Hypoxia-induced pulmonary hypertension (HPH) is a progressive disease that is mainly caused by chronic exposure to high altitude, chronic obstructive lung disease, and obstructive sleep apnea. The increased pulmonary vascular resistance and increased pulmonary arterial pressure result in increased right ventricular afterload, leading to right heart failure and increased morbidity. There are several clinical reports suggesting a link between PH and diabetes, insulin resistance, or obesity; however, it is unclear whether HPH is associated with diabetes as a progressive complication in diabetes. The major goal of this study is to examine the effect of diabetic ''preconditioning'' or priming effect on the progression of HPH and define the molecular mechanisms that explain the link between diabetes and HPH. Our data show that HPH is significantly enhanced in diabetic mice, while endothelium-dependent relaxation in pulmonary arteries is significantly attenuated in chronically hypoxic diabetic mice (DH). In addition, we demonstrate that mouse pulmonary endothelial cells (MPECs) isolated from DH mice exhibit a significant increase in mitochondrial reactive oxygen species (ROS) concentration and decreased SOD2 protein expression. Finally, scavenging mitochondrial ROS by mitoTempol restores endothelium-dependent relaxation in pulmonary arteries that is attenuated in DH mice. These data suggest that excessive mitochondrial ROS production in diabetic MPECs leads to the development of severe HPH in diabetic mice exposed to hypoxia.

Na presente dissertação objetivou-se avaliar a reatividade vascular e a repercussão do pré-tratamento com sinvastatina (SINV, 20mg/kg, p.o.), sob esse parâmetro, em artéria mesentérica superior (AMS) e pulmonar (AP) de ratos Wistar submetidos a 45 minutos de isquemia e 2 horas de reperfusão intestinal (iIR). Nas artérias avaliou-se a função dependente e independente do endotélio e a contração induzida pela fenilefrina agonista seletivo <font face=\"Symbol\">a1-adrenérgico, em preparações com e sem endotélio e na presença ou ausência de inibidores da NOS e da iNOS (L-NAME e 1400W, respectivamente). Pode-se concluir que a iIR modificou a reatividade vascular em AP, porém não em AMS. Na artéria pulmonar, a iIR causou disfunção endotelial por meio de ativação da iNOS, a qual levou à diminuição da resposta vasodilatadora dependente do endotélio e à hiporreatividade contrátil. Além disso, confirmando a segunda hipótese, uma única dose de sinvastatina antes da iIR previne as alterações de reatividade vascular, o que demonstra o efeito benéfico desse fármaco nessa doença. / This work aimed to evaluate the vascular reactivity and the effect of pre-treatment with simvastatin (SIMV, 20mg/kg, p.o.), under this parameter, in the superior mesenteric artery (SMA) and pulmonary artery (PA) of rats subjected to 45 minutes of ischemia and 2 hours of reperfusion (iIR). In these arteries, it was evaluated the endothelium-dependent and -independent function and the contraction induced by phenylephrine the selective <font face=\"Symbol\">a1-adrenergic agonist, in preparations with and without endothelium and at the presence or absence of non-selective NOS and of iNOS inhibitors (L-NAME and 1400W, respectively). It can be concluded that the iIR modified vascular reactivity in PA, but not in SMA. In the pulmonary artery, the iIR caused endothelial dysfunction via activation of iNOS, which led to decreased endothelium-dependent vasodilator response and to contractile hyporeactivity. Moreover, confirming the second hypothesis, a single dose of simvastatin prior to iIR prevents changes in vascular reactivity, which shows the beneficial effects of this drug in this disease.

