Splanchnic Vessels Research Articles

Effects of particle size and dry matter content of a total mixed ration on intraruminal equilibration and net portal flux of volatile fatty acids in lactating dairy cows

Effects of physical changes in consistency of ruminal contents on intraruminal equilibration and net portal fluxes of volatile fatty acids (VFA) in dairy cows were studied. Four Danish Holstein cows (121±17 d in milk, 591±24kg of body weight, mean ± SD) surgically fitted with a ruminal cannula and permanent indwelling catheters in the major splanchnic blood vessels were used. The experimental design was a 4 × 4 Latin square with a 2 × 2 factorial design of treatments. Treatments differed in forage (grass hay) particle size (FPS; 3.0 and 30mm) and feed dry matter (DM) content of the total mixed ration (44.3 and 53.8%). The feed DM did not affect chewing time, ruminal variables, or net portal flux of VFA. However, decreasing the FPS decreased the overall chewing and rumination times by 151±55 and 135±29 min/d, respectively. No effect of the reduced chewing time was observed on ruminal pH or milk fat percentage. Cows maintained average ventral ruminal pH of 6.65±0.02, medial ruminal pH of 5.95±0.04, and milk fat of 4.42±0.12% with chewing time of 28.0±2.1 min/kg of DM when fed short particles. The medial ruminal pool of wet particulate matter was decreased by 10.53±2.29kg with decreasing FPS, thereby decreasing the medial pool of total VFA, acetate, propionate, butyrate, isobutyrate, and isovalerate by 1,143±333, 720±205, 228±69, 140±51, 8.0±2.3, and 25.2±5.6 mmol, respectively. Ventral pool variables were not affected by treatments. Relatively large intraruminal differences of VFA concentrations and pH between the ventral and medial pools were observed, VFA concentrations being largest and pH being the lowest medially. This indicates that the ruminal mat acts as a barrier retaining VFA. The effects of reduced FPS were limited to the VFA pool sizes of the mat, leaving ruminal pH, ruminal VFA concentrations, and net portal flux of VFA unaffected. Consequently reduced FPS affected the intraruminal equilibration of VFA between mat and ventral rumen with an estimated turnover rate of isobutyrate increasing from 50±3%/h with long particles to 61±3%/h with short particles. The estimated ruminal fluid flow and therefore intraruminal VFA transport between medial and ventral phase was not affected by the FPS. In conclusion, the ruminal mat pool of VFA was proportional to the size of the mat and the only detected effects of decreasing FPS were decreasing the mat size and an increasing turnover of the mat pool of VFA.

CT angiography of the celiac trunk: anatomy, variants and pathologic findings

Celiac trunk variants and pathologies are relatively common occurrences. With the advent of computed tomography (CT) technology, these conditions are being diagnosed with an increased frequency even among asymptomatic patients. CT angiography is used noninvasively for preoperative staging and vascular mapping in patients with pancreatic and hepatobiliary neoplasm. Multidetector-row CT (MDCT) also allows the accurate depiction of the abdominal splanchnic vessels for stenosis, collateral vessels and atherosclerotic plaques. In this study, we describe the normal anatomy and variants of the celiac trunk as well as associated pathologic conditions, such as stenosis, occlusion, aneurysm and median arcuate ligament compression syndrome. The overall aim of this study was to emphasize the clinical importance of these abnormalities.

Abdominal angina due to recurrence of cancer of the papilla of Vater: a case report

IntroductionAbdominal angina is usually caused by atherosclerotic disease, and other causes are considered uncommon. This is the first report of a case of abdominal angina secondary to neoplastic vascular stenosis caused by local recurrence of an adenocarcinoma of the papilla of Vater.Case presentationAn 80-year-old woman of Caucasian origin presented with abdominal pain and diarrhea. She had undergone a pancreaticoduodenectomy for adenocarcinoma of the papilla of Vater four years earlier. Computed tomography revealed a mass surrounding her celiac trunk and superior mesenteric artery. Her abdominal pain responded poorly to analgesic drugs, but disappeared when oral feedings were withheld. A duplex ultrasonography of the patient's splanchnic vessels was consistent with vascular stenosis. Parenteral nutrition was started and the patient remained pain free until her death.ConclusionPain relief is an important therapeutic target in patients with cancer. In this case, abdominal pain was successfully managed only after the ischemic cause had been identified. The conventional analgesic therapy algorithm based on nonsteroidal anti-inflammatory drugs and opioids had been costly and pointless, whereas the simple withdrawal of oral feeding spared the patient of the discomfort of additional invasive procedures and allowed her to spend her remaining days in a completely pain-free state.

