[INNERVATION OF THE MESENTERIC LYMPHATIC VESSELS IN THE SMALL INTESTINE].
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A 2 1/2-year-old spayed Great Dane was evaluated for large, fluctuant, chyle-containing swellings on the ventral portion of the left side of the abdomen. Multiple abnormalities of the lymphatic system were diagnosed, including thoracic duct obstruction, lymphangioma, subcutaneous chyle reflux, intestinal lymphangiectasia, and dilatation of hepatic, mesenteric, and pleural lymphatic vessels. Mesenteric lymphangiography revealed leakage of contrast medium into the subcutaneous tissues adjacent and to the left of the second lumbar vertebral body. Dietary and surgical management to control the chylous reflux were unsuccessful, and the dog died approximately one year after the skin lesions were first observed.
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The electrical activity of smooth muscle of isolated lymphangiomas revealed spontaneous APs about 3.8 +/- 1.3 mV for 200-250 ms preceding the contractions. In Ca-free solution the APs and the contractions disappeared. The blockade of calcium channels suppressed electrical activity of smooth muscle cells. The increase of amplitude and time of the APs increased the amplitude and time of the contractions. The data suggest that spontaneous APs play a part in activation and coordination of the phasic contractions, and show that automaticity of lymphangiomas is revealed in smooth muscle cells of the circular layers of the valves, and that tonic and phasic contractions have a special type of membrane activating mechanisms.
Substantial evidence has accumulated that in certain vascular beds dopamine produces its relaxant effect through stimulation of specific dopamine receptors. The goal of this review is to describe several in vitro models (perfused mesenteric vessels of the dog; renal, mesenteric, splenic, coronary and cerebral arterial strips of rabbits, dogs and cats; perfused kidney of the rat) recently developed to demonstrate such specific relaxations induced by dopamine and dopaminomimetics. On these models studies on structure-activity relationship for activation of the dopamine receptor resulted in the following order of potency for agonists: SK&F 38393 (partial agonist) greater than epinine greater than A-6, 7-DTN greater than or equal to dopamine greater than N, N-di-n-propyl-dopamine (partial agonist) greater than apomorphine (partial agonist). The dopamine receptor antagonists (+)-butaclamol, cis-alpha-flupenthixol, metoclopramide, droperidol and bulbocapnine were found to competitively antagonize dopamine induced relaxation. In addition, in two isolated organ systems (rabbit mesenteric artery, rat perfused kidney) stereospecificity of the vascular dopamine receptor was demonstrated with the isomers of butaclamol. With the development of several in vitro models demonstrating a specific antagonism against dopamine induced relaxation an important requirement for definition of a specific dopamine receptor if fulfilled according to classical pharmacological criteria. Thus, there can be do doubt on the existence of post-synaptic dopamine receptors mediating vasodilation in certain vascular tissues.
A segmental necrosis of the ascending colon sometimes affecting the terminal ileum was observed 13 times in 12 end-stage renal disease patients over a 5400 patient-years observation period. In all but three cases the patient was operated within 24 h of onset of the abdominal pain. Three patients had a bowel perforation; nine had a limited intestinal necrosis. All underwent a partial resection or colectomy. Two died within 1 month. In all cases the mucosa was necrotic, the submucosa small vessels were congested and the mesenteric vessels were normal. Ischaemic bowel disease has been previously reported in uraemic patients, but our cases do not fit with the usual reported features of this complication. The absence of typical mesenteric infarction, vascular thrombosis, stenosis or major atherosclerotic lesions is surprising. The ascending colon topography of the lesions is very unusual. Ischaemia, constipation and other factors may play a role.
Neutrophils have been identified to play a major role in ischemia/reperfusion injury through several mechanisms. Neutrophil migration into reperfused gut may reduce bacterial translocation, but may also enhance the reperfusion injury. Ethanol ingestion impairs cutaneous chemotaxis, but its effects on neutrophil migration to postischemic small bowel are unknown. This study investigates the effects of ethanol on small bowel accumulation of neutrophils after ischemia/reperfusion. Ninety-five rats were divided into five groups; normal control, sham operation, ethanol-sham, ischemia, and ethanol-ischemia groups. Ethanol was given once acutely by gavage (3 g/kg, 20% solution) to the animals in the ethanol-sham and the ethanol-ischemia groups 4 hr before ischemic injury. Ischemia was produced for 1 hr by placing a vessel loop around the superior mesenteric vessels. After 1 hr, 87% of animals had gut ischemia and the loop was removed. Three hours later the small bowel was examined for necrosis and the reperfused viable small bowel was extirpated for measurement of neutrophil infiltration by colorimetric assay for myeloperoxidase (MPO), an enzyme restricted to neutrophils. Both ethanol and ischemia/reperfusion produced significant independent increase in the MPO activity. When ethanol was given prior to ischemia, the MPO activity was further increased by statistically significant margin. The present study demonstrated that ethanol enhanced the effects of gut ischemia/reperfusion injury on PMN accumulation into the intestinal wall. These observations suggest that ethanol may potentiate ischemic injury to the gut and lead to increased problems when gut blood flow is significantly impaired.
