Mesenteric Ischemia Publications (5933)

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Mesenteric Ischemia Publications

2017Jan
Neonatology
Neonatology 2017 Jan 17;111(4):337-343. Epub 2017 Jan 17.
Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

The etiology of necrotizing enterocolitis (NEC) remains elusive despite known associations with several factors, including intestinal ischemia related to the effects of umbilical arterial catheterization on the mesenteric circulation. However, the role of the mesenteric venous circulation has yet to be studied as a potential cause of NEC. We examined the association between umbilical venous catheter (UVC) position and the development of NEC in premature infants. Read More


A prospective cohort study was performed to examine the effect of UVC on portosystemic shunting via the ductus venosus (DV) and its potential role in NEC.
We recruited 132 premature infants, 62 of which had a birth weight ≤1,500 g. NEC was noted in 12 (19%) patients. All infants weighing ≤1,500 g underwent an attempt at UVC insertion. The UVC status was classified as appropriate (n = 39), unsuccessful (n = 9), or malpositioned (n = 14). Among the NEC patients, 7 (58%) had a UVC malposition and 3 (25%) had an unsuccessful attempt. These rates were significantly higher than in patients without NEC (14 and 12%, respectively). Multivariable logistic regression analysis confirmed birth weight (OR 2.2, 95% CI 1.2-4.7, p = 0.001) and UVC malpositioning (OR 6.9, 95% CI 1.6-35.4, p = 0.007) as independent risk factors associated with NEC.
Unrecognized withdrawal of a UVC into the portal vein or DV is associated with an increased incidence of NEC in infants weighing ≤1,500 g. The data support the need for additional studies to examine this effect. Confirmation of a causal relationship will raise the need to reassess UVC insertion criteria and strategies for more closely monitoring the catheter tip position.

2017Jan
Am. J. Physiol. Gastrointest. Liver Physiol.
Am J Physiol Gastrointest Liver Physiol 2017 Jan 12:ajpgi.00371.2016. Epub 2017 Jan 12.
University of California San Diego Health Sciences

Vagal nerve stimulation (VNS) has been shown to limit intestinal inflammation following injury, however, direct connection between vagal terminals and resident intestinal immune cells have yet to be identified. We have previously shown that enteric glia cell (EGC) expression is increased after injury through a vagal-mediated pathway to help restore gut barrier function. We hypothesize that EGCs modulate immune cell recruitment following injury and relay vagal anti-inflammatory signals to resident immune cells in the gut. Read More

EGCs were selectively ablated from an isolated segment of distal bowel with topical application of benzalkonium chloride (BAC) in male mice. Three days following BAC application, mice were subjected to an ischemia-reperfusion injury (I/R) by superior mesenteric artery occlusion for 30 minutes. VNS was performed in a separate cohort of animals. EGC(+) and EGC(-) segments were compared utilizing histology, flow cytometry, immunohistochemistry, and intestinal permeability. VNS significantly reduced immune cell recruitment after I/R injury in EGC(+) segments with cell percentages similar to sham. VNS failed to limit immune cell recruitment in EGC(-) segments. Histologic evidence of gut injury was diminished with VNS application in EGC+ segments, whereas EGC(-) segments showed features of more severe injury. Intestinal permeability increased following I/R injury in both EGC(+) and EGC(-) segments. Permeability was significantly lower after VNS application compared to injury alone in EGC(+) segments only (95.1 ± 30.0 vs. 217.6 ± 21.7 μg/mL, p<0.05). Therefore, EGC ablation uncouples the protective effects of VNS, suggesting that vagal-mediated signals are translated to effector cells through EGCs.

2017Jan
PLoS ONE
PLoS One 2017 6;12(1):e0169331. Epub 2017 Jan 6.
Abdominal Transplant Surgery, University Hospitals Leuven, & Department of Microbiology and Immunology, KU Leuven, Belgium.