Role of β3-adrenoceptors for intrahepatic resistance and portal hypertension in liver cirrhosis

Increased intrahepatic resistance and splanchnic blood flow cause portal hypertension in liver cirrhosis. Nonselective beta-adrenoceptor (beta-AR) antagonists have beneficial effects on hyperdynamic circulation and are in clinical use. In this context, the role of the beta(3)-AR is undefined. Here we investigated their expression and role in portal hypertension in patients and rats with liver cirrhosis. We analyzed cirrhotic human and rat tissues (liver, splanchnic vessels) and primary rat cells. Protein expression of beta(3)-AR was determined by western blot and messenger RNA (mRNA) levels by reverse-transcription polymerase chain reaction (RT-PCR). Activities of Rho-kinase and the nitric oxide (NO) effector protein kinase G (PKG) were assessed by way of substrate phosphorylation (moesin, vasodilator-stimulated phosphoprotein [VASP]). Cyclic 3',5' adenosine monophosphate (cAMP) accumulation was determined by an enzyme-immunoassay kit. The effects of selective beta(3)-AR agonists (CGP12177A, BRL37344) and antagonist (SR59230A) were investigated by collagen matrix contraction of hepatic stellate cells (HSCs), in situ liver perfusions, and in vivo hemodynamic parameters in bile duct ligation and carbon tetrachloride intoxication in cirrhotic rats. In cirrhosis of humans and rats, beta(3)-AR expression is markedly increased in hepatic and in splanchnic tissues. Stimulation of beta(3)-AR leads to relaxation of HSCs by way of cAMP accumulation, and by inhibition of Rho-kinase activity; any role of NO and its effector PKG was not observed. beta(3)-AR agonists decrease intrahepatic resistance and portal pressure in cirrhotic rats. There is a marked hepatic and mesenteric up-regulation of beta(3)-ARs in human cirrhosis and in two different animal models of cirrhosis. The beta(3)-AR-agonists should be further evaluated for therapy of portal hypertension.

Hybrid Procedures for Thoracoabdominal Aneurysms

(1) Observation. This option is usually tendered if the aneurysm is not large enough to be considered an immediate threat to the patient’s life or if the patient is too old or sick to benefit from intervention. Lifestyle improvements (i.e., weight loss, exercise, and smoking cessation) and optimization of medical therapy (i.e., an antiplatelet regimen, antihypertensive agents, statins, diabetes control, and physiotherapy) are crucial to improving life expectancy and quality of life in these patients; however, regrettably, they are often underutilized. (2) Open surgery. This is still considered the gold standard of treatment for TAAA. If patients are wisely selected and operated at a qualified institution, the life expectancy of surgically treated TAAA patients improves dramatically, achieving satisfactory postoperative functional status. There are, however, several drawbacks to this option. For one, mortality for more extensive TAAAs (i.e., type II) is not negligible. In survivors, the operation may be burdened by paraplegia, possibly one of the most catastrophic complications that may occur, and other cerebrovascular events. Cardiac events, as well as end-stage renal insufficiency requiring dialysis or respiratory insufficiency requiring prolonged mechanical ventilation, are other feared complications. (3) Endovascular procedure. This is clearly a less invasive and hugely appealing approach; however, it has many restrictions that limit its use to a very few centers worldwide. First, several anatomical requirements need to be met. Second, the required branched stentgrafts, which are custom-made by a single manufacturer, are expensive and typically take more than 8 weeks to produce. Lastly, top-level endovascular experience, technical expertise, and radiological equipment are required to accomplish these procedures. (4) Hybrid procedures. This approach consists of an open surgical procedure to debranch and reroute the renal and/or splanchnic vessels followed by endovascular deployment of an off-the-shelf commercial stent-graft for aneurysm exclusion. The open surgery is usually limited to the abdomen, which is particularly advantageous in patients with severe respiratory insufficiency or previous thoracotomy.