Pulmonary hypertension syndrome (PHS) in broiler chickens adequately represents idiopathic pulmonary arterial hypertension (IPAH) in humans, a condition that affects 300 new patients each year in the US. The factors that trigger IPAH are poorly understood but an increase in reactive oxygen species in the circulation coincides with the onset of these conditions. Broiler chickens (n=583) were fed a control diet (CTL), containing 3,200 kcal of ME / kg of feed, 23% CP, 1.55% (wt / wt) Arginine (Arg) and 40 IU of VE (alpha-tochopherol) / kg of feed; a high-Arg diet (HA), CTL diet plus 0.8% (wt / wt) supplemental L-Arg HCl; or a high Arg and vitamin diet (AEC), the HA diet plus 200 IU ?-tochopherol / kg of feed and 500 mg of ascorbic acid / L of drinking water 500 mg ascorbic acid / L of water (exp. 1 and 2) or Kg feed (exp. 3). Supplemented broilers were either exposed to hypobaric hypoxia or had a primary bronchus occluded (PBO) to induce PHS. Also, medial thickness was assessed in male broiler and Leghorn (n =80) chickens fed a CTL diet and subjected to pulmonary artery occlusion (PAO). The results show that supplementation with Arg and VE plus VC have an additive effect on the velocity at which the pulmonary arterial pressure returned to basal levels in hypoxic chickens challenged with epinephrine. Also, supplementation increased xanthine oxidase (XO) activity in the vicinity of the pulmonary endothelium with no effect on NAD(P)H-oxidase activity or oxidative stress in hypoxic chickens subjected to PBO. These enzymes are upregulated in humans with IPAH. Furthermore, supplementation reduced pulmonary artery reactivity to phenylephrine in hypoxemic broilers. Unsupplemented broiler chickens had a lower specific lung weight compared to unsupplemented Leghorns. Hypoxemic broilers showed thicker resistant pulmonary arteries and were more hypertensive than hypoxemic Leghorns. Leghorns were more hypoxemic and resistant to PHS than broilers. In conclusion, Arg and VE plus VC show an additive effect in the improvement of cardiovascular performance of hypoxemic broilers as well as in restoring reactivity to phenylephrine in hypoxemic pulmonary rings. Also, supplementation shows an additive effect in restoring XO activity in hypoxic broilers. Leghorns had a better ventilation capacity and better pulmonary vasodilation capacity than broiler chickens.

An adjustable systemic-pulmonary artery (SPA) shunt is being developed that consists of apolytetrafluoroethylene (PTFE) graft with a screw plunger mechanism. This device would allowfull control of flow through SPA shunts used to augment pulmonary blood flow in neonates bornwith single ventricle physiology. The objective of this study is to evaluate the changes this mechanismhas on flow fields for a 4 mm and 5 mm adjustable SPA shunt. Two in vitro models wereexamined; an idealized model with an axisymmetric constriction and a model developed from 3-Dreconstruction of the actual shunt under asymmetric constriction. These models were used to measurethe instantaneous velocity and vorticity fields using Particle Image Velocimetry (PIV) underboth steady and pulsatile flow conditions. Recirculation regions and maximum values of velocity,vorticity, and shear stress are compared between the 4 mm and 5 mm models. The results indicatethat for the idealized model of both shunts, separation regions are much smaller, persistingfor approximately 0-1.75 diameters downstream of the constriction, while for the realistic modelsseparation regions of 2.5 diameters downstream were observed. Additional models of a 4 mm and5 mm shunt were tested under pulsatile conditions matching Re of 1061 and 849 and a Womersleynumber of 4.09 and 5.12, respectively, as seen in vivo. The maximum shear rates observed in bothshunts are within an allowable range without inducing platelet aggregation or hemolysis. However,regions of reverse flow exist distal to the throat, leading to possible concerns of plaque formation.Further in vivo testing will be needed to address this concern. This work is part of an extensiveeffort in developing a completely implantable adjustable systemic-pulmonary artery shunt.

