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Pulmonary Vasculature (pulmonary + vasculature)
Selected AbstractsOff-Pump Total Cavopulmonary Connection in a Patient with Hypoplastic Right Pulmonary Artery and Right Lung Secondary to KyphoscoliosisJOURNAL OF CARDIAC SURGERY, Issue 5 2008Murat Ugurlucan M.D. Pulmonary vasculature and status of the lungs are critically important for the success of the operation. In this report, we present a 10-year-old patient with single ventricle heart and severely hypoplastic unilateral pulmonary artery and respective lung due to kyphoscoliosis who underwent extracardiac Fontan procedure without cardiopulmonary bypass, successfully. [source] Spasmogenic action of endothelin-1 on isolated equine pulmonary artery and bronchusEQUINE VETERINARY JOURNAL, Issue 2 2003A. E. M. BENAMOU Summary Reasons for performing study: There is currently little published information about the effects of endothelin-1 (ET-1), a potent endogenous spasmogen of vascular and airway smooth muscle, on pulmonary vasculature and airways or which ET receptor subtypes mediate ET-1-induced vasoconstrictive and bronchoconstrictive action in the horse. Objectives: To investigate the effect of endothelin-1 (ET-1) on smooth muscle from isolated equine pulmonary artery and bronchus. In addition, the roles of ETA and ETB receptors in ET-1 mediated contraction in these tissues were assessed. Methods: The force generation of ring segments from pulmonary arteries or third-generation airways (obtained from horses subjected to euthanasia fororthopaedic reasons) were studied in an organ bath at 37°C in response to exogenous endothelin and selective endothelin A (BQ123) or B receptor (BQ788) antagonists. Results: ET-1 produced concentration-dependent contractions of the equine pulmonary artery and bronchus. The threshold for contraction was 10,10 and 10,9 mol/l ET-1 for pulmonary artery and bronchus, respectively. The maximal contraction induced by the highest ET-1 concentration (10,7 mol/l) was 173 and 194% of the contraction obtained with 100 mmol/l KCl in pulmonary artery and bronchus, respectively. ET-1 potency was 25 times greater in equine pulmonary artery than in equine bronchus (concentration of ET-1 producing 50% of maximal contraction [EC50] = 5.6 10,9 mol/l and 2.2 10,8 mol/l, respectively). In pulmonary artery, ET-1 induced contractions were significantly inhibited by the ETA receptor antagonist BQ123 (1 ,mol/l; dose-response curve to ET-1 was shifted to the right by 5.4-fold), but not by the ETB antagonist BQ788. In bronchus, dose-responses curves to ET-1 were shifted to the right by BQ123 (1 ,mol/l; 2.5-fold), but not by BQ788 (1 ,mol/l). In the presence of both antagonists, the dose-response curve to ET-1 was shifted to the right by 4.5-fold. Conclusions: These functional studies demonstrate that ET-1 is a potent spasmogen of equine third generation pulmonary artery and bronchus, and that contractions are mediated via ETA receptors in the former and both ETA and ETB receptors in the latter. Potential clinical relevance: Endothelin receptor antagonists may have potential for treating equine pulmonary hypertension or bronchoconstriction. [source] Atrial septal defects: Magnetic resonance and computed tomography appearancesJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 3 2009ETD Hoey Summary Atrial septal defects are associated with significant morbidity and mortality. Echocardiography is the first-line imaging modality, but MR and CT imaging can provide complimentary information, especially for the detection of associated anomalies and for assessing changes in the pulmonary vasculature. The aim of this pictorial essay is to review the spectrum of atrial septal defects, with particular reference to their cross-sectional imaging appearances and issues pertaining to management. [source] Improvement in hepatopulmonary syndrome after methadone withdrawal: A case report with implications for disease mechanismLIVER TRANSPLANTATION, Issue 7 2010Edmund M. T. Lau Spontaneous resolution of hepatopulmonary syndrome (HPS) without liver transplantation or improvement in the underlying liver disease has rarely been reported in the literature. Increased endogenous production of nitric oxide has been implicated in the pathogenesis of HPS. We report the case of a 50-year-old man with hepatitis C cirrhosis who demonstrated dramatic improvement in HPS after withdrawal from chronic methadone therapy. We speculate on the potential role of opiate receptors in the pulmonary vasculature and their effect on nitric oxide signaling as a potential mechanism accounting for the patient's clinical improvement. Liver Transpl 16:870,873, 2010. © 2010 AASLD. [source] Time-resolved contrast-enhanced imaging with isotropic resolution and broad coverage using an undersampled 3D projection trajectoryMAGNETIC RESONANCE IN MEDICINE, Issue 2 2002Andrew V. Barger Abstract Time-resolved contrast-enhanced 3D MR angiography (MRA) methods have gained in popularity but are still limited by the tradeoff between spatial and temporal resolution. A method is presented that greatly reduces this tradeoff by employing undersampled 3D projection reconstruction trajectories. The variable density k -space sampling intrinsic to this sequence is combined with temporal k -space interpolation to provide time frames as short as 4 s. This time resolution reduces the need for exact contrast timing while also providing dynamic information. Spatial resolution is determined primarily by the projection readout resolution and is thus isotropic across the FOV, which is also isotropic. Although undersampling the outer regions of k -space introduces aliased energy into the image, which may compromise resolution, this is not a limiting factor in high-contrast applications such as MRA. Results from phantom and volunteer studies are