BALB/c mice (ischemia: 31; controls: 15) were studied to investigate the effects of intestinal ischemia on antibody synthesis to peptidoglycan polysaccharide (PGPS), a ubiquitous bacterial antigen found in both gram-positive and gram-negative bacteria. The gut ischemia model was produced by placing a vessel loop around the superior mesenteric vessels for 45 minutes. All animals in the ischemia group had visible gut ischemia. Eighteen animals (58%) in the ischemia group survived to 24 hours and all experienced total recovery of gut viability. Single-cell suspensions of splenic lymphocytes were made. After 5 days of culture with lipopolysaccharide, anti-PGPS immunoglobulin concentrations in culture supernatants were measured by ELISA using high-titer BALB/c anti-PGPS serum as control. The synthesis of immunoglobulin by 10(5) lymphocytes was significantly increased in the ischemia group compared with the controls. These results represent the translocation of bacteria after intestinal ischemia, and this antibody response may be important in resistance to sepsis and multiple organ dysfunction attributed to bacterial translocation.
Posttraumatic arteriovenous fistulas affecting the superior mesenteric artery and vein are extremely rare. Twenty-four cases of posttraumatic superior mesenteric arteriovenous fistulas (SMAVFs) have been reported. We presented two cases of SMAVFs occurring in a young woman and man secondary to a gunshot and a grenade shrapnel wound in the epigastrium, respectively. Nausea, heartburn, emesis, and cramping abdominal pain were the clinical signs of SMAVF. Abdominal pains, particularly after meals, tense and meteoristic abdomen, frequent liquid bowel movements, oliguria, subfebrility, abdominal thrill, and bruit were also present. Abdominal duplex ultrasonic scanning and computed tomograms with a contrast agent were especially useful screening tools. As our results demonstrated, those methods were not only suitable for clinical use, but were also as good as arteriography in defining both the exact location and the extent of the mesenteric vessel involvement. However, the superior mesenteric arteriogram remains mandatory for complete preoperative evaluation. Arteriovenous fistulas were successfully treated by suturing the arterial and venous sides of the fistula in one case, and resectioning the fistula and end-to-end anastomosis in the other case.
PURPOSE: To evaluate the computed tomographic (CT) features of systemic lupus erythematosus (SLE) in patients with acute abdominal pain. Special emphasis was placed on the analysis of ischemic bowel disease. MATERIALS AND METHODS: The authors retrospectively reviewed the images from 39 abdominal CT examinations performed in 33 patients with SLE and acute abdominal pain. Images were evaluated for bowel wall changes, mesenteric changes, fluid collection, retroperitoneal lymphadenopathy, peritoneal enhancement, and hepatomegaly as well as for changes in other abdominal organs. Ischemic bowel disease was diagnosed if at least three of the following signs were seen: bowel wall thickening, target sign, dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat. RESULTS: Thirty-one (79%) of the 39 examinations had CT findings diagnostic of ischemic bowel disease, including symmetric bowel wall thickening (n = 29), target sign (n = 26), and mesenteric vascular engorgement and haziness (n = 31). In 24 cases, bowel wall thickening was multifocal, with variable length, and did not appear to be confined to a single vascular territory. CONCLUSION: The most common CT finding in patients with SLE and acute abdominal pain is ischemic bowel disease. CT is useful for detecting the primary cause of gastrointestinal symptoms, planning treatment, and monitoring for infarction or perforation.
We observed the synthesis and release of vasoactive polypeptides (VPs) in the endothelial cells of human umbilical blood vessels (HUVEC). The results showed: (1) The content of VPs in the endothelial cells of non-innervated human umbilical vessels is higher than that of mesenteric vessels. (2) These VPs are synthesized by endothelial cells and released into the outside of cell bodies. (3) VIP and SP can stimulate the proliferation of HUVEC, but somatostatin (SOM) inhibits it. (4) VIP and SP increase opening probability of the Ca2+ channel in the membrane of HUVEC, while SOM decrease it, but VIP, SP and SOM result in the increase of concentrations of intracytosolic free Ca2+ and cAMP, while decreasing that of cGMP in HUVEC. In conclusion, we proved that there are local regulatory mechanisms in non-innervated human umbilical blood vessels, and VPs within endothelial cells may play an important role.
Techniques have been developed for the study of isolated small arteries. To pressurize and perfuse segments of these vessels, a cannula with a low resistance to flow was developed. This cannula consisted of two concentric micropipettes. The end of a vessel segment was sucked into the inner pipette and clamped by applying subatmospheric pressure on the outer pipette. Subsequently, the vessel was pressurized via the inner pipette. To enable perfusion, the segment was cannulated at both ends. Mean cross-sectional area (CSA) of the cannulated segments was continuously measured using a fluorescence technique. The emission of light by fluorescein isothiocyanate (FITC) labeled dextran in the vessel lumen was measured using a photomultiplier tube (PMT). PMT current was linearly related to the vessel CSA. Twenty-nine rat mesenteric vessels with inside diameters ranging from 110 to 350 microns (mean 226 microns) when maximally dilated at 80 mm Hg were cannulated. CSA was monitored during variations in perfusion pressure and addition of vasoactive agents.