Το πεδίο έρευνας της παρούσας διδακτορικής διατριβής είναι η υπολογιστική καρδιολογία και συγκεκριμένα η μέτρηση όγκου δεξιάς κοιλίας με χρήση υπερήχων σε καθετήρα πνευμονικής αρτηρίας (ΚΠΑ) για την αποτελεσματικότερη διαχείριση των βαριά πασχόντων ασθενών. Μέχρι τώρα ο ΚΠΑ μετράει μόνο τις πιέσεις ενδοκοιλοτικά. Τα αποτελέσματα από τη χρήση του δεν είναι επαρκώς ενθαρρυντικά. Έχει βρεθεί ότι για την καλύτερη αντιμετώπιση των βαριά πασχόντων στην μονάδα εντατικής θεραπείας (ΜΕΘ), ή στην μονάδα εμφραγμάτων, ή ακόμα και κατά την προετοιμασία ή τη διάρκεια μιας σοβαρής χειρουργικής επέμβασης, σημαντική παράμετρος πέρα από την πίεση είναι ο τελοσυστολικός και ο τελοδιαστολικός όγκος της δεξιάς κοιλίας. Αυτές οι παράμετροι συνδυαζόμενες με τις πιέσεις, προσφέρουν σαφώς καλύτερη εκτίμηση και αποτελεσματικότερη αιμοδυναμική διαχείριση των βαριά πασχόντων ασθενών με απώτερο στόχο την ελάττωση της νοσηρότητας και θνησιμότητας. Γι’ αυτό το λόγο μοντελοποιήθηκε σύστημα μέτρησης όγκου δεξιάς κοιλίας από εικόνες MRI (μαγνητικού συντονισμού) με προσομοίωση υπερήχων. Επίσης το γεγονός ότι δεν υπάρχει μέθοδος υπολογισμού όγκου ενδοκοιλιακά που να συνδυάζεται με τον δεξιό καθετηριασμό, καθιστά την παρούσα διατριβή ως καινοτόμα αφ’ ενός στον υπολογισμό του όγκου της δεξιάς κοιλίας και αφ’ ετέρου στην διαχείριση της αιμοδυναμικής κατάστασης των βαριά πασχόντων. / The research field of this PhD thesis is the computational cardiology and more specifically the right ventricle’s volume measurement using ultrasound technology on the pulmonary artery catheter (PAC) for the effective management of critically ill patients. Hitherto, right cardiac catheterization with a pulmonary artery catheter provides only intracavity pressure measurements. Several studies showed that the use of PAC in critically illness does not make any effect in patient management. It was found that for the reliable management of critical ill patients in intensive care unit (ICU), or in infarctions unit, or even during serious surgery, pressures, is the right ventricle end-diastolic and end-systolic volume. The combination of those parameters with pressures, provides obviously better estimation and effective hemodynamic management of critically ill patients seeking in mortality and morbidity reduction. For that reason, a right ventricle’s volume measurement system was modeled from cardiac MRIs with ultrasound simulation. The fact that there is not any intraventricular volume calculation method combined with right catheterization, makes this PhD thesis innovative as the right ventricle’s volume and the hemodynamic management of critically ill patients regards.

Na presente dissertação objetivou-se avaliar a reatividade vascular e a repercussão do pré-tratamento com sinvastatina (SINV, 20mg/kg, p.o.), sob esse parâmetro, em artéria mesentérica superior (AMS) e pulmonar (AP) de ratos Wistar submetidos a 45 minutos de isquemia e 2 horas de reperfusão intestinal (iIR). Nas artérias avaliou-se a função dependente e independente do endotélio e a contração induzida pela fenilefrina agonista seletivo <font face=\"Symbol\">a1-adrenérgico, em preparações com e sem endotélio e na presença ou ausência de inibidores da NOS e da iNOS (L-NAME e 1400W, respectivamente). Pode-se concluir que a iIR modificou a reatividade vascular em AP, porém não em AMS. Na artéria pulmonar, a iIR causou disfunção endotelial por meio de ativação da iNOS, a qual levou à diminuição da resposta vasodilatadora dependente do endotélio e à hiporreatividade contrátil. Além disso, confirmando a segunda hipótese, uma única dose de sinvastatina antes da iIR previne as alterações de reatividade vascular, o que demonstra o efeito benéfico desse fármaco nessa doença. / This work aimed to evaluate the vascular reactivity and the effect of pre-treatment with simvastatin (SIMV, 20mg/kg, p.o.), under this parameter, in the superior mesenteric artery (SMA) and pulmonary artery (PA) of rats subjected to 45 minutes of ischemia and 2 hours of reperfusion (iIR). In these arteries, it was evaluated the endothelium-dependent and -independent function and the contraction induced by phenylephrine the selective <font face=\"Symbol\">a1-adrenergic agonist, in preparations with and without endothelium and at the presence or absence of non-selective NOS and of iNOS inhibitors (L-NAME and 1400W, respectively). It can be concluded that the iIR modified vascular reactivity in PA, but not in SMA. In the pulmonary artery, the iIR caused endothelial dysfunction via activation of iNOS, which led to decreased endothelium-dependent vasodilator response and to contractile hyporeactivity. Moreover, confirming the second hypothesis, a single dose of simvastatin prior to iIR prevents changes in vascular reactivity, which shows the beneficial effects of this drug in this disease.

