RESUMO
BACKGROUND: This study sought to define duplex ultrasound (DUS) velocity criteria predicting ≥70% stenosis in superior mesenteric artery (SMA) stents by correlating in-stent peak systolic velocity (PSV) with computed tomographic angiography (CTA) measurements of percent stenosis. METHODS: A retrospective review of 109 patients undergoing SMA stenting between 2003 and 2018 was conducted at a single institution. Thirty-seven surveillance duplex ultrasound studies were found to have a CTA performed within 30 days of study completion. Bare metal (nâ¯=â¯20) and covered stents (nâ¯=â¯17) were included. Velocities were paired to in-stent restenosis (ISR) measured by mean vessel diameter reduction on SMA centerline reconstructions from CTA. Receiver operating characteristic (ROC) curves was generated and logistic regression models for ≥70% ISR probability were used to define velocity criteria in the stented SMA. RESULTS: At a PSV of 300 cm/sec, the sensitivity is 100% and specificity 80% for a ≥70% in-stent SMA stenosis. At a PSV of 400 cm/sec, the sensitivity and positive predictive value (PPV) is 63% and the specificity and negative predictive value (NPV) is 90%. A PSV of 450 cm/sec was consistent with the highest specificity (100%) and PPV (100%) but lower sensitivity (50%) and NPV (87.9%). One patient with a PSV of 441 cm/sec on surveillance DUS died from complications of acute-on-chronic mesenteric ischemia. CONCLUSIONS: A PSV of 400 cm/sec on mesenteric DUS can predict ≥70% ISR with high sensitivity and should be considered as a diagnostic threshold for SMA in-stent restenosis.
Assuntos
Procedimentos Endovasculares/instrumentação , Artéria Mesentérica Superior/diagnóstico por imagem , Isquemia Mesentérica/terapia , Oclusão Vascular Mesentérica/terapia , Stents , Ultrassonografia Doppler Dupla , Idoso , Idoso de 80 Anos ou mais , Velocidade do Fluxo Sanguíneo , Doença Crônica , Angiografia por Tomografia Computadorizada , Procedimentos Endovasculares/efeitos adversos , Feminino , Humanos , Masculino , Artéria Mesentérica Superior/fisiopatologia , Isquemia Mesentérica/diagnóstico por imagem , Isquemia Mesentérica/fisiopatologia , Oclusão Vascular Mesentérica/diagnóstico por imagem , Oclusão Vascular Mesentérica/fisiopatologia , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Recidiva , Reprodutibilidade dos Testes , Estudos Retrospectivos , Medição de Risco , Fatores de Risco , Circulação Esplâncnica , Fatores de Tempo , Resultado do Tratamento , Grau de Desobstrução VascularRESUMO
Haemosuccus pancreaticus (HP) is an uncommon cause of upper gastrointestinal (GI) bleeding, most often intermittent, making it difficult to diagnose, becoming fatal. It usually occurs in patients with chronic pancreatitis and is caused by the rupture of a visceral aneurysm within the main pancreatic duct. The association between pseudoaneurysm formation and pancreatitis is well established. Pseudoaneurysm occurs in 3.5%-10% of pancreatitis cases and its rupture is a rare but life-threatening complication of chronic pancreatitis occurring in 6%-8% of patients with pseudocysts and corresponds to less than 1% of cases of GI bleeding.Its diagnosis is challenging, given the intermittent nature of bleeding. Angiographic therapy is considered the first-choice treatment, especially in patients who are stable haemodynamically. We present a case of embolisation of inferior pancreaticoduodenal branches with polyvinyl alcohol microparticles in the treatment of HP.
