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At least 397 records · Page 22Linked to original sources
PubMed2003

Mesenteritic panniculitis: detection by abdominal ultrasonography.

OBJECTIVE: to describe the findings that allowed us to detect mesenteric panniculitis in sonographic abdominal studies. PATIENTS AND METHODS: we retrospectively evaluated the images of 10 patients diagnosed of mesenteric panniculitis, initially detected by sonography. Diagnosis was confirmed by computed tomography (CT) in all cases, and by surgical biopsy in one of them. Two patients were symptomatic, and it was an incidental finding in the remaining eight cases. RESULTS: the characteristic sonographic appearance consisted of thickening of mesenteric fat around mesenteric vessels, with an elliptical or rounded shape, a convex or lobulated and well-defined anterior border and an homogeneous or slightly heterogeneous structure, with nodular images in three of the cases. Mesenteric vessels were identified, without evidence of distortion. There was a reduction of compressibility in relation to normal mesenteric tissue. CONCLUSION: although we cannot presently state the specificity of the findings described, mesenteric panniculitis can be detected by abdominal sonography. This technique provides guidance for the diagnosis and, eventually, percutaneous biopsy.

Abdomen↗
PubMed2004

Isoform switching from SM-B to SM-A myosin results in decreased contractility and altered expression of thin filament regulatory proteins.

We previously generated an isoform-specific gene knockout mouse in which SM-B myosin is permanently replaced by SM-A myosin. In this study, we examined the effects of SM-B myosin loss on the contractile properties of vascular smooth muscle, specifically peripheral mesenteric vessels and aorta. The absence of SM-B myosin leads to decreased velocity of shortening and increased isometric force generation in mesenteric vessels. Surprisingly, the same changes occur in aorta, which contains little or no SM-B myosin in wild-type animals. Calponin and activated mitogen-activated protein kinase expression is increased and caldesmon expression is decreased in aorta, as well as in bladder. Light chain-17b isoform (LC(17b)) expression is increased in aorta. These results suggest that the presence or absence of SM-B myosin is a critical determinant of smooth muscle contraction and that its loss leads to additional changes in thin filament regulatory proteins.

Animals↗
PubMedDate not supplied

Contractile and dilatory action of neuropeptides on isolated human mesenteric blood vessels.

Neuropeptide Y (NPY), substance P (SP), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), lysyl-bradykinin, somatostatin, Met- and Leu-enkephalin were tested for their smooth muscle activity in isolated human mesenteric arteries and veins. Only NPY regularly contracted both arteries and veins. Alpha-adrenergic and 5-HT2 antagonists did not affect the response. Somatostatin contracted the veins, but not the arteries, in a variable but concentration-dependent way. The other neuropeptides were without contractile effect. CGRP, bradykinin, and SP regularly dilated, in a concentration-dependent way, both arteries and veins precontracted with prostaglandin F2 alpha or uridine triphosphate. CGRP and bradykinin were the most potent dilators. VIP and somatostatin usually caused a moderate dilatation in the arteries, whereas in the veins, somatostatin was without dilatory effect and the VIP-induced dilatation was irregular. In both types of vessels Met-enkephalin seldom gave any significant dilatation, and no response occurred in the presence of Leu-enkephalin or NPY. The SP-antagonist (D-Arg, D-Trp, Leu)-SP (spantide) caused a dextal shift of the concentration-response curves for SP, in the case of the arteries also including a reduced maximum effect.

Adult↗
PubMed2003

Contractions to histamine in pulmonary and mesenteric arteries from endotoxemic rabbits: modulation by vascular expressions of inducible nitric-oxide synthase and histamine H1-receptors.

The inducible isoform of nitric-oxide synthase (iNOS) is highly expressed after induction of endotoxemia and contributes to vascular hypocontractility in endotoxemia. Circulating levels of histamine are elevated in animal models of sepsis and in patients with septic shock. This study assessed whether the vascular effects of histamine play a significant role in the pathophysiology of endotoxemic shock despite the hyporesponsiveness to vasoconstrictors associated with iNOS up-regulation. Rabbits were rendered endotoxemic by lipopolysaccharide (LPS; 100 microg/kg, i.v.). In mesenteric arteries taken from animals at 6 h of LPS administration, the contractile response to histamine was significantly impaired but histamine-evoked contractions in pulmonary arteries were unchanged. Western blot revealed a drastic increase in iNOS expression in mesenteric vessels after LPS, but endotoxin-induced iNOS increase was not so marked in pulmonary vessels. On the other hand, expression of endothelial nitric-oxide synthase was suppressed under LPS challenge in both types of vessels. In the presence of NG-nitro-l-arginine or (S)-ethylisothiourea used for iNOS inhibition, histamine-evoked contractions of endotoxemic pulmonary and mesenteric vessels were significantly enhanced. This was possibly associated with a dramatic increase in H1-receptor expression at the gene and protein levels, as determined by Northern blot and immunoblot analyses. Furthermore, we found that LPS-induced endotoxemia caused prominent increases in production of histamine through induction of histidine decarboxylase in tissues, including blood vessels. From these results, we propose that histamine may contribute to the development of endotoxin-induced pulmonary hypertension.