1061: Splanchnic Vessel Aneurysms: Ultrasound Findings in Combining with MSCT 64 in Vietnam

1061: Splanchnic Vessel Aneurysms: Ultrasound Findings in Combining with MSCT 64 in Vietnam

The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years

The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years

Essential thrombocythaemia as a causative agent of portal vein thrombosis: A case report

Thrombosis of splanchnic blood vessels is one of the most difficult complications and most frequent causes of death in patients with myeloproliferative disorders. We report a 48-year-old man with recurring haemorrhage from the upper digestive tract. Doppler ultrasonography of the portal system revealed a thrombosed portal vein, with marginal flow of 10 cm/s. Peroral fiber panendoscopy of the oesophagus showed III-IV degree varices together with varices in the stomach fundus. Blood count revealed thrombocytosis (Pt. 900 x 109/l), and haematological analysis led to the diagnosis of essential thrombocythaemia. However, two years after the established diagnosis, the patient was hospitalized again for bleeding from esophageal varicosity. During haemorrhage, anticoagulant therapy was discontinued. Eight days after anticoagulant discontinuation, mesenterial thrombosis and small intestinal gangrene developed. Surgical intervention was carried out, including resection of 2.5 m of the small intestine. In spite of intensive postoperative therapy, the lethal outcome ensued. The bleeding from oesophageal and/or gastric varicosity is often the presenting manifestation of up to that time undetected myeloproliferative disease. The following question still remains open: should anticoagulant therapy be continued in the phase of acute bleeding of these patients?

Spontaneous Resolution of Extreme Essential Thrombocytosis in a Child

Essential Thrombocytosis (ET) is rare in children and its clinical course is considered to be different from the adult disease. Unlike adults, most children with ET do not need treatment; however, children with extreme thrombocytosis present the treating physician with a therapeutic dilemma. We report a girl with a spontaneous resolution of extreme essential thrombocytosis. A 13 year old previously healthy girl presented to our ER with a 3 months history of intermittent mild abdominal pain with short episodes of diarrhea, intermittent episodes of paraesthesia in lower limbs and 3000 × 109/L platelets on CBC with pseudohyperkalemia of 6.4 mEq/L. Physical examination was unremarkable except for some diffuse mild tenderness on abdominal palpation. Laboratory work-up revealed normal WBC and Hb, Platelets 4100 × 109/L, mild microcytosis, Iron - 21.9 mcg/dL, transferin saturation 5.6%, serum potassium − 6.5 mEq/L, LDH 1000 IU. Liver, renal and thyroid function tests were within normal limits. PTT was mildly elevated 49.3 seconds (normal – 24.3–35), LAC-R mildly positive – 1.205 (0.8–1.20), KCT 58.2 sec. Anticardiolipin IgG −4.82 U/ml (negative), IgM - 11.24 U/ml (negative < 7 U/ml). Anti dsDNA and Anti nuclear antibodies were negative. Studies for hypercoagulable state included Protein C, Antitrombin, Factor VIII, IX, XI, Factor V R506Q, and Apolipoprotein a; all were normal. A heterozygosity for PT G20210A was found, as well as homozygosity for MTHFR C667T with a normal level of Homocysteine (7.7mmole/L). Bone marrow aspiration showed increased cellularity of all cell lines, with many young megakaryocytes including some in clusters. No malignant cells were seen. Reticulin score on bone marrow biopsy was 0. Platelets function tests with adenosine di-phosphate and epinephrine were normal. Serum TPO level was 31.0 pg/ml (normal). A karyotype examination revealed a normal 46XX female. FISH for BCR/ABL was negative. DNA mutations for JAK2 on both the 12 and the14 exons and c-mpl mutations were not found. Spontaneous clone formation was normal. Helicobacter pylori IgG was 2.89 U/ml (normal) and stool was negative for parasites. Imaging studies included high resolution abdominal contrast CT scan, upper gastrointestinal tract imaging with gastrografin, Doppler sonography of splanchnic vessels and capsule endoscopy; all were interpreted as normal. Aspirin 75 mg/d was started without antimetabolite therapy. Abdominal pain and diarrhea gradually improved. After 3 month of antiagregant therapy, platelets count declined, gradually but steadily. One year after presentation the child is asymptomatic with platelet count of 600 × 109/L. The spontaneous remission of the extreme ET achieved by conservative treatment with no complications adds to the growing evidence, that childhood ET is a unique entity with different biology than adult ET, which might not need antimetabolite therapy.