Assuntos
Falso Aneurisma/diagnóstico por imagem , Embolização Terapêutica , Hemorragia Gastrointestinal/diagnóstico por imagem , Artéria Mesentérica Superior/diagnóstico por imagem , Pâncreas/irrigação sanguínea , Pancreatopatias/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Dor Abdominal/diagnóstico por imagem , Adulto , Falso Aneurisma/fisiopatologia , Falso Aneurisma/terapia , Angiografia , Hemorragia Gastrointestinal/etiologia , Hemorragia Gastrointestinal/terapia , Humanos , Masculino , Melena , Artéria Mesentérica Superior/fisiopatologia , Pâncreas/diagnóstico por imagem , Pancreatopatias/fisiopatologia , Pancreatopatias/terapia , Álcool de Polivinil/administração & dosagem , Resultado do TratamentoRESUMO
BACKGROUND: High fat diet (HFD) induces insulin resistance in various tissues, including the vasculature. HFD also increases plasma levels of TNF-α, a cytokine that contributes to insulin resistance and vascular dysfunction. Considering that the enzyme phosphatase and tension homologue (PTEN), whose expression is increased by TNF-α, reduces Akt signaling and, consequently, nitric oxide (NO) production, we hypothesized that PTEN contributes to TNF-α-mediated vascular resistance to insulin induced by HFD. Mechanisms underlying PTEN effects were determined. METHODS: Mesenteric vascular beds were isolated from C57Bl/6J and TNF-α KO mice submitted to control or HFD diet for 18 weeks to assess molecular mechanisms by which TNF-α and PTEN contribute to vascular dysfunction. RESULTS: Vasodilation in response to insulin was decreased in HFD-fed mice and in ex vivo control arteries incubated with TNF-α. TNF-α receptors deficiency and TNF-α blockade with infliximab abolished the effects of HFD and TNF-α on insulin-induced vasodilation. PTEN vascular expression (total and phosphorylated isoforms) was increased in HFD-fed mice. Treatment with a PTEN inhibitor improved insulin-induced vasodilation in HFD-fed mice. TNF-α receptor deletion restored PTEN expression/activity and Akt/eNOS/NO signaling in HFD-fed mice. CONCLUSION: TNF-α induces vascular insulin resistance by mechanisms that involve positive modulation of PTEN and inhibition of Akt/eNOS/NO signaling. Our findings highlight TNF-α and PTEN as potential targets to limit insulin resistance and vascular complications associated with obesity-related conditions.
Assuntos
Dieta Hiperlipídica , Resistência à Insulina , Artéria Mesentérica Superior/enzimologia , Óxido Nítrico Sintase Tipo III/metabolismo , Óxido Nítrico/metabolismo , PTEN Fosfo-Hidrolase/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismo , Animais , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Infliximab/farmacologia , Insulina/metabolismo , Masculino , Artéria Mesentérica Superior/efeitos dos fármacos , Artéria Mesentérica Superior/fisiopatologia , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fosforilação , Receptores do Fator de Necrose Tumoral/genética , Receptores do Fator de Necrose Tumoral/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fatores de Tempo , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/farmacologia , Vasodilatação , Vasodilatadores/farmacologiaRESUMO
BACKGROUND: Resistance exercise effects on cardiovascular parameters are not consistent. OBJECTIVES: The effects of resistance exercise on changes in blood glucose, blood pressure and vascular reactivity were evaluated in diabetic rats. METHODS: Wistar rats were divided into three groups: control group (n = 8); sedentary diabetic (n = 8); and trained diabetic (n = 8). Resistance exercise was carried out in a squat device for rats and consisted of three sets of ten repetitions with an intensity of 50%, three times per week, for eight weeks. Changes in vascular reactivity were evaluated in superior mesenteric artery rings. RESULTS: A significant reduction in the maximum response of acetylcholine-induced relaxation was observed in the sedentary diabetic group (78.1 ± 2%) and an increase in the trained diabetic group (95 ± 3%) without changing potency. In the presence of NG-nitro-L-arginine methyl ester, the acetylcholine-induced relaxation was significantly reduced in the control and trained diabetic groups, but not in the sedentary diabetic group. Furthermore, a significant increase (p < 0.05) in mean arterial blood pressure was observed in the sedentary diabetic group (104.9 ± 5 to 126.7 ± 5 mmHg) as compared to that in the control group. However, the trained diabetic group showed a significant decrease (p < 0.05) in the mean arterial blood pressure levels (126.7 ± 5 to 105.1 ± 4 mmHg) as compared to the sedentary diabetic group. CONCLUSIONS: Resistance exercise could restore endothelial function and prevent an increase in arterial blood pressure in type 1 diabetic rats.
