Omental Arteries Research Articles

LDL-c/HDL-c Ratio and NADPH-Oxidase-2-Derived Oxidative Stress as Main Determinants of Microvascular Endothelial Function in Morbidly Obese Subjects.

The identification of obese subjects at higher risk for cardiovascular disease (CVD) is required. We aimed to characterize determinants of endothelial dysfunction, the initial step to CVD, in small omental arteries of visceral fat from obese subjects. The influences of analytical parameters and vascular oxidative stress mediated by NADPH-oxidase-2 (NOX2) on endothelial function were determined. Specimens were obtained from 51 obese subjects undergoing bariatric surgery and 14 non-obese subjects undergoing abdominal surgery. Obese subjects displayed reduced endothelial vasodilation to bradykinin (BK). Endothelial vasodilation (pEC50 for BK) among obese subjects was significantly and negatively associated with low-density lipoprotein cholesterol (LDL-c)/high-density lipoprotein cholesterol (HDL-c) ratio (r = -0.510, p = 0.0001) in both women and men, while other metabolic parameters and comorbidities failed to predict endothelial function. The vascular expression of NOX2 was upregulated in obese subjects and was related to decreased endothelial vasodilation (r = -0.529, p = 0.0006, n = 38) and increased oxidative stress (r = 0.783, p = 0.0044, n = 11) in arterial segments. High LDL-c/HDL-c (>2) and high NOX2 (above median) were independently associated with reduced endothelial function, but the presence of both conditions was related to a further impairment. Concomitant elevated LDL-c/HDL-c ratio and high vascular expression of NOX2 would exacerbate endothelial impairment in obesity and could reveal a deleterious profile for cardiovascular outcomes among obese subjects.

Exploring the Therapeutic Potential of C-Type Natriuretic Peptide for Preeclampsia.

Preeclampsia is a serious condition of pregnancy, complicated by aberrant maternal vascular dysfunction. CNP (C-type natriuretic peptide) contributes to vascular homeostasis, acting through NPR-B (natriuretic peptide receptor-B) and NPR-C (natriuretic peptide receptor-C). CNP mitigates vascular dysfunction of arteries in nonpregnant cohorts; this study investigates whether CNP can dilate maternal arteries in ex vivo preeclampsia models. Human omental arteries were dissected from fat biopsies collected during cesarean section. CNP, NPR-B, and NPR-C mRNA expression was assessed in arteries collected from pregnancies complicated by preeclampsia (n=6) and normotensive controls (n=11). Using wire myography, we investigated the effects of CNP on dilation of arteries from normotensive pregnancies. Arteries were preconstricted with either serum from patients with preeclampsia (n=6) or recombinant ET-1 (endothelin-1; vasoconstrictor elevated in preeclampsia; n=6) to model vasoconstriction associated with preeclampsia. Preconstricted arteries were treated with recombinant CNP (0.001-100 µmol/L) or vehicle and vascular relaxation assessed. In further studies, arteries were preincubated with NPR-B (5 µmol/L) and NPR-C (10 µmol/L) antagonists before serum-induced constriction (n=4-5) to explore mechanistic signaling. CNP, NPR-B, and NPR-C mRNAs were not differentially expressed in omental arteries from preeclamptic pregnancies. CNP potently stimulated maternal artery vasorelaxation in our model of preeclampsia (using preeclamptic serum). Its vasodilatory actions were driven through the activation of NPR-B predominantly; antagonism of this receptor alone dampened CNP vasorelaxation. Interestingly, CNP did not reduce ET-1-driven omental artery constriction. Collectively, these data suggest that enhancing CNP signaling through NPR-B offers a potential therapeutic strategy to reduce systemic vascular constriction in preeclampsia.

