Abstract 495: Mouse Model of Mesenteric Ischemia Secondary to Vascular Calcification and Atherosclerosis

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Konstantinos Damiris ◽  
Filippo Romanelli ◽  
Alexei Savinov ◽  
José Luis Millan ◽  
Jes Kuruvilla ◽  
...  
Keyword(s):  
Weight Loss ◽  
Mouse Model ◽  
Mesenteric Ischemia ◽  
Intestinal Ischemia ◽  
Density Lipoprotein ◽  
Body Weight Loss ◽  
Goblet Cells ◽  
Mesenteric Arteries ◽  
Chronic Mesenteric Ischemia

Objective: Atherosclerosis is a leading cause of chronic mesenteric ischemia (CMI), defined as intestinal hypoperfusion resulting from stenosis of mesenteric arteries. Symptoms of CMI range from non-specific abdominal pain and weight loss to aversion of food resulting in cachexia. In this study we aim to define intestinal ischemia and its effects on gastrointestinal structure and function in an in vivo model of atherosclerosis. Hypothesis: Overexpression of tissue-nonspecific alkaline phosphatase (TNAP) under conditions of hypercholesterolemia in a mouse model will lead to atherosclerosis causing intestinal ischemia. Methods and Results: We have previously established that endothelial TNAP overexpression (eTNAP) results in calcification of medium-sized arteries including mesenteric. In this study eTNAP was combined with a point mutation in the low-density lipoprotein receptor ( ldlr ^WHC). When fed an atherogenic diet (Paigen’s diet, starting at 8 weeks of age), WHC-eTNAP mice developed acute body weight loss (>15% from baseline), whereas WHC mice continued to gain weight. Examination of the mesenteries of WHC-eTNAP demonstrated eccentric vascular remodeling and stiffening, as well as calcification of atherosclerotic plaques (n=4). Mesenteric arteries of WHC were not affected (n=3). WHC-eTNAP (n=2) mice developed extensive atherosclerosis of submucosal arterioles in the colon where most vessels were narrowed or occluded. Examination of the small intestine in WHC-eTNAP mice showed structurally distressed villi accompanied with an increase in goblet cells and fragmentation of the epithelial layer possibly reflecting cell death. The colon demonstrated loss of goblet cells and signs of denuding of the epithelium. Conclusion: Atherosclerosis induced by overexpression of TNAP causes occlusion of mesenteric arteries as well as structural pathology in the small and large intestine

Stenting of stenotic mesenteric arteries for symptomatic chronic mesenteric ischemia

VASA ◽  
2012 ◽  
Vol 41 (6) ◽  
pp. 425-431 ◽  
Author(s):  
Aschenbach ◽  
Bergert ◽  
Kerl ◽  
Zangos ◽  
Neumeister ◽  
...  
Keyword(s):  
Weight Loss ◽  
Abdominal Pain ◽  
Gastrointestinal Bleeding ◽  
Mesenteric Artery ◽  
Mesenteric Ischemia ◽  
Celiac Artery ◽  
Lower Gastrointestinal Bleeding ◽  
Mesenteric Arteries ◽  
Chronic Mesenteric Ischemia ◽  
Technical Failure

Background: We report the results of our single center series of patients with chronic mesenteric ischemia (CMI) to determine the role of stenting in the management of patients. Patients and methods: We retrospectively reviewed all patients with CMI treated endovascularly with stent revascularisation from January 2008 to January 2011.CMI diagnosis was made according to clinical symptoms, including postprandial abdominal pain, food fear, and weight loss. Additionally, the diagnosis was confirmed by duplex ultrasonography and/or computed tomography angiography and/or contrast-enhanced magnetic resonance angiography. Results: All 45 patients presented with typical CMI symptoms: 45/45 (100 %) had postprandial pain, 31/45 (68.8 %) had a weight loss of more than 10 kilograms, and 11/45 (24.4 %) suffered from ischemic colitis combined with lower gastrointestinal bleeding. In three patients occlusion could not be crossed, therefore considered as technical failure. A total of 55 arteries were stented in the remaining 42 patients. Nineteen patients underwent SMA stenting alone, eight underwent celiac stenting, alone and three patients underwent stenting of inferior mesenteric artery (IMA) alone. We performed combined stenting of the celiac artery and superior mesenteric artery in ten patients, and one patient underwent a combined stenting of the celiac artery and the IMA. All three mesenteric arteries were stented in only one patient. Primary technical success was achieved in 42/45 (94.8 %) patients. Clinical symptom relief was achieved in 39/45 (86.6 %) patients with abdominal pain. Increased body weight was observed in 28/31 (90.3 %) patients with an average weight gain of 8.8 kilograms (5 - 12 kilograms), and 10/11 (90.9 %) patients recovered from ischaemic colitis/lower gastrointestinal bleeding. Conclusions: Stent revascularisation can be considered as the first-line therapy for patients with chronic mesenteric ischemia.