Assuntos
Pressão Sanguínea/fisiologia , Diabetes Mellitus Experimental/fisiopatologia , Diabetes Mellitus Tipo 1/fisiopatologia , Endotélio Vascular/fisiopatologia , Condicionamento Físico Animal/fisiologia , Treinamento Resistido/métodos , Acetilcolina/farmacologia , Animais , Glicemia/efeitos dos fármacos , Glicemia/fisiologia , Pressão Sanguínea/efeitos dos fármacos , Agonistas Colinérgicos/farmacologia , Inibidores Enzimáticos/farmacologia , Masculino , Artéria Mesentérica Superior/fisiopatologia , Modelos Animais , NG-Nitroarginina Metil Éster/farmacologia , Ratos WistarRESUMO
Background: Resistance exercise effects on cardiovascular parameters are not consistent. Objectives: The effects of resistance exercise on changes in blood glucose, blood pressure and vascular reactivity were evaluated in diabetic rats. Methods: Wistar rats were divided into three groups: control group (n = 8); sedentary diabetic (n = 8); and trained diabetic (n = 8). Resistance exercise was carried out in a squat device for rats and consisted of three sets of ten repetitions with an intensity of 50%, three times per week, for eight weeks. Changes in vascular reactivity were evaluated in superior mesenteric artery rings. Results: A significant reduction in the maximum response of acetylcholine-induced relaxation was observed in the sedentary diabetic group (78.1 ± 2%) and an increase in the trained diabetic group (95 ± 3%) without changing potency. In the presence of NG-nitro-L-arginine methyl ester, the acetylcholine-induced relaxation was significantly reduced in the control and trained diabetic groups, but not in the sedentary diabetic group. Furthermore, a significant increase (p < 0.05) in mean arterial blood pressure was observed in the sedentary diabetic group (104.9 ± 5 to 126.7 ± 5 mmHg) as compared to that in the control group. However, the trained diabetic group showed a significant decrease (p < 0.05) in the mean arterial blood pressure levels (126.7 ± 5 to 105.1 ± 4 mmHg) as compared to the sedentary diabetic group. Conclusions: Resistance exercise could restore endothelial function and prevent an increase in arterial blood pressure in type 1 diabetic rats. .
Fundamento: Os efeitos do exercício resistido sobre os parâmetros cardiovasculares não são consistentes. Objetivos: Foram avaliados os efeitos do exercício resistido sobre as alterações na glicemia, reatividade vascular e pressão arterial de ratos diabéticos. Métodos: Ratos Wistar foram divididos em três grupos: grupo controle (n = 8), diabético sedentário (n = 8) e diabético treinado (n = 8). O exercício resistido foi realizado no aparelho de agachamento para ratos e consistiu em três séries de dez repetições com uma intensidade de 50%, três vezes por semana, durante 8 semanas. As alterações na reatividade vascular foram avaliadas em anéis de artéria mesentérica superior. Resultados: Foi observada uma redução significativa da resposta máxima dos relaxamentos induzidos por acetilcolina no grupo diabético sedentário (78,1% ± 2) e um aumento do grupo diabético treinado (95 ± 3%), sem alterar a potência. Na presença de NG-nitro-L-arginina metil éster, os relaxamentos induzidos por acetilcolina foram significativamente reduzidos nos grupos controle e diabético treinado, mas não no grupo diabético sedentário. Além disso, foi observado um aumento significativo (p < 0,05) da pressão arterial média no grupo diabético sedentário de 104,9 ± 5 para 126,7 ± 5 mmHg, quando comparado ao grupo controle. Por outro lado, o grupo diabético treinado apresentou redução significativa (p < 0,05) nos níveis da pressão arterial média de 126,7 ± 5 mmHg para 105,1 ± 4 mmHg, quando comparado ao diabético sedentário. Conclusões: O exercício resistido foi capaz de restaurar a funcionalidade endotelial e impedir o aumento da pressão arterial em ratos com ...
