed tomography of the normal mesentery.

Thirty patients were studied to evaluate the CT appearance of the normal mesentery and its vasculature. Mesenteric vessels were identified by determining their relations to segments of the small bowel and colon in the 30 patients. Jejunal and ileal branches supplying small bowel were identified in all patients. The ileocolic and right colic branches of the ascending colon were identified in 27 and 26 patients, respectively; middle colic vessels were identified in 29 patients. Left colic branches were identified in only 14 patients; sigmoid branches were identified in 23 patients. The vessels showed a characteristic wavy appearance as they coursed through mesenteric fat. The average attenuation of the mesenteric fat was -117.4 +/- 7.9 H. Normal lymph nodes were not routinely identified within the mesentery. Various pathologic processes altered the normal appearance of the components of the mesentery.

Adipose Tissue↗
PubMed1979

[Necrotizing enterocolitis in the neonatal period. Revue of 19 cases proved by anatomopathologic examination].

Nineteen newborn infants with necrotizing enterocolitis, proved by autopsy or surgical examination, are presented. In this study the absence of blood in the stools and of pneumatosis intestinalis did not exclude the diagnosis of necrotizing enterocolitis. The role of umbilical arterial and venous catheters and of exchange transfusion in the pathogenesis of the disease was less than has been previously reported. There was no evidence for emboli of thrombosis in the mesenteric vessels. On the other hand, the probable importance of nonocclusive mesenteric arterial insufficiency is supported by several observations, including the high incidence of antecedent hypoxaemic episodes, the time of onset of the subsequent gastrointestinal pathology and the localization of the lesions. An infectious component was demonstrated, but our results do not allow to state precisely the time of its occurrence.

Catheterization↗