Purinergic signaling in the gastrointestinal tract

Purinergic signaling in the gastrointestinal tract

Hepatic Circulation

Hepatic Circulation

Purinergic receptors in the splanchnic circulation

There is considerable evidence that purines are vasoactive molecules involved in the regulation of blood flow. Adenosine is a well known vasodilator that also acts as a modulator of the response to other vasoactive substances. Adenosine exerts its effects by interacting with adenosine receptors. These are metabotropic G-protein coupled receptors and include four subtypes, A(1), A(2A), A(2B) and A(3). Adenosine triphosphate (ATP) is a co-transmitter in vascular neuroeffector junctions and is known to activate two distinct types of P2 receptors, P2X (ionotropic) and P2Y (metabotropic). ATP can exert either vasoconstrictive or vasorelaxant effects, depending on the P2 receptor subtype involved. Splanchnic vascular beds are of particular interest, as they receive a large fraction of the cardiac output. This review focus on purinergic receptors role in the splanchnic vasomotor control. Here, we give an overview on the distribution and diversity of effects of purinergic receptors in splanchnic vessels. Pre- and post-junctional receptormediated responses are summarized. Attention is also given to the interactions between purinergic receptors and other receptors in the splanchnic circulation.

Degos' disease with delayed involvement of the gastrointestinal tract

A 75-year-old woman presented with pink papules over the trunk and limbs. Over the next few weeks, the papules became umbilicated and then developed into porcelain-white lesions with a rose or violaceous rim. A biopsy of one of these lesions revealed superficial and deep dermal lymphohistiocytic inflammation, mainly perivascular with a central zone of infarction consistent with Degos' disease. Three years later, she presented with increasing abdominal pain, anaemia, raised inflammatory markers and an abdominal bruit. Angiography showed splanchnic vessel stenosis possibly secondary to vasculitis and she underwent successful balloon dilatation. Treatment with prednisolone was commenced. There has been no recurrence of lesions in the 12 months since the balloon dilatation.

Diagnosis and management of splanchnic ischemia.

Splanchnic or gastrointestinal ischemia is rare and randomized studies are absent. This review focuses on new developments in clinical presentation, diagnostic approaches, and treatments. Splanchnic ischemia can be caused by occlusions of arteries or veins and by physiological vasoconstriction during low-flow states. The prevalence of significant splanchnic arterial stenoses is high, but it remains mostly asymptomatic due to abundant collateral circulation. This is known as chronic splanchnic disease (CSD). Chronic splanchnic syndrome (CSS) occurs when ischemic symptoms develop. Ischemic symptoms are characterized by postprandial pain, fear of eating and weight loss. CSS is diagnosed by a test for actual ischemia. Recently, gastro-intestinal tonometry has been validated as a diagnostic test to detect splanchnic ischemia and to guide treatment. In single-vessel CSD, the complication rate is very low, but some patients have ischemic complaints, and can be treated successfully. In multi-vessel stenoses, the complication rate is considerable, while most have CSS and treatment should be strongly considered. CT and MR-based angiographic reconstruction techniques have emerged as alternatives for digital subtraction angiography for imaging of splanchnic vessels. Duplex ultrasound is still the first choice for screening purposes. The strengths and weaknesses of each modality will be discussed. CSS may be treated by minimally invasive endoscopic treatment of the celiac axis compression syndrome, endovascular antegrade stenting, or laparotomy-assisted retrograde endovascular recanalization and stenting. The treatment plan is highly individualized and is mainly based on precise vessel anatomy, body weight, co-morbidity and severity of ischemia.