Assuntos
Animais , Masculino , Pressão Sanguínea/fisiologia , Diabetes Mellitus Experimental/fisiopatologia , Diabetes Mellitus Tipo 1/fisiopatologia , Endotélio Vascular/fisiopatologia , Condicionamento Físico Animal/fisiologia , Treinamento Resistido/métodos , Acetilcolina/farmacologia , Glicemia/efeitos dos fármacos , Glicemia/fisiologia , Pressão Sanguínea/efeitos dos fármacos , Agonistas Colinérgicos/farmacologia , Inibidores Enzimáticos/farmacologia , Modelos Animais , Artéria Mesentérica Superior/fisiopatologia , NG-Nitroarginina Metil Éster/farmacologia , Ratos WistarRESUMO
Vascular hyporeactivity is an important factor in irreversible shock, and post-shock mesenteric lymph (PSML) blockade improves vascular reactivity after hemorrhagic shock. This study explored the possible involvement of myosin light chain kinase (MLCK) in PSML-mediated vascular hyporeactivity and calcium desensitization. Rats were divided into sham (n=12), shock (n=18), and shock+drainage (n=18) groups. A hemorrhagic shock model (40 ± 2 mmHg, 3 h) was established in the shock and shock+drainage groups. PSML drainage was performed from 1 to 3 h from start of hypotension in shock+drainage rats. Levels of phospho-MLCK (p-MLCK) were determined in superior mesenteric artery (SMA) tissue, and the vascular reactivity to norepinephrine (NE) and sensitivity to Ca²âº were observed in SMA rings in an isolated organ perfusion system. p-MLCK was significantly decreased in the shock group compared with the sham group, but increased in the shock+drainage group compared with the shock group. Substance P (1 nM), an agonist of MLCK, significantly elevated the decreased contractile response of SMA rings to both NE and Ca²âº at various concentrations. Maximum contractility (Emax) in the shock group increased with NE (from 0.179 ± 0.038 to 0.440 ± 0.177 g/mg, P<0.05) and Ca²âº (from 0.515 ± 0.043 to 0.646 ± 0.096 g/mg, P<0.05). ML-7 (0.1 nM), an inhibitor of MLCK, reduced the increased vascular response to NE and Ca²âº at various concentrations in the shock+drainage group (from 0.744 ± 0.187 to 0.570 ± 0.143 g/mg in Emax for NE and from 0.729 ± 0.037 to 0.645 ± 0.056 g/mg in Emax for Ca²âº, P<0.05). We conclude that MLCK is an important contributor to PSML drainage, enhancing vascular reactivity and calcium sensitivity in rats with hemorrhagic shock.