Diminished insulin-induced vasodilation of the posterior cerebral artery in db/db mice is associated with reduced presence of endothelial insulin receptor alpha and inward remodeling

Type 2 diabetes (T2D) is a major risk factor for cardiovascular disease (CVD) development and associated mortality. In the cerebral circulation, T2D-related vascular disfunction also contributes to diverse cerebrovascular diseases including stroke, cognitive impairment, and dementia. Previous research has documented that endothelial dysfunction and inward remodeling are prevalent pathophysiological characteristics of the arterial circulation in T2D. We have further documented that reduced presence of endothelial insulin receptor alpha (IRα) contributes to impaired insulin-dependent vasodilation in omental arteries from T2D patients. Herein, we tested the hypothesis that, compared to wild-type (WT) mice, diabetic db/db mice have reduced insulin-induced vasodilation of the posterior cerebral artery (PCA) in association with reduced presence of endothelial IRα and inward remodeling. We used pressure myography in isolated PCAs to assess vascular reactivity and remodeling, and confocal microscopy to determine IRα content on the endothelial surface. All reported differences are significant at P<0.05. Our results indicate that, when compared with WT controls, PCAs from db/db mice have reduced insulin-induced vasodilatory responses in association with reduced presence of endothelial IRα, inward remodeling, and increased arterial stiffness. The amount of IRβ, elastin, or collagen present in the PCAs did not differ between groups. These findings provide evidence of cerebrovascular endothelial dysfunction in the form of impaired insulin-induced vasodilation in db/db mice, a defect likely attributed to the reduced presence of endothelial IRα and associated with vascular inward remodeling. These changes may contribute to cerebrovascular disease development and progression in T2D, including stroke, cognitive impairment, and associated dementias. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Role of neuraminidase in promoting the shedding of endothelial mechanosensing structures in type 2 diabetes

Endothelial dysfunction represents a causal factor in the pathogenesis of cardiovascular disease associated with type 2 diabetes (T2D). Previous work shows that endothelial mechanosensing structures are degraded in T2D, resulting in impaired shear stress mechanotransduction and decreased endothelial-derived nitic oxide (NO) bioavailability. Recent evidence suggests that glypican-1, a well-known mechanosensor, is a substrate of the proinflammatory enzyme a disintegrin and metalloproteinase-17 (ADAM17). A key step in ADAM17 activation is externalization of phosphatidylserine (PS) to the outer leaflet of the plasma membrane, which can be mediated by the phospholipid scramblase anoctamin-6 (ANO6). However, whether ANO6-mediated activation of ADAM17 leads to glypican-1 shedding in endothelial cells remains unknown. Also unknown are the mechanisms by which this pathway becomes overactive in T2D. We recently reported that T2D is associated with increased circulating levels of neuraminidase, a soluble enzyme that cleaves sialic acid residues. We also showed that intraluminal exposure of isolated arteries to neuraminidase impairs shear stress mechanotransduction. Herein, we tested the hypothesis that neuraminidase-induced impaired shear stress mechanotransduction is mediated by ANO6-induced ADAM17 activation and consequent shedding of glypican-1. All reported differences are significant at P<0.05. In support of our hypothesis, we show that neuraminidase and ADAM17 activities are increased, while nitrite (NO surrogate) is decreased, in plasma of men and women with T2D who also display evidence of impaired shear stress mechanotransduction ( i.e., diminished flow-mediated dilation). In cultured endothelial cells, we show that neuraminidase exposure decreases sialic acid content and increases intracellular Ca2+ mobilization, adhesion of lactadherin (a peptide that binds externalized PS), ADAM17 activity, and shedding of glypican-1. Also in cultured endothelial cells, overexpression of ADAM17 increases shedding of glypican-1 and impairs shear stress-induced activation of endothelial NO synthase. Congruently, intraluminal exposure of human omental arteries to active ADAM17 recombinant protein impairs flow-mediated dilation. Furthermore, silencing of ANO6 reduces ADAM17 activity, leading to increased presence of glypican-1 on the endothelial cell surface. Taken together, we provide evidence that neuraminidase, an enzyme increased in the circulation of individuals with T2D, promotes ANO6-dependent externalization of PS in endothelial cells, which in turn leads to ADAM17 activation and consequent shedding of glypican-1. Thus, this work supports the idea that the neuraminidase-ANO6-ADAM17 axis should be considered as a potential target for restoring endothelial mechanosensation and improving NO bioavailability in T2D. R01HL151384 (to LAML and JP), R01HL153264 (to LAML and JP), R01HL137769 (to JP), and R21DK116081 (to CM-A). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Efficacy and safety of transcatheter arterial embolization of omental artery aneurysm: A single-center experience.