scholarly journals Clinical implications of chronic mesenteric ischemia in elderly and senile patients

2020 ◽  
Vol 92 (2) ◽  
pp. 74-80
Author(s):  
A. I. Dolgushina ◽  
A. S. Kuznecova ◽  
A. A. Seljanina ◽  
V. V. Genkel ◽  
A. G. Vasilenko
Keyword(s):  
Weight Loss ◽  
Abdominal Pain ◽  
Mesenteric Artery ◽  
Mesenteric Ischemia ◽  
Clinical Manifestations ◽  
Pain Syndrome ◽  
Celiac Trunk ◽  
Mesenteric Arteries ◽  
Chronic Mesenteric Ischemia ◽  
Clinical Criteria

Aim.To evaluate the sensitivity and specificity of the clinical criteria for the diagnosis of chronic mesenteric ischemia in elderly and senile patients with mesenteric atherosclerosis. Materials and methods.The study included 142 patients (82 men and 60 women). The median age of patients is 66.0 [62.0; 72.0] years. Results.According to MDCT atherosclerotic lesions of the abdominal aorta and its unpaired visceral branches were diagnosed in 105 (73.9%) patients. A combination of atherosclerosis of the celiac trunk and the superior mesenteric artery with the presence of hemodynamically insignificant stenosis was revealed. Hemodynamically significant atherosclerotic narrowing of at least one mesenteric artery was present in 15% of cases. Among them, a single vascular lesion was found in 6 patients (4.2%), a combination of hemodynamically significant lesions of two arteries in 15 (11%) patients. Depending on the clinical manifestations, all patients are divided into two groups: the first group 30 (21.1%) patients with the presence of symptoms characteristic of chronic mesenteric ischemia (CMI). The second group consisted of 112 (78.8%) patients without a characteristic triad of symptoms. The clinical symptom complex of СMI, including postprandial abdominal pain, intestinal dysfunction and progressive weight loss, as a diagnostic criterion showed low sensitivity 13.3% and specificity 77.9%. At the same time, the sensitivity of such a clinical combination as a combination of atherosclerosis of the arteries of the lower extremities, weight loss and abdominal pain syndrome with a severity of more than 5.5 points, with respect to the detection of hemodynamically significant stenoses of two or more mesenteric arteries was sensitivity 86.7%, specificity 74.0%.

scholarly journals Mid-term outcomes of endovascular treatment for symptomatic chronic mesenteric ischemia

2011 ◽  
Vol 1 (1) ◽  
pp. 2 ◽  
Author(s):  
Eva Schönefeld ◽  
Susanne Szesny ◽  
Konstantinos P. Donas ◽  
Georgios A. Pitoulias ◽  
Giovanni Torsello
Keyword(s):  
Endovascular Treatment ◽  
Mesenteric Ischemia ◽  
Primary Patency ◽  
Mesenteric Arteries ◽  
Primary Study ◽  
Symptom Improvement ◽  
Initial Symptom ◽  
Secondary Patency ◽  
Chronic Mesenteric Ischemia