Assuntos
Cálcio/metabolismo , Linfa/fisiologia , Artéria Mesentérica Superior/fisiopatologia , Músculo Liso Vascular/fisiopatologia , Quinase de Cadeia Leve de Miosina/fisiologia , Choque Hemorrágico/fisiopatologia , Animais , Masculino , Artéria Mesentérica Superior/metabolismo , Contração Muscular , Músculo Liso Vascular/metabolismo , Cadeias Leves de Miosina/metabolismo , Quinase de Cadeia Leve de Miosina/análise , Distribuição Aleatória , Ratos Wistar , Choque Hemorrágico/enzimologiaRESUMO
Vascular hyporeactivity is an important factor in irreversible shock, and post-shock mesenteric lymph (PSML) blockade improves vascular reactivity after hemorrhagic shock. This study explored the possible involvement of myosin light chain kinase (MLCK) in PSML-mediated vascular hyporeactivity and calcium desensitization. Rats were divided into sham (n=12), shock (n=18), and shock+drainage (n=18) groups. A hemorrhagic shock model (40±2 mmHg, 3 h) was established in the shock and shock+drainage groups. PSML drainage was performed from 1 to 3 h from start of hypotension in shock+drainage rats. Levels of phospho-MLCK (p-MLCK) were determined in superior mesenteric artery (SMA) tissue, and the vascular reactivity to norepinephrine (NE) and sensitivity to Ca2+ were observed in SMA rings in an isolated organ perfusion system. p-MLCK was significantly decreased in the shock group compared with the sham group, but increased in the shock+drainage group compared with the shock group. Substance P (1 nM), an agonist of MLCK, significantly elevated the decreased contractile response of SMA rings to both NE and Ca2+ at various concentrations. Maximum contractility (Emax) in the shock group increased with NE (from 0.179±0.038 to 0.440±0.177 g/mg, P<0.05) and Ca2+ (from 0.515±0.043 to 0.646±0.096 g/mg, P<0.05). ML-7 (0.1 nM), an inhibitor of MLCK, reduced the increased vascular response to NE and Ca2+ at various concentrations in the shock+drainage group (from 0.744±0.187 to 0.570±0.143 g/mg in Emax for NE and from 0.729±0.037 to 0.645±0.056 g/mg in Emax for Ca2+, P<0.05). We conclude that MLCK is an important contributor to PSML drainage, enhancing vascular reactivity and calcium sensitivity in rats with hemorrhagic shock.
Assuntos
Animais , Masculino , Cálcio/metabolismo , Linfa/fisiologia , Artéria Mesentérica Superior/fisiopatologia , Músculo Liso Vascular/fisiopatologia , Quinase de Cadeia Leve de Miosina/fisiologia , Choque Hemorrágico/fisiopatologia , Contração Muscular , Artéria Mesentérica Superior/metabolismo , Músculo Liso Vascular/metabolismo , Cadeias Leves de Miosina/metabolismo , Quinase de Cadeia Leve de Miosina/análise , Distribuição Aleatória , Ratos Wistar , Choque Hemorrágico/enzimologiaRESUMO
PURPOSE: To investigate the role of protein kinase G (PKG) in blocking post-shock mesenteric lymph (PSML) return ameliorating the calcium sensitivity in hemorrhagic shock rats. METHODS: Male Wistar rats were randomly divided into sham, shock, shock+ligation (shock plus mesenteric lymph duct ligation (MLDL)), shock+drainage (shock plus PSML drainage) groups. After shock (hypotension 40 mm Hg) for three hours or corresponding times, the superior mesenteric artery (SMA) was taken out for detecting the PKG and phospho PKG (p-PKG) contents, and the vascular rings of SMA were prepared for assaying the calcium sensitivity using an isolated organ perfusion system. RESULTS: The PKG and p-PKG contents of SMA in shock group were significantly increased than that of sham group, and MLDL or PSML drainage reducing the levels of PKG and p-PKG. Meanwhile, the vascular calcium sensitivity in shock group was significantly lower than that of sham group, MLDL or PSML drainage enhanced the calcium sensitivity. After incubating with PKG regulators in shock+ligation and shock+drainage groups, the PKG agonist 8Br-cGMP reduced the contractility of vascular rings to gradient calcium ions and Emax and the PKG inhibitor agonist KT5823 elevated the calcium sensitivity significantly. CONCLUSION: Protein kinase G plays an important role in post-shock mesenteric lymph blockage improving vascular calcium sensitivity.