Omental artery aneurysm (OAA) is an extremely rare visceral artery aneurysm. Ruptured OAAs are associated with a high mortality rate. Transcatheter arterial embolization (TAE) has been used to treat OAA in recent years. However, the risk of omental ischemia due to TAE remains unclear. Therefore, this study aimed to investigate the efficacy and safety of TAE of OAA as a first-line treatment. Fifteen patients with true aneurysms or pseudoaneurysms who underwent OAA-TAE between 1 April 2010 and 31 December 2022 were included in this study. The technical and clinical outcomes, the incidence of omental infarction after TAE as a major complication, OAA-TAE techniques, radiological findings on computed tomography angiography and angiogram, and patient characteristics were evaluated. Fifteen patients (nine men, six women; age, 69.8 ± 18.59 years) underwent TAE of OAAs (mean aneurysm size of 9.30 ± 6.10 mm) located in the right gastroepiploic (n = 9), left gastroepiploic (n = 1), and epiploic (n = 5) arteries. All patients with ruptured (n = 6) and unruptured (n = 9) OAA successfully underwent TAEs using coils, n-butyl-2-cyanoacrylate, or gelatin sponges. Hepatic artery thrombosis and coil migration were observed during the procedure; however, these adverse events were manageable. Transfusion of red blood cell units (4.66 ± 1.63 units) was required only in cases with ruptured OAAs after TAE. Additional surgery or TAE due to rupture or rerupture of OAA and omental infarction was not required during the postoperative and follow-up periods. The OAA-TAE can effectively treat ruptured and unruptured OAAs, and the risk of omental infarction after OAA-TAE may not be high.

Commentary on: Increased stiffness of omental arteries from late pregnant women at advanced maternal age.

Worldwide, pregnancy at age 35 or older, termed 'advanced maternal age (AMA)', is increasing exponentially. As the incidence of pregnancy at AMA has increased, a growing body of evidence has suggested that AMA is also associated with increased risk for adverse maternal and fetal outcomes outside of genetic anomalies. Importantly, despite the mounting evidence and the increased global risk of adverse perinatal outcomes observed, few studies have examined the potential mechanisms underlying this elevated risk in pregnant people ≥35 years of age. Wooldridge and colleagues begin to address this gap in the literature. In their recent report, they examine vessel stiffness in omental resistance vessels obtained from pregnant individuals ≥35 years of age compared with pregnant individuals <35 years of age. Omental arteries were isolated and assessed via pressure myography (mechanical properties) and histological analysis for collagen and elastin content. Overall, the findings from this investigation report that maternal resistance arteries collected from women of AMA were less compliant and had less elastin than arteries obtained from women <35 years of age, suggesting that maternal resistance vessel stiffening in AMA may contribute to increased risk of adverse pregnancy outcomes. The authors should be commended for completing these studies in human resistance vessels, which now open new avenues for investigation and provoke a cascade of questions related to maternal cardiovascular adaptations to pregnancy in women ≥35 years of age.

Hepatocellular carcinoma vascularization: CT angiography variations identifying arteries feeding the tumour

BackgroundHepatic arterial anatomy is important in performing many surgical and endovascular procedures. Familiarity with variations in the hepatic arterial anatomy is essential to achieving adequate embolization. In some patients, in addition to anatomic variations of the hepatic arteries, different extrahepatic collateral arteries may provide partial or total vascular supply to hepatocellular carcinoma (HCC), which makes transcatheter arterial chemoembolization (TACE) technically challenging. We aim to evaluate the different feeding vessels of HCC using multi-detector computed tomography angiography (MDCTA) as a pre-procedural step before planning suitable management.ResultsOne hundred patients with 150 focal HCC lesions were involved in our study. The anatomy of the blood supply and the morphological characteristics of HCC, including the size, location, and history of previous hepatitis, were quantitatively assessed and statistically analysed. The number of patients who had classic hepatic arterial supply for the HCC lesions in our study was 54 (54%). The number of patients with additional extrahepatic supply is 26, while the number of patients with anatomical vascular variants is 20. Among these 26 patients with extrahepatic (parasitic) blood supply, six patients were supplied by the right inferior phrenic artery, four patients were supplied by the right internal mammary artery, and two patients were supplied by each other type of extrahepatic feeder, which are the left inferior phrenic artery, left internal mammary artery, left gastric artery, cystic artery, right lumbar artery, direct branch from the aorta, omental arteries, right renal artery, and LHA from the LGA. Twelve of the 20 patients with anatomical vascular variants had replaced RHA from the SMA; four patients had replaced LHA from the LGA; two patients had replaced RHA from the GDA; and two patients had replaced CHA from the SMA. Only 50 cases of CT findings were correlated with the data from the interventional procedures of these patients.ConclusionsBecause of the differences in HCC blood supply between typical, parasitic, and anatomical vascular variants, MDCTA has significant clinical significance prior to TACE and any interventional procedure.