Background-Pulmonary artery hypertension (PAH) is characterized by progressive vascular changes causing increased pulmonary resistance and eventual right heart failure (HF). It has been suggested that altered myocardial substrate utilization may be associated with right HF, however these changes have not yet been well characterized. The aim of this study was to evaluate in vivo right ventricular (RV) function and RV glucose and fatty acid metabolism in an experimental model of PAH using non-invasive positron emission tomography (PET) imaging and to investigate the effect of a novel endothelin receptor antagonist, Macitentan, on the development of PAH and RV energetics. Methods and Results-Severe PAH was induced in a total of 11 male Sprague-Dawley rats using a single injection of Sugen5416 followed by chronic hypoxia. The rats were then randomized to treatment or no treatment with Macitentan (30 mg/kg daily) Five and eight weeks post injection, substrate utilization was serially assessed with 2-[18F]fluoro-2-deoxyglucose (FDG) and 4-[18F]fluoro-6-thia-heptadecanoate (FTHA) PET scans for glucose and fatty acid metabolism respectively, and reported as a standardized uptake value (SUV). This data was correlated with in vivo functional measurements with echocardiography and multi gated acquisition scans. The Sugen-hypoxia (SuHx) model resulted in an increase in RV FDG uptake over 8 weeks (SUV control: 1.56 ± 0.38, week 5 SuHx: 4.06 ± 1.90, week 8 SuHx: 4.00 ± 1.60, p<0.005 between control and week 5 SuHx). RV FTHA data showed a trend towards increased uptake with onset of PAH at week 5 SuHx (SUV control: 1.50 ± 0.40, week 5 SuHx: 3.06 ± 1.10, p>0.05). Macitentan significantly decreased RV FDG uptake (SUV week 8 SuHx: 4.00 ± 1.60, week 8 SuHx +ERA: 2.54 ± 0.90, p<0.05). This was associated with improved RV ejection fraction (PAH week 8 untreated: 53.15 ± 9.9% vs PAH week 8 treated: 73.22 ± 4.8%, p<0.01) and improved pulmonary artery pressures measured by pulmonary artery acceleration time (PAH week 8 untreated: 17.32 ± 2.30 ms vs. PAH week 8 treated: 24.38 ± 3.90 ms, p<0.001). There was a strong correlation between increased pulmonary artery pressures and increased RV FDG uptake (r=0.87, p=0.001) as well as a significant inverse relationship between improved RV ejection fraction and decreased RV FDG uptake (r=-0.72, p=0.01). Conclusion-PAH is associated with metabolic changes in the RV, characterized by increased glucose uptake and a trend towards increased RV fatty acid uptake with onset of PAH. Macitentan attenuated RV FDG uptake and significantly increased RV function as well as hemodynamics compared to untreated group.

