Mesenteric Ischemia Publications (5933)
Mesenteric Ischemia Publications
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.
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.
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.
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.
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.
IMA and bilateral IIA preservation with covered self-expanding stents during endovascular aneurysm repair is a safe and effective method.
He was started with anticoagulation and decision was to treat long term. He was admitted with mesenteric artery ischemic symptoms in February 2012 on anticoagulation. CT scan abdomen and pelvis in February 2012 showed tumor thrombus involving the superior mesenteric vein, portal vein, and splenic vein with hepatic metastasis. His tumor marker chorioembryonic antigen was 34 µg/L. He was continued on anticoagulation. A repeat CT scan abdomen after 2 years (in January 2014) showed, increase in size of hepatic metastasis, extensive thrombus involving the superior mesenteric vein, portal vein, and splenic vein with collaterals. Mesentery was congested due to extensive superior mesenteric vein thrombus. He finally succumbed in June 2014. It is very important to differentiate PVT from PVTT as the prognosis is different. PVTT progresses despite of long-term anticoagulation with poor prognosis.
HuR bound to the Cdc42 mRNA via its 3' -untranslated region and this association specifically enhanced Cdc42 translation without effect on Cdc42 mRNA level. Intestinal epithelium-specific HuR knockout not only decreased Cdc42 levels in mucosal tissues, but it also inhibited repair of damaged mucosa induced by mesenteric ischemia/reperfusion in the small intestine and by dextran sulphate sodium in the colon. Furthermore, Cdc42 silencing prevented HuR-mediated stimulation of cell migration over the wounded area by altering the subcellular distribution of F-actin. These results indicate that HuR promotes early intestinal mucosal repair after injury by increasing Cdc42 translation and demonstrate the importance of HuR deficiency in the pathogenesis of delayed mucosal healing in certain pathological conditions.
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.