Idiopathic omentum hemorrhage as a cause of hemoperitoneum

Hemorrhage into the large omentum is a general term for a pathological condition in which an omental artery and/or vein ruptures with bleeding into the abdominal cavity and/or forming an omental hematoma. There is a high probability of its diagnosis only during surgery. This is an extremely rare condition, which is described only in clinical case reports. There are primary and secondary omental hemorrhage. Secondary hemorrhage occurs due to various reasons, primary (idiopathic) in the absence of morphological changes that could lead to bleeding to the large omentum. The article is devoted to a rare case of idiopathic omentum bleeding complicated by hemoperitoneum, diagnosed intraoperatively. The article presents the results of a literary review of the last twenty years on English-language and Russian-language publications on omental hemorrhage, presented in the databases of PubMed and the Russian scientific electronic library (eLIBRARY.RU). According to the results of the analysis of the literature data, ultrasound can be used as a first-line imaging method to assess the presence of hemoperitoneum. But CT angiography is the method of choice in assessing acute intra-abdominal bleeding and determining the cause of bleeding due to its speed, availability and ability to diagnose alternative causes of abdominal pain, and it is also recommended to be performed in cases where ultrasound data do not allow to unambiguously establish the presence of bleeding or localize its source. Also, taking into account the age characteristics and gender of patients, the presence of bleeding into the omentum may be due to conditions such as cystic lymphangioma and interrupted ectopic pregnancy. Other causes may be vascular pathologies, tumors and anticoagulant therapy. When detecting signs of bleeding into the large omentum, in addition to determining the fact of hemoperitoneum and its volume, the most important tasks are to establish the causes of hemorrhage and differential diagnosis between idiopathic and secondary bleeding.

The Regulation of Endothelin-1 in Pregnancies Complicated by Gestational Diabetes: Uncovering the Vascular Effects of Insulin.

Gestational diabetes mellitus (GDM) is a condition of pregnancy defined by new-onset hyperglycemia. GDM is associated with impaired maternal endothelial and vascular reactivity. Endothelin-1 (ET-1) is a potent vasoconstrictor that contributes to endothelial dysfunction, however, its abundance and actions in GDM are unclear. Maternal plasma was obtained from pregnancies complicated by GDM (n = 24) and gestation-matched controls (n = 42); circulating ET-1 levels were assessed by ELISA. Human omental arteries from healthy pregnancies and those complicated by GDM were dissected from omental fat biopsies and collected at cesarean section. mRNA expression of ET-1 and its receptors, ETA and ETB, in addition to vascular cell adhesion molecule-1 (VCAM1) and intercellular adhesion molecule-1 (ICAM1) were assessed by qPCR (n = 28). Using wire myography, we investigated vascular constriction to ET-1 (10-11-10-4 M) in omental arteries from pregnancies complicated by GDM, compared to gestation-matched controls (n = 7). GDM cases were stratified by clinical management, diet intervention (n = 5), or insulin treatment (n = 6). Additionally, arteries from healthy pregnancies were treated with insulin (1 mU/mL (n = 7) and 10 mU/mL (n = 5)) or vehicle control. Vasoactive response to ET-1 was measured via wire myography. Circulating ET-1 levels and mRNA expression of the ET-1 system in omental arteries were not found to be significantly different between pregnancies complicated by GDM compared to healthy controls. However, we found insulin treatment during pregnancy and in ex vivo models reduced ET-1 vasoconstriction of maternal vasculature in GDM. These data suggest insulin may improve vascular function in GDM, however, further investigation is needed to define the role of ET-1 in pregnancy.

Calcitonin gene-related peptide protects from soluble fms-like tyrosine kinase-1-induced vascular dysfunction in a preeclampsia mouse model.