The farnesoid X receptor (FXR) is abundantly expressed in the ileum, where it exerts an enteroprotective role as a key regulator of intestinal innate immunity and homeostasis, as shown in pre-clinical models of inflammatory bowel disease. Since intestinal ischemia reperfusion injury (IRI) is characterized by hyperpermeability, bacterial translocation and inflammation, we aimed to investigate, for the first time, if the FXR-agonist obeticholic acid (OCA) could attenuate intestinal ischemia reperfusion injury.
In a validated rat model of intestinal IRI (laparotomy + temporary mesenteric artery clamping), 3 conditions were tested (n = 16/group): laparotomy only (sham group); ischemia 60min+ reperfusion 60min + vehicle pretreatment (IR group); ischemia 60min + reperfusion 60min + OCA pretreatment (IR+OCA group). Read More

Vehicle or OCA (INT-747, 2*30mg/kg) was administered by gavage 24h and 4h prior to IRI. The following end-points were analyzed: 7-day survival; biomarkers of enterocyte viability (L-lactate, I-FABP); histology (morphologic injury to villi/crypts and villus length); intestinal permeability (Ussing chamber); endotoxin translocation (Lipopolysaccharide assay); cytokines (IL-6, IL-1-β, TNFα, IFN-γ IL-10, IL-13); apoptosis (cleaved caspase-3); and autophagy (LC3, p62).
It was found that intestinal IRI was associated with high mortality (90%); loss of intestinal integrity (structurally and functionally); increased endotoxin translocation and pro-inflammatory cytokine production; and inhibition of autophagy. Conversely, OCA-pretreatment improved 7-day survival up to 50% which was associated with prevention of epithelial injury, preserved intestinal architecture and permeability. Additionally, FXR-agonism led to decreased pro-inflammatory cytokine release and alleviated autophagy inhibition.
Pretreatment with OCA, an FXR-agonist, improves survival in a rodent model of intestinal IRI, preserves the gut barrier function and suppresses inflammation. These results turn FXR into a promising target for various conditions associated with intestinal ischemia.

2016Nov
J Clin Diagn Res
J Clin Diagn Res 2016 Nov 1;10(11):OD03-OD04. Epub 2016 Nov 1.
Assistant Professor, Department of Cardiology, Kasturba Medical College , Manipal, Karnataka, India .

Chronic Mesenteric Ischemia (CMI) presenting as acute abdomen can be treated percutaneously. An endovascular intervention has surpassed surgical revascularization over the past decade due to its lesser perioperative complication rate. Trans-femoral approach of revascularising is limited by its difficulty in coaxial alignment of the guiding catheter and hence, brachial artery and recently the radial approach have been utilized for mesenteric artery revascularisation for over a decade. Read More

Here by we report a case of chronic mesenteric ischemia having total occlusion of two and 70% occlusion of one of the three mesenteric vessels. The patient had presented with acute abdomen which in turn was percutaneously revascularised via the left brachial artery for the two major abdominal visceral vessels being superior mesenteric artery and inferior mesenteric artery.

2017Jan
Semin. Thorac. Cardiovasc. Surg.
Semin Thorac Cardiovasc Surg 2016 Summer;28(2):221-237. Epub 2016 Jul 17.
Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; Department of Cardiovascular Surgery, Texas Heart Institute, Houston, Texas; Department of Cardiovascular Surgery, CHI St. Luke׳s Health-Baylor St. Luke׳s Medical Center, Houston, Texas; Surgical Research Core, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas.

The primary risks associated with thoracoabdominal aortic aneurysm (TAAA) repair-namely operative death, paraplegia, and renal failure necessitating dialysis-are commonly related to the distal ischemia that occurs during aortic clamping and the disruption of vital branching arteries. Our technique for open TAAA repair has evolved over the course of 3 decades, from the unheparinized, simple "clamp-and-sew" approach learned directly from E. Stanley Crawford himself to a contemporary, multimodal strategy that uses an array of surgical adjuncts. Read More