Animals↗
PubMedDate not supplied

CT of the mesenteric vascular anatomy.

BACKGROUND: To evaluate the appearance of the arrangement of the superior mesenteric artery (SMA) and superior mesenteric vein (SMV) on computed tomography (CT) in normal patients and in patients with abdominal masses. METHODS: One hundred seventy-seven consecutive abdominal CT examinations of 143 adults and two children were reviewed. The relationship of the SMV to the SMA was recorded at four locations: the beginning of the mesenteric vessels and levels 3 cm, 6 cm, and 9 cm caudad to the beginning. The relationship of the SMV to the SMA was divided into four quadrants in relation to the SMA: I, ventral right or directly ventral; II, dorsal right or directly right; III, dorsal left or directly dorsal; and IV, ventral left or directly left. RESULTS: In the beginning of the SMV-SMA complex and levels 3 cm, 6 cm, and 9 cm caudal to the beginning, the SMV was located in quadrant I in 146, 84, 69, and 43 examinations, in quadrant II in 31, 93, 71, and 27 examinations, in quadrant III in zero, zero, five, and three examinations, and in quadrant IV in zero, zero, nine, and 15 examinations, respectively. The cases with SMV inversion had neither malrotation nor adjacent tumor compression. All the cases with an adjacent tumor-induced compression of the SMV-SMA complex had a normal SMV-SMA relationship. CONCLUSION: In the first 3 cm, the SMV is always to the right of the SMA. Caudal to the level of 6 cm, the SMV may be located to the left of the SMA without evidence of malrotation. A midgut nonrotation is more likely to be present when a proximal SMV inversion is coexistent with a rightward direction of the proximal jejunal vessels. A hypothetical depiction of the step-by-step change of the SMV-SMA relationship during embryologic development may explain the arrangement patterns of the mesenteric vessels in normal rotation and midgut nonrotation.

Abdominal Neoplasms↗
PubMed1993

Intestinal ischemia secondary to thromboangiitis obliterans.

A 38-year-old woman presented with a 10-month history of postprandial abdominal pain and weight loss. She smoked two packs of cigarettes a day, but her history did not indicate diabetes mellitus, hyperlipidemia, or hypercoagulability. A lateral aortogram documented complete occlusion of all three mesenteric arteries but showed no evidence of atherosclerosis, arteritis, or medial fibroplasia. Two retrograde aortomesenteric grafts, one to the superior mesenteric artery and another to the meandering mesenteric artery, utilizing the greater saphenous vein were placed. Pathologic examination of the inferior mesenteric artery demonstrated changes that were considered diagnostic of thromboangiitis obliterans. We found only 10 confirmed cases of thromboangiitis obliterans involving the mesenteric vessels in the English language literature. The present case appears to be the first involving a woman and the only one in which the main trunk of all three mesenteric vessels was involved.

Adult↗
PubMed1996

Effects of ultra-low-dose aspirin on embolization in a model of laser-induced thrombus formation.

A laser-induced rat mesenteric vessel thrombosis model was used to evaluate the effect of acetylsalicylic acid (ASA) at ultra-low doses. A partial occlusion was induced in small mesenteric vessels (diameter 40-50 microns) by an argon laser. The laser induced damage of endothelial cells. Thrombi formed within seconds after the laser lesion and grew rapidly. Embolization began during the minute following the laser injury. Compared to placebo, the administration of ASA at ultra-low doses (334 x 10(-11) mol/mL) by subcutaneous injection in the thorax region (0.2 mL) induced three different phenomena: (1) a decrease in the number of laser injuries required to induce thrombus formation, (2) an increase in number of emboli removed by the blood stream, and (3) an increase in the duration of embolization. The ultra-low doses of ASA showed a strong increase in the number of emboli and in the duration of embolization.

Animals↗
PubMed2006

Effects of h1-calponin ablation on the contractile properties of bladder versus vascular smooth muscle in mice lacking SM-B myosin.

The functional significance of smooth muscle-specific h1-calponin up-regulation in the smooth muscle contractility of SM-B null mice was studied by generating double knockout mice lacking both h1-calponin and SM-B myosin. The double knockout mice appear healthy, reproduce well and do not show any smooth muscle pathology. Loss of h1-calponin in the SM-B null mice bladder resulted in increased maximal shortening velocity (V(max)) and steady-state force generation. The force dilatation pressure, which was decreased in the SM-B null mesenteric vessels, was restored to wild-type levels in the double knockout vessels. In contrast, the half-time to maximal constriction was significantly increased in the double knockout vessels similar to that of SM-B null mice and indicating decreased shortening velocity in the double knockout vessels. Biochemical analyses showed that there is a significant reduction in smooth muscle alpha-actin levels, whereas h-caldesmon levels are increased in the double knockout bladder and mesenteric vessels, suggesting that these changes may also partly contribute to the altered contractile function. Taken together, our studies suggest that up-regulation of h1-calponin in the SM-B null mice may be necessary to maintain a reduced level of cross-bridge cycling over time in the absence of SM-B myosin and play an important role in regulating the smooth muscle contraction.