Introduction: Preeclampsia (PE) is a hypertensive disorder during pregnancy associated with elevated levels of soluble FMS-like tyrosine kinase (sFLT-1) and increased vascular sensitivity to angiotensin II (ATII). Calcitonin gene-related peptide (CALCA) is a potent vasodilator that inhibits the ATII-induced increase in blood pressure and protects against ATII-induced increases in oxidative stress through a mitochondrial-dependent pathway in male mice. In rodent pregnancy, CALCA facilitates pregnancy-induced vascular adaptation. Most of the vascular effects of CALCA are mediated by vascular smooth muscle cells (VSMCs). We recently reported that CALCA treatment inhibits sFLT-1-induced decreases in cAMP synthesis in omental artery smooth muscle cells (OASMCs) isolated from pregnant women and has relaxant effects in omental arteries (OAs) isolated from pregnant women with preeclamptic (PE) pregnancies. The current study was designed to assess the effects of sFLT-1 on mitochondrial bioenergetics in OASMCs isolated from pregnant women in the presence or absence of CALCA and assess the development of vascular dysfunction in sFLT-1 using a mouse model of PE pregnancy. Methods: OASMCs were isolated from pregnant women to assess the effects of sFLT-1 on mitochondrial bioenergetics and oxidative stress using the Seahorse assay and quantitative PCR. Pregnant mice overexpressing sFLT-1 via adenoviral delivery were used to assess the effects of CALCA infusion on the sFLT-1-induced increase in blood pressure, ATII hypersensitivity, fetal growth restriction, and the elevated albumin-creatinine ratio. Systemic blood pressure was recorded in conscious, freely moving mice using implantable radio telemetry devices. Results: CALCA inhibited the following sFLT-1-induced effects: 1) increased oxidative stress and the decreased oxygen consumption rate (OCR) in response to maximal respiration and ATP synthesis; 2) increases in the expression of mitochondrial enzyme complexes in OASMCs; 3) increased mitochondrial fragmentation in OASMCs; 4) decreased expression of mitophagy-associated PINK1 and DRAM1 mRNA expression in OASMCs; and 5) increased blood pressure, ATII hypersensitivity, fetal growth restriction, and the albumin-creatinine ratio in sFLT-1-overexpressing pregnant mice. Conclusion: CALCA inhibits sFLT-1-induced alterations in mitochondrial bioenergetics in vascular smooth muscle cells and development of maternal vascular dysfunction in a mouse model of PE.

Increased stiffness of omental arteries from late pregnant women at advanced maternal age.

Advanced maternal age (≥35 years) is a risk factor for poor pregnancy outcomes. Pregnancy requires extensive maternal vascular adaptations, and with age, our blood vessels become stiffer and change in structure (collagen and elastin). However, the effect of advanced maternal age on the structure of human resistance arteries during pregnancy is unknown. As omental resistance arteries contribute to blood pressure regulation, assessing their structure in pregnancy may inform on the causal mechanisms underlying pregnancy complications in women of advanced maternal age. Omental fat biopsies were obtained from younger (<35 years) or advanced maternal age (≥35 years) women during caesarean delivery (n = 7-9/group). Arteries (200-300 µm) were isolated and passive mechanical properties (circumferential stress and strain) assessed with pressure myography. Collagen (Masson's Trichrome) and elastin (Verhoff) were visualized histologically and % positively-stained area was assessed. Median maternal age was 32 years (range 25-34) for younger, and 38 years (range 35-42) for women of advanced maternal age. Circumferential strain was lower in arteries from advanced maternal age versus younger women but circumferential stress was not different. Omental artery collagen levels were similar, while elastin levels were lower with advanced maternal age versus younger pregnancies. The collagen:elastin ratio was greater in arteries from advanced maternal age versus younger women. In conclusion, omental arteries from women of advanced maternal age were less compliant with less elastin compared with arteries of younger controls, which may affect how vascular stressors are tolerated during pregnancy. Understanding how vascular aging affects pregnancy adaptations may contribute to better pregnancy outcomes.