The authors would present the mid-term outcomes with the use of stent-supported angioplasty in the treatment of symptomatic chronic mesenteric ischemia (CMI). The present study is a retrospective analysis of 36 patients undergoing endovascular treatment of symptomatic CMI, between November 2000 and September 2009. Primary study endpoints were defined as primary patency, periprocedural and midterm mortality and complications, and symptom improvement after intervention. Forty-one mesenteric arteries (77.3% stenotic and 22.7% occluded vessels) were treated in 36 patients with 42 stents. In 30 patients (83.3%) one visceral artery and in 6 cases (16.7%) two visceral arteries were treated. Overall mortality was 16.7% (n=6) after a 60-month follow-up (mean follow-up period 30.1 months). Two early (<30-day) deaths were caused by visceral ischemia (n=2: 5.5%). Late death was procedure-related in one patient with re-occlusion of the superior mesenteric artery after 12 months. The other 3 patients died from non procedure-related causes; e.g. twice myocardial infarction. Initial symptom relief was observed in 29 patients (80.5%); 7 patients reported no change. Primary patency was 83.3% after 5 years and secondary patency was 90.5% (38 out of 42 stents) among all patients. Two conversions to open surgery were documented. First-line endovascular approach of CMI is a reasonable strategy. Close follow-up is mandatory due to symptom recurrence and restenosis.

Leptin causes body weight loss in the absence of in vivo activities typical of cytokines of the IL-6 family

1998 ◽  
Vol 275 (3) ◽  
pp. R913-R919 ◽  
Author(s):  
Davide Agnello ◽  
Cristina Meazza ◽  
Christopher G. Rowan ◽  
Pia Villa ◽  
Pietro Ghezzi ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Peripheral Blood Cell ◽  
Serum Corticosterone ◽  
Amyloid A ◽  
Cell Counts ◽  
Control Body ◽  
The One

To investigate if leptin shares in vivo activities with interleukin (IL)-6 family cytokines, it was tested in normal mice for the ability, after a single injection, to induce the acute-phase protein serum amyloid A, to potentiate the induction by IL-1 of serum corticosterone and IL-6, and to inhibit the induction by lipopolysaccharide of serum tumor necrosis factor and, after seven daily injections, to cause body weight loss and to change peripheral blood cell counts. At a 0.5 mg/kg dose, leptin caused body weight loss but did not show any of the other activities above. At a dose of 5 mg/kg, which also caused body weight loss, leptin potentiated the induction by IL-1 of serum corticosterone and IL-6 but did not show any other activity. In addition to causing body weight loss, leptin shows only some of the in vivo activities typical of IL-6 family cytokines and only if used at a dose that exceeds the one sufficient to affect body weight. In vivo, leptin seems to chiefly control body weight and not inflammatory or hematopoietic processes.

scholarly journals P069 CD73 promotes colitis-associated tumourigenesis in mice

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S170-S170
Author(s):  
X Wu ◽  
X Liu ◽  
N Lan ◽  
X Zheng ◽  
Y Chen ◽  
...  
Keyword(s):  
Weight Loss ◽  
Mouse Model ◽  
Rna Sequencing ◽  
Inflammatory Cytokines ◽  
Adenosine Receptors ◽  
Tumour Size ◽  
Body Weight Loss ◽  
Model Group ◽  
Adenosine Receptor Agonist ◽  
Pro Inflammatory Cytokines

Abstract Background Patients with inflammatory bowel disease (IBD) are at a higher risk of developing colitis-associated colorectal cancer. The aim of the present study was to investigate the role of CD73 in IBD-associated tumourigenesis. Methods A mouse model of colitis-associated tumourigenesis (CAT) induced by azoxymethane and dextran sulphate sodium (AOM/DSS) was successfully constructed. Model mice were injected with CD73 inhibitor or adenosine receptor agonist. Colon length, body weight loss and tumour formation were assessed macroscopically. Measurement of inflammatory cytokines and RNA sequencing on colon tissues were performed. Results Inhibition of CD73 by adenosine 5′-(α,β-methylene) diphosphate (APCP) suppressed the severity of CAT with attenuated weight loss, longer colons, lower tumour number and smaller tumour size when compared with the model group. On the other hand, activation of adenosine receptors using 1-(6-amino-9H-purin-9-yl)-1-deoxy-N-ethyl-β-d-ribofuranuronamide (NECA) exacerbated CAT. Histological assessment indicated that inhibition of CD73 reduced while activation of adenosine receptors exacerbated the histological damage of the colon compared with the model group. Increased expression of pro-inflammatory cytokines (tumour necrosis factor-α and interleukin-6) in colonic tissue was detected in the NECA group. According to the results of RNA sequencing, potential oncogenes such as ALOX15, Bcl2l15 and Nat8l were found to be downregulated in the APCP group and upregulated in the NECA group compared with the model group. Conclusion Therefore, inhibition of CD73 attenuated IBD-associated tumourigenesis, while activation of adenosine receptors exacerbated tumourigenesis in a C57BL/6J mouse model. This effect may be associated with the expression of pro-inflammatory cytokines and the regulation of ALOX15, Bcl2l15 and Nat8l.