Assuntos
Cálcio/metabolismo , Proteínas Quinases Dependentes de GMP Cíclico/fisiologia , Artéria Mesentérica Superior/metabolismo , Choque Hemorrágico/metabolismo , Animais , Western Blotting , Cálcio/análise , Proteínas Quinases Dependentes de GMP Cíclico/análise , Ensaio de Imunoadsorção Enzimática , Masculino , Artéria Mesentérica Superior/fisiopatologia , Contração Muscular , Distribuição Aleatória , Ratos , Ratos Wistar , Choque Hemorrágico/fisiopatologiaRESUMO
PURPOSE: To investigate the role of protein kinase G (PKG) in blocking post-shock mesenteric lymph (PSML) return ameliorating the calcium sensitivity in hemorrhagic shock rats. METHODS: Male Wistar rats were randomly divided into sham, shock, shock+ligation (shock plus mesenteric lymph duct ligation (MLDL)), shock+drainage (shock plus PSML drainage) groups. After shock (hypotension 40mmHg) for three hours or corresponding times, the superior mesenteric artery (SMA) was taken out for detecting the PKG and phospho PKG (p-PKG) contents, and the vascular rings of SMA were prepared for assaying the calcium sensitivity using an isolated organ perfusion system. RESULTS: The PKG and p-PKG contents of SMA in shock group were significantly increased than that of sham group, and MLDL or PSML drainage reducing the levels of PKG and p-PKG. Meanwhile, the vascular calcium sensitivity in shock group was significantly lower than that of sham group, MLDL or PSML drainage enhanced the calcium sensitivity. After incubating with PKG regulators in shock+ligation and shock+drainage groups, the PKG agonist 8Br-cGMP reduced the contractility of vascular rings to gradient calcium ions and Emax and the PKG inhibitor agonist KT5823 elevated the calcium sensitivity significantly. CONCLUSION: Protein kinase G plays an important role in post-shock mesenteric lymph blockage improving vascular calcium sensitivity.
Assuntos
Animais , Masculino , Ratos , Cálcio/metabolismo , Proteínas Quinases Dependentes de GMP Cíclico/fisiologia , Artéria Mesentérica Superior/metabolismo , Choque Hemorrágico/metabolismo , Western Blotting , Cálcio/análise , Proteínas Quinases Dependentes de GMP Cíclico/análise , Ensaio de Imunoadsorção Enzimática , Contração Muscular , Artéria Mesentérica Superior/fisiopatologia , Distribuição Aleatória , Ratos Wistar , Choque Hemorrágico/fisiopatologiaRESUMO
OBJECTIVES: Intestinal neovascularization and abnormal abdominal arterial flow rates have been reported in Crohn's disease. The aim of this study was to evaluate Doppler sonography as a method for assessing Crohn's disease activity based on changes in splanchnic hemodynamics. METHODS: Forty-eight patients with Crohn's disease, 22 healthy volunteers and 12 patients with irritable bowel syndrome were evaluated by Doppler ultrasound for flow parameters of the aorta and superior mesenteric artery. This evaluation included the cross-sectional area, maximum flow volume, peak systolic velocity, end diastolic velocity, resistance and the pulsatility index. Disease activity was classified according to the Crohn's disease activity index. RESULTS: Most measurements in the aorta and superior mesenteric artery were significantly different between Crohn's disease patients and both control groups. Only the aortic maximum flow volume (CC = 0.37, p = 0.009) and aortic peak systolic velocity (CC = 0.30, p = 0.035) showed a significant positive correlation with the Crohn's disease activity index. The determination of cut-off points for the aortic maximum flow volume and peak systolic velocity measurements increased the sensitivity (80 and 75% for flow volume and velocity, respectively), specificity (57 and 75%), accuracy (67 and 75%) and positive (57 and 68%) and negative (80 and 81%) predictive values. These cut-off values permitted the correct classification of most of the patients with Crohn's disease with respect to disease activity. None of the superior mesenteric artery measurements were able to discriminate patients in relation to disease activity. CONCLUSION: The aortic maximum flow volume and peak systolic velocity levels estimated by Doppler sonography reflected disease activity in Crohn's disease. Doppler sonography of the aorta is therefore a novel noninvasive adjunct method that may be useful in the clinical follow-up of patients with Crohn's disease.