Submitted by Nadir Basilio (nadirsb@uninove.br) on 2018-07-17T21:13:23Z No. of bitstreams: 1 Jessica Julioti Urbano.pdf: 3065396 bytes, checksum: 1e38f15e601296f027d3fd4cd280d051 (MD5) / Made available in DSpace on 2018-07-17T21:13:23Z (GMT). No. of bitstreams: 1 Jessica Julioti Urbano.pdf: 3065396 bytes, checksum: 1e38f15e601296f027d3fd4cd280d051 (MD5) Previous issue date: 2016-11-30 / The actual scientific approach to bioengineering organs is based on the use of natural extracellular matrix of decellularized lung as initial departure for subsequent reconstruction of the organ for recellularization in a bioreactor. The decellularization technique can be performed by two infusion ways, one through the trachea and other by pulmonary artery. The aim of this studies was to investigate in an experimental animal model, by the occlusion at the end of inspiration (OEI) and movement equation (ME), the behavior of the elastic, viscous and viscoelastic mechanical properties, of mice lungs after the process of decellularization through the trachea and the pulmonary artery. Were used 30 male mice C57BL/6, weighing 17-18 g (7-8 weeks of age), anesthetized and euthanized by exsanguination through the abdominal aorta. The decellularization protocol comprised the following steps: collecting, cleaning, freezing and thawing, rinsing with sodium dodecyl sulfate and phosphate buffered saline. For the studies I and II, the lungs were divided into the control group (GC = 10), the decellularization group by the trachea (TDG = 10) and the pulmonary artery decellularization group (PDG = 10), 5 lungs in each group for the study I that had the analysis through the technique of OEI and 5 lungs in each group for the study II with analysis through the ME. In the study I, the values of static elastance (Eest = CG: 226.9 ± 4.1, PDG: 162.6 ± 3.9, TDG: 154.8 ± 1.7) and dynamics (Edyn = CG: 240 , 9 ± 6.7, PDG: 176 ± 5.4, TDG: 177.6 ± 1.6) were significantly lower in TDG and PDG when compared to CG. In study II, the value of lung resistance presented in TDG was significantly lower in relation to the other two groups (R = CG: 5.32 ± 0.26; PDG: 5.94 ± 0.24; TDG: 2.85 ± 0.14) and GC elastance was significantly higher in comparison with TDG and PDG, and in PDG the difference was significantly lower in relation to TDG (E = CG: 279 ± 13.81; PDG: 146 ± 19.04, TDG: 209.6 ± 12.06). We can observe in both the two-way decellularization are effective to provide a scaffold ideal for pulmonary later recellularization when evaluated by the OEI and ME. Furthermore, the decellularized lungs through the pulmonary artery may be used to create a pulmonary scaffold in less time, because the protocol can be performed in a day, which facilitates the process for obtaining functional lungs scaffolds. / A abordagem científica atual para a bioengenharia de órgãos é baseada na utilização da matriz extracelular natural do pulmão descelularizado como partida inicial para posterior reconstrução do órgão por recelularização em um biorreator. A técnica de descelularização pode ser realizada por duas vias de perfusão, uma através da traqueia e a outra pela artéria pulmonar. O objetivo deste estudo foi investigar em um modelo experimental animal, através da técnica de oclusão ao final da inspiração (OFI) e equação do movimento (EM), o comportamento das propriedades mecânicas elásticas, viscosas e viscoelásticas de pulmões descelularizados de camundongos pelos métodos de perfusão através da traqueia e da artéria pulmonar. Foram utilizados 30 camundongos machos da raça C57BL/6, com peso de 17-18 g (7-8 semanas de idade), anestesiados e eutanasiados por exsanguinação pela aorta abdominal. O protocolo de descelularização seguiu as etapas de coleta, limpeza, congelamento