Intraperitoneal hemorrhage secondary to ruptured omental artery aneurysm associated with polyarteritis nodosa: a case report

BackgroundPolyarteritis nodsa (PAN) is a rare disease characterized by acute focal inflammatory damage to small and medium arteries. PAN complicated by ruptured aneurysm is an infrequent presentation with the most affected arteries being the renal and mesenteric arteries.Case presentationA 76-year-old female presented with a low-grade fever, generalized body aches, and abdominal pain. Investigation revealed intraperitoneal bleeding secondary to a ruptured and actively bleeding right omental artery aneurysm. Clinical manifestation, angiography and histology were consistent with PAN. Laparotomy was performed for stabilization and resection of the bleeding aneurysm followed by post operative steroids and cyclophosphamide. Patient was discharged in a stable condition. We reviewed seven cases found in the literature of omental artery aneurysm and rupture. Four cases were proceeded with laparotomy and aneurysm resection while three cases were proceeded with a less invasive approach of arterial embolization.ConclusionsOmental artery aneurysm is a rare occurrence with even fewer reported cases associated with PAN. Of the seven reported cases, all patients were treated with a surgical intervention. In addition, PAN patients should be treated post-operatively with a course of steroids and cyclophosphamide.

Investigating the Effects of Atrial Natriuretic Peptide on the Maternal Endothelium to Determine Potential Implications for Preeclampsia.

Preeclampsia is associated with an increased lifelong risk of cardiovascular disease (CVD). It is not clear whether this is induced by persistent systemic organ and vascular damage following preeclampsia or due to a predisposition to both conditions that share cardiovascular pathophysiology. Common to both CVD and preeclampsia is the dysregulation of corin and its proteolytic product, atrial natriuretic peptide (ANP). ANP, a hypotensive hormone converted from pro-ANP by corin, is involved in blood pressure homeostasis. While corin is predominantly a cardiac enzyme, both corin and pro-ANP are significantly upregulated in the gravid uterus and dysregulated in preeclampsia. Relatively little is known about ANP function in the endothelium during a pregnancy complicated by preeclampsia. Here, we investigated the effect of ANP on endothelial cell proliferation and migration, markers of endothelial dysfunction, and receptor expression in omental arteries exposed to circulating preeclamptic toxins. ANP receptor expression is significantly upregulated in preeclamptic vasculature but not because of exposure to preeclampsia toxins tumour necrosis factor α or soluble fms-like tyrosine kinase-1. The supplementation of endothelial cells with ANP did not promote proliferation or migration, nor did ANP improve markers of endothelial dysfunction. The role of ANP in preeclampsia is unlikely to be via endothelial pathways.

Serum Collected from Preeclamptic Pregnancies Drives Vasoconstriction of Human Omental Arteries-A Novel Ex Vivo Model of Preeclampsia for Therapeutic Development.

New-onset maternal hypertension is a hallmark of preeclampsia, driven by widespread endothelial dysfunction and systemic vasoconstriction. Here, we set out to create a new ex vivo model using preeclamptic serum to cause injury to the endothelium, mimicking vascular dysfunction in preeclampsia and offering the potential to evaluate candidate therapeutic interventions. Human omental arteries were collected at caesarean section from normotensive pregnant patients at term (n = 9). Serum was collected from pregnancies complicated by preterm preeclampsia (birth < 34 weeks’ gestation, n = 16), term preeclampsia (birth > 37 weeks’ gestation, n = 5), and healthy gestation-matched controls (preterm n = 16, term n = 12). Using wire myography, we performed ex vivo whole vessel assessment where human omental arteries were treated with increasing doses of each serum treatment (2–20%) and vasoreactivity was assessed. All pregnant serum treatments successfully drove vasoconstriction; no significant difference was observed in the degree of vasoconstriction when exposed to preeclamptic or control serum. We further demonstrated the ability of esomeprazole (a candidate therapeutic for preeclampsia; 0.1–100 µM) to drive vasorelaxation of pre-constricted vessels (only with serum from preeclamptic patients). In summary, we describe a novel human physiological model of preeclamptic vascular constriction. We demonstrate its exciting potential to screen drugs for their therapeutic potential as treatment for vasoconstriction induced by preeclampsia.