Discrepant effects of inducible nitric oxide synthase modulation on systemic and splanchnic endothelial nitric oxide synthase activity and expression in cirrhotic rats

Arterial vasodilatation, which is a major factor in the pathogenesis of the hyperkinetic circulatory state and portal hypertension in cirrhosis, is due to arterial nitric oxide (NO) overproduction secondary to endothelial NO synthase (eNOS) and inducible NOS (iNOS) upregulation. However, in cirrhosis, the respective roles of eNOS and iNOS isoforms in NO overproduction are still unknown and the effect of iNOS modulation on eNOS activity and expression has not been evaluated in the systemic or splanchnic vessels. The aim of this study was to evaluate the effects of modulating aortic and superior mesenteric arteries (SMA) iNOS on arterial eNOS activity and expression in rats with cirrhosis. eNOS and iNOS protein expression and eNOS activity (assessed by its phosphorylation at serine 1177) were measured in the aortas and SMA in untreated and treated cirrhotic rats with lipopolysaccharide (LPS), N-iminoethyl-L-lysine (L-NIL), a selective iNOS inhibitor, and LPS plus L-NIL. LPS administration significantly increased eNOS and iNOS protein expression and eNOS activity in the aortas of both sham-operated and cirrhotic rats. However, in SMA, LPS administration induced a decrease in eNOS protein expression and activity and an increase in iNOS protein expression. The results of this study may explain the worsening of the hyperdynamic state in cirrhosis during septic shock by direct LPS-induced eNOS activation in large systemic vessels, and its inhibition in concomitant small splanchnic vasculature by iNOS synthesized NO.

What Is the Best Diagnostic Approach for Chronic Gastrointestinal Ischemia?

Chronic gastrointestinal ischemia is still a difficult diagnosis to establish. The diagnosis depends on a high degree of clinical suspicion as well as selective angiography. Duplex sonography may serve as a screening tool, providing information on splanchnic vessel patency and flow patterns. GET is a minimally invasive test that can be used for diagnosis in patients with chronic gastrointestinal ischemia, and can differentiate between symptomatic and asymptomatic splanchnic artery stenosis. In the present study, we compared four different diagnostic approaches. Between 1997 and 2000, 84 patients were evaluated for suspected chronic gastrointestinal ischemia. All underwent splanchnic arterial angiography, duplex sonography, and GET. For the presence or absence of stenosis, angiography was used as the gold standard. For diagnosing ischemia, we relied on a panel decision. The diagnostic approaches studied were: (a) angiography, only in patients with classic abdominal angina; (b) screening with duplex sonography, angiography if sonography abnormal or unreliable; (c) screening with gastric tonometry and angiography if tonometry not normal; (d) both gastric tonometry exercise and duplex sonography, angiography if one of both screening tests not normal. In 28 patients, chronic gastrointestinal ischemia was diagnosed. Using clinical suspicion only, 16 patients (57%) would have been missed. Screening by duplex sonography or gastric tonometry only would have missed 4 or 6 patients, respectively. Screening with combined gastric tonometry and duplex sonography would not have missed patients with symptomatic ischemia, while 21% of angiographies would have been avoided. Screening by combined GET and duplex sonography has excellent diagnostic accuracy. Currently, this approach represents the best diagnostic workup strategy in patients with suspected chronic gastrointestinal ischemia.

Expression of somatostatin receptors in splanchnic blood vessels of normal and cirrhotic rats

Somatostatin has been used for over two decades to treat acute variceal bleeding. Although it is assumed that somatostatin lowers portal pressure by constriction of the splanchnic arteries, little is known about the expression of somatostatin receptors (SSTR) in splanchnic blood vessels. In this study we investigated SSTR expression in splanchnic blood vessels from normal and cirrhotic rats. Cirrhosis was induced by intraperitoneal injection of 50 mg thioacetamide twice a week for 14 weeks. In portal vein, mesenteric artery and aorta of normal and cirrhotic rats, mRNA for the five known SSTR was measured by quantitative reverse transcriptase-polymerase chain reaction. SSTR subtypes 1, 2, 3 and 4 were expressed, but subtype 5 was undetectable. In the portal vein of cirrhotic animals, SSTR1 was significantly down-regulated as compared with controls. Otherwise, no major differences in receptor expression between normal and cirrhotic animals were observed. Using immunohistochemistry, we identified all five receptors, although the staining of receptor 5 was very weak. All five SSTR are expressed in splanchnic blood vessels. Our results suggest that cirrhosis reduces expression of SSTR1 in portal vein. In other vessels, no major differences between the normal and cirrhotic state were noted.