Actins↗
PubMed1992

Management of pancreatic injuries.

With the aim of aiding the accurate diagnosis and treatment of patients with pancreatic injuries, we reviewed the medical records of all those patients, treated for traumatic pancreatic lesions at our hospital in the period between 1971 and 1987. For all twenty-four male patients the mechanism of the injury, the diagnostic methods employed, associated injuries, location of the pancreatic injury, the presence of pancreatic duct lesion, treatment, the final outcome, and complications are described. In our view, the high mortality rate of patients with pancreatic trauma is due not to the pancreatic injury per se, but to the severe concomitant injuries resulting from a high-energy trauma. On the basis of the literature and our own experience we designed a flow chart for the management of pancreatic injuries. If the history and physical examination indicate that intra-abdominal injury might be present, radiographic and ultrasound investigation are the diagnostic methods of choice. Patients without pancreatic duct injury can be treated with debridement and external suction drainage. If pancreatic duct lesion is presented and is located to the right of the superior mesenteric vessels, treatment should consist of partial pancreatic resection and pancreatico-jejunostomy or a Whipple procedure. If the pancreatic duct lesion is located to the left of the superior mesenteric vessels, distal pancreatectomy and splenectomy with pancreatico-jejunostomy, should be performed.

Adolescent↗
PubMed2005

Peroxisome proliferator-activated receptor gamma regulates angiotensin II-stimulated phosphatidylinositol 3-kinase and mitogen-activated protein kinase in blood vessels in vivo.

Angiotensin (Ang) II is implicated in hypertension, vascular remodeling, and insulin resistance. Peroxisome proliferator-activated receptor (PPAR) gamma activators increase insulin sensitivity and improve Ang II-induced vascular remodeling. We evaluated the effects of the PPAR-gamma activator rosiglitazone on Ang II signaling in aorta and mesenteric arteries. Rats received Ang II by subcutaneous infusion and/or rosiglitazone per os for 7 days. Blood pressure rise in Ang II-infused rats was attenuated by rosiglitazone. Ang II significantly increased Ang II type 1 receptor expression in the mesenteric arteries (P<0.001), whereas that of the aorta was decreased (P<0.05), changes which were reversed by rosiglitazone. Akt activity was increased by Ang II and returned to basal levels under rosiglitazone in both vascular beds. However, Ang II-induced extracellular signal-regulated kinase 1/2 activity increased in aorta but not in mesenteric vessels (P<0.001), where 4E-binding protein 1 activity was significantly increased by Ang II and inhibited by PPAR-gamma activation. In response to Ang II, Src homology (SH) 2-containing inositol phosphatase 2 activity was increased (P<0.05) in both vascular beds. In conclusion, PPAR-gamma activator rosiglitazone attenuated Ang II-induced blood pressure elevation and intracellular signaling on aorta and mesenteric vessels. There was differential inhibition of Ang II type 1 receptor receptors/phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase 1/2 in both vessels. Effects of PPAR-gamma activators on these pathways could contribute to regression of vascular remodeling in models of hypertension and diabetes and, accordingly, in hypertensive diabetic patients.

Angiotensin II↗
PubMed1988

Mesenteric vascular responses to i.v. administration of lipoxin A4 and lipoxin B4 in the conscious rat.

Lipoxin A4 and lipoxin B4 are newly discovered lipoxygenase-interacting products of leukocytes which might have a role in cardiovascular events associated with anaphylaxis. We have tested this possibility by systemic administration of both LXA4 and LXB4 to the conscious rat while monitoring systemic and regional hemodynamic changes. LXA4 and LXB4 (1-100 micrograms/kg) produced dose-dependent constriction of the mesenteric vessels, up to +123 +/- 23% and +50 +/- 9% for LXA4/B4, respectively. Dose-related changes were not observed in arterial blood pressure, heart rate, renal (LXB4) and hindquarter blood flow. We suggest that LXA4 and LXB4 might affect selective vascular beds, such as the mesenteric vessels, and contribute to variations in blood flow in specific pathophysiological states.

Animals↗
PubMed1998

[Complete remission of a mesenteric fibromatosis after taking sulindac].

We report the case of a 22-year-old-man having a familial adenomatous polyposis coli treated by total colectomy with ileo-rectal anastomosis. Two years after the operation, an asymptomatic mesenteric fibromatosis appeared which was nonresectable due to mesenteric vessels infiltration. Nine years later, sulindac therapy was started for residual polyps in the rectal stump. This treatment was taken intermittently, during periods of 1 to 8 months, for 6 years. After 4 years of treatment, the tumor was no longer palpable. Four years after sulindac discontinuation, the patient was operated on for suspicion of intestinal adhesion. The mesenteric fibromatosis had completely disappeared and mesenteric vessels were free. This complete macroscopic regression of a desmoid tumor after sulindac therapy emphasizes again the interest of this treatment for mesenteric fibromatosis.

Adenomatous Polyposis Coli↗