Efficacy and safety of endovascular therapy for delayed hepatic artery post-pancreatectomy hemorrhage: development of extrahepatic collateral circulation and complications of post endovascular therapy

BackgroundEndovascular therapy (ET) for delayed hepatic artery post-pancreatectomy hemorrhage (HA-PPH) may require complete hepatic artery occlusion (HAO). Nonetheless, the development of extrahepatic collateral circulation (EHC) and the relationship between radiological factors (EHC, portal vein stenosis, and HAO) and adverse hepatic events after ET remain unclear. This study aimed to evaluate the efficacy and safety of ET for delayed PPH and examine the development of EHC.MethodsA total of 19 ET cases for delayed HA-PPH were reviewed. Hepatic adverse events, portal vein stenosis, HAO, and mortality rate after ET were evaluated. Moreover, EHC from the left gastric artery (LGA), right inferior phrenic artery (RIPA), left inferior phrenic artery (LIPA), right internal thoracic artery (RITA), left internal thoracic artery (LITA), renal artery (RA), omental artery (OA), intercostal artery (IA), and branch of superior mesenteric artery (BSMA) was assessed using angiogram and computed tomography angiography (CTA).ResultsAll cases were successfully treated using transcatheter arterial embolization (n = 17) and stent-graft placement (n = 2) without mortality. EHC from the LGA (8/19), RIPA (10/19), LIPA (4/19), and RITA (3/19) was observed on post-ET CTA. The incidence of hepatic adverse events was significant in the group with both HAO and portal vein stenosis (p < 0.001) and absence of EHC from LIPA and RITA (p < 0.05).ConclusionET for delayed HA-PPH might be effective and safe. While avoiding both HAO and portal vein stenosis is important, the development of EHCs from LIPA and RITA may prevent hepatic adverse events after ET.

Assessment of the Proton Pump Inhibitor, Esomeprazole Magnesium Hydrate and Trihydrate, on Pathophysiological Markers of Preeclampsia in Preclinical Human Models of Disease.

Previously, we demonstrated that the proton pump inhibitor, esomeprazole magnesium hydrate (MH), could have potential as a repurposed treatment against preeclampsia, a serious obstetric condition. In this study we investigate the difference in the preclinical effectiveness between 100 µM of esomeprazole MH and its hydration isomer, esomeprazole magnesium trihydrate (MTH). Here, we found that both treatments reduced secretion of sFLT-1 (anti-angiogenic factor) from primary cytotrophoblast, but only esomeprazole MH reduced sFLT-1 secretion from primary human umbilical vein endothelial cells (assessed via ELISA). Both drugs could mitigate expression of the endothelial dysfunction markers, vascular cell adhesion molecule-1 and endothelin-1 (via qPCR). Neither esomeprazole MH nor MTH quenched cytotrophoblast reactive oxygen species production in response to sodium azide (ROS assay). Finally, using wire myography, we demonstrated that both compounds were able to induce vasodilation of human omental arteries at 100 µM. Esomeprazole is safe to use in pregnancy and a candidate treatment for preeclampsia. Using primary human tissues and cells, we validated that esomeprazole is effective in enhancing vascular relaxation, and can reduce key factors associated with preeclampsia, including sFLT-1 and endothelial dysfunction. However, esomeprazole MH was more efficacious than esomeprazole MTH in our in vitro studies.

Idiopathic Omental Infarction to Be a Rare Cause of Acute Abdomen: A Case Report

Omental infarction is a rare entity, representing hemorrhagic omental necrosis as a result of impaired omental perfusion. It can occur secondary to omental torsion or to inflammatory and neoplastic infiltration of the omental segment from adjacent organs. If the foregoing reasons can be excluded, omental infarction is called primary or idiopathic omental infarction. Occlusions of small omental arteries are rare and may be found in patients with thromboembolic disease, arteriolosclerosis, arteritis, or amyloidosis. The author presents a case of idiopathic omental infarction in a 66-year-old male presenting with abdominal pain. The patients underwent an emergent operation and recovered without any complication after surgery.

Artificial sweeteners sucralose and acesulfame potassium: A bittersweet story for the cardiovascular system?