e descongelamento, lavagem com dodecil-sulfato de sódio e tampão fosfato-salino. Para a realização dos estudos I e II, os pulmões foram divididos em grupo controle (GC = 10), grupo descelularização pela traqueia (TDG = 10) e grupo descelularização pela artéria pulmonar (PDG = 10), sendo 5 pulmões em cada grupo para o estudo I que teve a análise através da técnica de OFI e 5 pulmões em cada grupo para o estudo II com análise através da EM. No estudo I, os valores de elastância estática (Eest = CG: 226,9 ± 4,1; PDG: 162,6 ± 3,9; TDG: 154,8 ± 1,7) e dinâmica (Edyn = CG: 240,9 ± 6,7; PDG: 176 ± 5,4; TDG: 177,6 ± 1,6) foram significativamente menores em TDG e PDG quando comparados com o CG. Já no estudo II, o valor da resistência pulmonar apresentado no TDG foi significativamente menor em relação aos outros dois grupos (R = CG: 5,32 ± 0,26; PDG: 5,94 ± 0,24; TDG: 2,85 ± 0,14) e o valor da elastância de CG apresentou-se maior de forma significativa em comparação com a TDG e PDG, e no PDG a diferença foi menor significativamente em relação à TDG (E = CG: 279 ± 13,81; PDG: 146 ± 19,04; TDG: 209,6 ± 12,06). Podemos observar que, quando avaliadas pelas técnicas de OFI e EM, as duas vias de descelularização foram eficazes na geração de um scaffold pulmonar ideal para posterior recelularização. Além disso, a técnica de descelularização através da artéria pulmonar mostrou-se eficaz para a obtenção de um scaffold pulmonar em menor período de tempo, uma vez que o protocolo pode ser realizado em um dia, o que facilita o processo de obtenção de pulmões funcionais.

no / We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of in vivo phenomena to alterations in protein activity (or vice versa). We have applied this approach to electrical and mechanical remodelling in right ventricular failure caused by monocrotaline-induced pulmonary artery hypertension in rats. We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca2+]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca2+-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate. Echocardiography was used to estimate increased wall stress in failure, in vivo. Stretch of intact and skinned single myocytes revealed no effect on the Frank-Starling mechanism in failing myocytes. In isolated hearts acute stretch-induced arrhythmias occurred in all preparations. Significant shortening of the early APD was seen in control but not failing hearts. These observations may be linked to changes in the gene expression of candidate mechanosensitive ion channels (MSCs) TREK-1 and TRPC1/6. Computer simulations incorporating MSCs and changes in ion channels with failure, based on altered gene expression, largely reproduced experimental observations.

Οι καρδιαγγειακές παθήσεις αποτελούν την κύρια αιτία θανάτου στις αναπτυγμένες χώρες. Η στένωση σε μία αρτηρία, είτε αυτή προκαλείται από μία πάθηση όπως το ανεύρυσμα, είτε προκαλείται από μία περίδεση, όπως στις περιπτώσεις των συγγενών καρδιοπαθειών, μπορεί να μεταβάλλει σε σημαντικό βαθμό τα χαρακτηριστικά της ροής του αίματος. Η μελέτη της φυσιολογικής παλλόμενης ροής μέσα από στένωση είναι ιδιαίτερα σημαντική για τη διάγνωση και αντιμετώπιση των αγγειακών νόσων. Το ιατρικό πρόβλημα το οποίο εξετάζουμε στην παρούσα εργασία, είναι η στένωση της πνευμονικής αρτηρίας από περίδεση. Η περίδεση γίνεται προφανώς για να μειωθεί η υψηλή αρτηριακή πίεση και τελικά η ροή του αίματος προς τους πνεύμονες. Πρόκειται για μία χειρουργική μέθοδο αντιμετώπισης συγγενών καρδιοπαθειών. Η περίδεση της πνευμονικής αρτηρίας (pulmonary artery banding - PAB) είτε με συμβατικό τρόπο, ή με την πλέον σύγχρονη μέθοδο μέσω της συσκευής FloWatchTM προκαλεί τη στένωσή της. Με τον συμβατικό τρόπο η στένωση μπορεί να θεωρηθεί αξονικά συμμετρική, ωστόσο