Doppler Study of Splanchnic Hemodynamics in Hirschsprung’s Disease

Background: Doppler studies of splanchnic vessels have demonstrated alteration in blood flow in bowel obstruction and strangulation. The aim of this study was to evaluate hemodynamic changes in celiac artery (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA) using pulsed Doppler sonography (PDS) in Hirschsprung’s disease. Material and Methods: Fasting splanchnic flowmetry of CA, SMA, and IMA arteries was performed using PDS preoperatively in 13 patients with Hirschsprung’s disease and 13 healthy age- and sex-matched controls. Diagnostic workup for Hirschsprung’s disease included a barium enema and a rectal biopsy. A primary transanal pull through was performed if the transition zone was at rectosigmoid or midsigmoid. Doppler studies were repeated on the 1st and 7th postoperative day under similar conditions. Mean flow velocity (V_mean) and the pulsatility index (PI) of the three major vessels was measured. Results: Patients with Hirschsprung’s disease showed increased blood flow velocities in CA, SMA, and IMA (p < 0.001), an increased resistance to blood flow in IMA (p < 0.001) and a decreased resistance to blood flow in CA and SMA (p < 0.005 and p < 0.001, respectively). The blood flow velocity for IMA normalized after resection of the aganglionic segment (r = 0.41, p < 0.005, 95% CI: 45.4–52.7). Conclusions: Hirschsprung’s diseaseis associated with alterations in splanchnic vessel hemodynamics which are reversible after corrective surgery. Doppler studies may play an important role in the assessment of bowel function after surgery.

Doppler Flow Velocimetry in the Superior Mesenteric Artery on the First Day of Life in Preterm Infants and the Risk of Neonatal Necrotizing Enterocolitis

The purpose of this work was to relate Doppler indices of splanchnic perfusion and vascular resistance to the risk of developing necrotizing enterocolitis. We conducted a prospective cohort study with analysis of Doppler flow velocity waveforms of splanchnic vessels on the first day of life. Clinical management and diagnosis of necrotizing enterocolitis were performed blind to the Doppler results in a tertiary NICU on 64 eligible preterm neonates admitted for intensive care. We measured necrotizing enterocolitis using an objective diagnostic classification. When adjusted for gestational age at birth, the following indices of the Doppler flow velocity wave form in the superior mesenteric artery were significantly predictive of the risk of necrotizing enterocolitis: end-diastolic velocity, mean velocity, and pulsatility index. The association between necrotizing enterocolitis and Doppler velocimetry indicative of high vascular resistance was independent of a range of other factors and comorbidities (race, mode of delivery, umbilical arterial catheter, growth restriction, patent ductus arteriosus, jaundice, respiratory distress syndrome, mechanical ventilation, and hypotension). We concluded that neonates with high resistance patterns of blood flow velocity in the superior mesenteric artery on the first day of life are at increased risk of developing necrotizing enterocolitis.

Die Ösophagus-/Fundus-Varizen-Blutung

Oesophageal and fundic varices belong to the most frequent complications of cirrhosis and portal hypertension. Due to their significant morbidity and mortality, bleedings from oesophageal or fundic varices represent a challenge for the emergency medical team as well as for the gastroenterologist. The patient with a variceal bleeding should be accurately monitored and his/her hemodynamic parameters should be maintained stable with the administration of plasma expanders and blood units when indicated. An antibiotic prophylaxis in this setting--norfloxacin or ceftriaxon--has been demonstrated to significantly reduce morbidity and mortality. Additionally, the early administration of vasoactive compounds, such as terlipressin, somatostatin or octreotide, is associated with beneficial effects in reducing the bleeding. An upper gastrointestinal endoscopy should be generally performed within the first twelve hours from the beginning of the bleeding in order to obtain an accurate diagnosis and to provide an adequate treatment. Endoscopic procedures to control the bleeding include the rubber band ligation, the treatment of the varix with a sclerosing agent or the injection of tissue glue into the varix. In case of recurrent bleeding, beyond the above methods, different techniques, such as the transjugular porto-caval shunt, surgical shunt procedures, as well as embolisation of splanchnic blood vessels, represent additional therapeutic options. However, they are associated with very high mortality rates and their indication has to be discussed case by case by an interdisciplinary team of experts. Future therapies include the optimisation and the improvement of the current medical and endoscopic armamentarium, as well as the application of treatments to novel targets, such as the coagulation cascade.