Artificial sweeteners (AS) are well known to activate two categories of receptors; sweet taste receptor with high affinity and bitter taste receptors with low affinity. Interestingly, recent data from our and other groups suggested that these two receptors families are expressed throughout the arterial tree. Therefore, it could be interesting to explore if AS may have an impact on vascular function, and to decipher the role of these taste receptors. The aims of this ongoing work is to investigate whether AS, like sucralose and acesulfame potassium (AceK) (1) exhibit vasomotor effect and (2) in that case determine the underlying mechanisms. Biomolecular and functional investigations have been performed on isolated rodent aortas, human dermal micro-arteries and omental arteries. Ex vivo vasomotor function was assessed using isometric tension measurements in organ bath systems. We first confirmed that both endothelial and smooth muscle cells from rodent and human arteries express the transcripts encoding for TAS1R2 and TAS1R3; the heterodimer receptor known to be responsible for the sweet taste. Our ex vivo data showed that only high concentrations (about 10 mM) of AceK and sucralose induce vasomotor responses. While AceK exhibited a vasoconstrictive effect, sucralose induced vasorelaxation. Both responses were found to be independent of the endothelium. Pharmacological inhibition (gurmarin and lactisol) and the use of a TAS1R3 KO mice model demonstrated that AS vasomotor effects do not rely on the sweet taste receptors. In contrast, inhibition of TAS2Rs abolished all responses suggesting that bitter taste receptors are more likely responsible for the AS-induced vascular effects. Additionally, our last observations show that the vasoconstrictive effect of AceK is mediated by RhoA/ROCK pathway. These evidences support the idea that AS can alter vasomotor signaling in the smooth muscle cells. These acute effects are probably mediated by the bitter taste receptor family. Their activation at the vascular level as well as the underlying pathways remains poorly understood, and the physiopathological consequences need to be further investigated.

Autologous Bone Marrow Cell Infusion for the Treatment of Decompensated Liver Cirrhosis Patients With Type 2 Diabetes Mellitus.

This study aimed to indicate whether autologous bone marrow cell infusion (ABMI) via the right omental vein (ROV) could have a regulatory effect on decompensated liver cirrhosis (DLC) patients with type 2 diabetes mellitus (T2DM). For this purpose, 24 DLC patients with T2DM were divided into observation group (n=14) and control group (n=10). Patients in the observation group were given ABMI through the ROV and right omental artery (ROA), and cases in the control group received ABMI through the ROV. At 1, 3, 6, and 12months after ABMI, it was revealed that the prothrombin time, the total bilirubin levels, and the amount of ascites were significantly lower, while the serum albumin levels in the two groups were markedly higher compared with those before ABMI (p<0.01), and there was no significant difference between the two groups at each time point (p>0.05). The fasting blood glucose and glycosylated hemoglobin levels at 6 and 12months after ABMI in the two groups significantly decreased compared with those before ABMI (p<0.05 or p<0.01), while the decreased levels in the observation group were more obvious than those in the control group at each time point (p<0.01). The amount of insulin in the observation group at 3, 6, and 12months after ABMI was significantly less than that before ABMI in the control group (p<0.01). In summary, ABMI showed a significant therapeutic efficacy for DLC patients with T2DM through ROV and ROA.

Surgical Considerations in Parasitic Fibroid Excision

<h3>Study Objective</h3> To provide an overview of the etiology and risk factors of parasitic fibroids and to demonstrate laparoscopic considerations during the excision of abdominal and pelvic parasitic fibroids. <h3>Design</h3> Surgical video. <h3>Setting</h3> Academic hospital. <h3>Patients or Participants</h3> 38-year-old with symptomatic uterine fibroids and four prior myomectomies who presents for second opinion regarding the management of uterine and extra-uterine fibroids. <h3>Interventions</h3> Parasitic fibroids are a rare variant that has no connection with the uterus itself and may develop de novo or iatrogenically from prior fibroid surgery. Limited retrospective data estimates occurrence in 0.2-1.25% of cases after laparoscopic myomectomy and 0.1%-1% of cases specifically using uncontained power morcellation. These fibroids often occur along large vessels including the omental and mesenteric arteries, adding surgical complexity during excision. Proposed methods to prevent dissemination include removal through an in-bag containment system, intact removal, and irrigation. We demonstrate a successful laparoscopic myomectomy with excision of abdominal and pelvic parasitic fibroids located proximal to key anatomic structures, and we exhibit measures to prevent further dissemination. <h3>Measurements and Main Results</h3> N/A. <h3>Conclusion</h3> Consider parasitic fibroids on the differential of pelvic mass after previous myomectomy. Consider the possible proximity of parasitic fibroids to key anatomic structures to avoid vascular, urinary, bowel complications. To date, the best preventative measures include in-bag containment, intact removal and irrigation but continued study is needed.