Today, our approach to TAAA repair is largely standardized and based on the Crawford extents of TAAA repair, but we have maintained flexibility to explore new techniques and to adapt to the specific needs of patients. To protect the spinal cord, we routinely use mild passive hypothermia, cerebrospinal fluid drainage, left heart bypass, and reimplantation of crucial intercostal or lumbar arteries. The renal arteries are perfused with cold solution to protect the kidneys from ischemic damage, and the celiac axis and superior mesenteric artery are perfused with isothermic blood from the left heart bypass circuit, which minimizes the duration of abdominal-organ ischemia. The most extensive repair, Crawford extent II repair, typically replaces the aorta from just beyond the left subclavian artery to the aortic bifurcation; unsurprisingly, it commonly poses greater operative risk than do less extensive TAAA repairs (extent I, III, and IV). Subsequently, most surgical adjuncts used today were developed to ameliorate risk in extent II repair. Here, we provide a detailed description of our approach to open extent II TAAA repair.

2016Dec
Vasc Specialist Int
Vasc Specialist Int 2016 Dec 31;32(4):190-194. Epub 2016 Dec 31.
Department of Thoracic and Cardiovascular Surgery, College of Medicine and Institute of Health Sciences, Gyeongsang National University Changwon Hospital, Changwon, Jinju, Korea.

We report an endovascular aneurysm repair in a patient with isolated bilateral common iliac artery aneurysms, a prominent inferior mesentery artery (IMA), and bilateral proximal internal iliac artery (IIA) aneurysms using covered self-expanding stents to preserve the IMA and bilateral internal iliac arteries. A follow-up computed tomography angiography was obtained at 1 month. Pelvic circulation was well preserved without bowel ischemia. Read More

IMA and bilateral IIA preservation with covered self-expanding stents during endovascular aneurysm repair is a safe and effective method.

2016Dec
Int. J. Angiol.
Int J Angiol 2016 Dec 30;25(5):e73-e76. Epub 2014 Jul 30.
North Shore Long Island Jewish Hospital, Manhasset, New York.

Superior mesenteric artery (SMA) syndrome or Wilkie syndrome is a rare condition that arises when the distal third of the duodenum becomes trapped between the SMA and the abdominal aorta causing intestinal obstruction. It is most commonly described in adolescents and rarely in adult patients. We present an interesting case of an adult who developed SMA syndrome from an uncommon gastric mantle cell lymphoma that was recognized early and treated surgically. Read More

2016Dec
Mol. Cell. Biol.
Mol Cell Biol 2016 Dec 28. Epub 2016 Dec 28.
Cell Biology Group, Department of Surgery, and Department of Pathology, University of Maryland School of Medicine, and Baltimore Veterans Affairs Medical Center, Maryland 21201

Intraamniotic meconium has been responsible for intestinal damage in gastroschisis and meconium-dependent intestinal ischemia has been proposed to induce additional intestinal damage in gastroschisis. This study is aimed to determine the effects of lipid and water-soluble meconium subfractions on the contractility of the superior mesenteric artery (SMA).
The study was conducted on 18-day fertilized chick embryos (Gallus Domesticus). Read More

Meconium is fractioned into water and lipid-soluble components. Only one SMA tissue was prepared from each embryo and suspended in the organ bath. Isometric contraction responses (ICR) were created in SMA tissues by one hour of incubation in Krebs-Henseleit solution for each group. Groups consisted of control, meconium, water-soluble meconium subfraction and lipid-soluble meconium subfraction. ICR of the SMA specimens were evaluated with a transducer-amplifier system on a computer. The data were expressed (mean±1SD) as milliNewton (mN).
The ICR of the meconium, water-soluble meconium subfraction and lipid-soluble meconium subfraction groups were significantly high when compared to the control group (p<0.01). The meconium and water-soluble meconium subfraction created more contraction response than the lipid-soluble meconium subfraction (p<0.01). The ICR of the meconium group was not different from the ICR of the water-soluble meconium subfraction group (p>0.05).
Water-soluble meconium subfraction has a profound vasoconstrictor effect on the SMA compared to the lipid-soluble meconium subfraction.