scholarly journals The Extract of Arctium lappa L. Fruit (Arctii Fructus) Improves Cancer-Induced Cachexia by Inhibiting Weight Loss of Skeletal Muscle and Adipose Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3195
Author(s):  
Yo-Han Han ◽  
Jeong-Geon Mun ◽  
Hee Dong Jeon ◽  
Dae Hwan Yoon ◽  
Byung-Min Choi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Cancer Cachexia ◽  
Uncoupling Protein ◽  
Body Weight Loss ◽  
In Vivo Experiments ◽  
Wasting Syndrome

Background: Cachexia induced by cancer is a systemic wasting syndrome and it accompanies continuous body weight loss with the exhaustion of skeletal muscle and adipose tissue. Cancer cachexia is not only a problem in itself, but it also reduces the effectiveness of treatments and deteriorates quality of life. However, effective treatments have not been found yet. Although Arctii Fructus (AF) has been studied about several pharmacological effects, there were no reports on its use in cancer cachexia. Methods: To induce cancer cachexia in mice, we inoculated CT-26 cells to BALB/c mice through subcutaneous injection and intraperitoneal injection. To mimic cancer cachexia in vitro, we used conditioned media (CM), which was CT-26 colon cancer cells cultured medium. Results: In in vivo experiments, AF suppressed expression of interleukin (IL)-6 and atrophy of skeletal muscle and adipose tissue. As a result, the administration of AF decreased mortality by preventing weight loss. In adipose tissue, AF decreased expression of uncoupling protein 1 (UCP1) by restoring AMP-activated protein kinase (AMPK) activation. In in vitro model, CM increased muscle degradation factors and decreased adipocytes differentiation factors. However, these tendencies were ameliorated by AF treatment in C2C12 myoblasts and 3T3-L1 cells. Conclusion: Taken together, our study demonstrated that AF could be a therapeutic supplement for patients suffering from cancer cachexia.

Chronic mesenteric ischemia: stenting of mesenteric arteries

2006 ◽  
Vol 32 (3) ◽  
pp. 304-309 ◽  
Author(s):  
Philipp J. Schaefer ◽  
Fritz K. W. Schaefer ◽  
Stefan Mueller-Huelsbeck ◽  
Thomas Jahnke
Keyword(s):  
Mesenteric Ischemia ◽  
Mesenteric Arteries ◽  
Chronic Mesenteric Ischemia

scholarly journals Weight Loss: A Significant Cue To The Diagnosis of Chronic Mesenteric Ischemia

Cureus ◽  
2019 ◽  
Author(s):  
Ayesha Bakhtiar ◽  
Adeel S Yousphi ◽  
Ali R Ghani ◽  
Zain Ali ◽  
Waqas Ullah
Keyword(s):  
Weight Loss ◽  
Mesenteric Ischemia ◽  
Chronic Mesenteric Ischemia

scholarly journals A case of chronic mesenteric ischemia managed by ascending aorta to superior mesenteric and hepatic artery bypass

2017 ◽  
Vol 4 (8) ◽  
pp. 2836
Author(s):  
Harilal V. Nambiar ◽  
Robin George Manappallil ◽  
Sylesh Aikot ◽  
Pramod V.
Keyword(s):  
Hepatic Artery ◽  
Mesenteric Ischemia ◽  
Artery Bypass ◽  
Aortic Disease ◽  
Artery Occlusion ◽  
Ascending Aorta ◽  
Mesenteric Arteries ◽  
Chronic Mesenteric Ischemia ◽  
Threatening Condition ◽  
Life Threatening

Chronic mesenteric ischemia is a rare and life-threatening condition which occurs due to occlusion of two or more mesenteric arteries following atherosclerosis. Multi-vessel revascularization forms the mainstay of treatment. This is a case of a middle-aged smoker who presented with abdominal angina and was diagnosed to have chronic mesenteric ischemia due to atherosclerotic occlusive aortic disease with coeliac artery and superior mesenteric artery occlusion. He was successfully managed with extra anatomic bypass from the ascending aorta to superior mesenteric and hepatic artery.

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