με τη χρήση του FloWatchTM είναι μη αξονικά συμμετρική. Έχει αποδειχθεί ότι τόσο η αξονικά συμμετρική, όσο και η μη συμμετρική περίδεση δημιουργεί διαφόρου βαθμού ίνωση του τοιχώματος της πνευμονικής αρτηρίας. Η αναδόμηση της πνευμονικής αρτηρίας είναι πολύ ηπιότερη στην περίπτωση της περίδεσης με το FloWatchTM. Η διαφοροποίηση αυτή έγκειται κυρίως στο ότι η συμβατική περίδεση προκαλεί για συγκεκριμένη μείωση της διατομής ισχυρότερη μείωση της περιμέτρου της διατομής από εκείνης της περίδεσης με το FloWatchTM. Στην παρούσα εργασία γίνεται αναφορά και ανάλυση των διαφόρων περιπτώσεων ροής σε στενώσεις αρτηριών, των συγγενών καρδιοπαθειών και των τεχνικών περίδεσης της πνευμονικής αρτηρίας. Επιπρόσθετα, μελετήθηκαν και υπολογίστηκαν η μόνιμη και η παλλόμενη ροή σε αξονικά συμμετρική 25% στένωση προκαλούμενη από συμβατική περίδεση, καθώς και η μόνιμη και παλλόμενη ροή σε μη συμμετρική 25% στένωση της πνευμονικής αρτηρίας όπως προκαλείται από το FloWatchTM, μέσω των πακέτων Fluent και Gambit. Η υπολογιστική μελέτη του πεδίου ροής περιλαμβάνει την κατανομή ταχυτήτων, τον προσδιορισμό των περιοχών ανακυκλοφορίας, την κατανομή των πιέσεων και την σύγκριση των παραπάνω μεγεθών με τα αντίστοιχα αποτελέσματα της βιβλιογραφίας. Τέλος, με βάση τα αποτελέσματα γίνεται η σύγκριση των δύο μελετούμενων μεθόδων περίδεσης. Αριθμητικά ρεαλιστικά δεδομένα ελήφθησαν από την καρδιοχειρουργική κλινική του νοσοκομείου Παίδων «Αγία Σοφία». / Cardiovascular diseases are the leading cause of death in developed countries. A stenosis in an artery , caused either by a disease such as an aneurism or by a banding (such as in congenital diseases) can change the characteristics of the blood flow very seriously. The study of the physiological pulsatile flow through a stenosis is very important for the diagnosis and treatment of the arterial diseases. The medical problem which is examined in this study is pulmonary artery stenosis caused by a banding. The banding takes place to reduce the high arterial pressure and finally the blood flow from the heart to the lungs. It is a surgical method used for treatment of congenital heart diseases. The pulmonary artery banding either with the use of the conventional method or the most modern with the use of the FloWatchTM technology causes stenosis of the artery. With the conventional method, stenosis can be considered axially symmetrical while with the use of FloWatchTM it is asymmetrical. It has been proven that both the axially symmetrical and asymmetrical banding cause fibrosis of the pulmonary artery walls of different degrees. The reconstruction of the pulmonary artery is milder where there is banding with FloWatchTM. This differentiation is based mainly on the fact that the conventional banding causes, for a specific decrease of the cross-section, a decrease in the perimeter of the cross-section higher than that of banding with FloWatchTM. In this assignment there is a report of different cases of flow in arterial stenosis, in congenital heart diseases and pulmonary banding techniques. In addition what was studied and appreciated was the steady and pulsatile flow in axially symmetrical 25% stenosis caused by the conventional banding, as well as the steady and pulsatile flow in asymmetrical 25% stenosis of pulmonary artery caused by FloWatchTM with the use of Fluent and Gambit. The numerical study of flow distribution includes velocity distribution, designation of back flow area, distribution of pressure and comparison of these quantities with the results in bibliography. Finally, based on the results, there is a comparison of the two banding methods under study. The numerical realistic data were received from the cardio-surgical clinic of children’s hospital “Aghia Sophia”.