presented demonstrating isotropic resolution, broad coverage with an isotropic field of view (FOV), minimal projection reconstruction artifacts, and temporal information. In one application, a single breath-hold exam covering the entire pulmonary vasculature generates high-resolution, isotropic imaging volumes depicting the bolus passage. Magn Reson Med 48:297,305, 2002. © 2002 Wiley-Liss, Inc. [source] Relationship of Ultrafiltration and Anastomotic Flow in Isolated Rat LungsMICROCIRCULATION, Issue 5 2001WEN LIN ABSTRACT Objective: When arterial and venous pressures are increased to equal values in "stop-flow" studies, perfusate continues to enter the pulmonary vasculature from the arterial and venous reservoirs. Losses of fluid from the pulmonary vasculature are due to ultrafiltration and flow through disrupted anastomotic (bronchial) vessels. This study compared the relative sites of ultrafiltration and anastomotic flows at low and high intravascular pressures. Methods: Isolated rat lungs were perfused for 10 minutes with FITC-dextran, which was used to detect ultrafiltration. Arterial and venous catheters were then connected to reservoirs containing radioactively labeled dextrans at 20 or 30 cm H2O for 10 minutes. The vasculature was subsequently flushed into serial vials, and ultrafiltration and vascular filling during the equal-pressure interval were calculated. Results: Ultrafiltration equaled 0.43 ± 0.11 mL at 20 cm H2O and was similar to the volume of fresh arterial and venous perfusate which entered and remained in the pulmonary vasculature during the equal-pressure interval (0.45 ± 0.10 mL). At 30 cm H2O, 0.80 ± 0.23 mL entered and remained in the vasculature during the equal-pressure interval, replacing the original perfusate, and calculated transudation (0.56 ± 0.09 mL) was not significantly more than at 20 cm H2O. Fluid also entered the airspaces at 30 cm H2O but not at 20 cm H2O. Conclusions: At 20 cm H2O, flow through anastomotic vessels occurs at sites that are at the arterial and venous ends of the microcirculation. Flow in exchange vessels remains minimal, permitting measurements of ultrafiltration and exchange. Losses of perfusate from the pulmonary vessels complicate measurements of ultrafiltration at 30 cm H2O. [source] Pulmonary tumor thrombotic microangiopathy resulting from metastatic signet ring cell carcinoma of the stomachPATHOLOGY INTERNATIONAL, Issue 6 2007Naomi Sakashita Pulmonary tumor thrombotic microangiopathy is an unusual malignancy-related respiratory complication characterized by multiple microthrombi and intimal myofibroblast proliferation. Its clinical manifestation is subacute respiratory failure with pulmonary hypertension. Herein is reported a case of pulmonary tumor thrombotic microangiopathy associated with gastric signet ring cell carcinoma. A 51-year-old woman with gastric cancer died of subacute respiratory failure. Autopsy showed gastric signet ring cell carcinoma with diffuse metastasis of pulmonary lymphatics and pleurae; every organ examined lacked a space-occupying tumor mass. Histologically, proliferated intimal myofibroblasts obliterated most of the pulmonary vascular lumen, and a few stenosed vascular lumina contained cancer cells. In addition, pulmonary vasculature associated with intimal proliferation contained microthrombi. Most cancer cells in the stomach and pulmonary lymphatics were typical signet ring cells, whereas those in vascular lesions were cells of poorly differentiated adenocarcinoma without mucous production. Consistent with a previous report, the latter expressed vascular endothelial growth factor (VEGF) and tissue factor (TF). The proliferated intimal myofibroblasts also expressed type 2A serotonin receptor (5-HT2A). These findings suggest that local expression of VEGF, TF, and 5-HT2A may be linked to the pathogenesis of this unusual pulmonary complication. [source] Expression and function of phosphodiesterases in nitrofen-induced congenital diaphragmatic hernia in ratsPEDIATRIC PULMONOLOGY, Issue 4 2010Irene W.J.M. van der Horst MD Abstract Background Congenital diaphragmatic hernia (CDH) is an anomaly associated with pulmonary hypoplasia and pulmonary hypertension (PH). The limited efficacy of current approaches to treat PH in CDH, including inhaled nitric oxide (NO), drives the search for other therapies. Phosphodiesterases (PDEs) degrade cyclic nucleotide second messenger cAMP and cGMP downstream of NO thereby limiting the vasodilatory response to NO. Objective To identify therapeutic targets by cataloguing the expression and function of PDE isoforms in the pulmonary vasculature in nitrofen-induced CDH in fetal rats. Methods/Results Quantitative RT-PCR revealed PDE1,5 and PDE9 mRNA expression in pulmonary arteries (PAs) of control and nitrofen-induced CDH term fetal rats. In this order of potency, the PDE inhibitors Sildenafil (PDE5),>,EHNA (PDE2),>,Rolipram (PDE4),>,Cilostamide (PDE3) all dilated isolated third generation PA after pre-constriction with the thromboxane analog U46619. Hyperoxic pre-incubation of PAs significantly attenuated vasodilatation induced by the PDE5 inhibitor Sildenafil (65% vs. 33%, P,<,0.004). CDH PAs dilated significantly less to PDE2 inhibitor EHNA compared to control (51% vs. 72%, P,<,0.05). Subsequently PDE2 protein expression was higher in PAs of CDH animals. Conclusion Most PDE isoforms exist in the PAs of fetal rats and their inhibition causes pulmonary vasodilatation. PDE5 inhibition was the most potent vasodilator, however, there were no differences between groups. PDE5-induced vasodilatation was attenuated by hyperoxic pre-incubation. PDE inhibitors might be considered therapeutic targets in combination with iNO in neonates with CDH. Pediatr Pulmonol. 2010; 45:320,325. © 2010 Wiley-Liss, Inc. [source] The Extracellular Signal-Regulated Kinase Is Involved in the Effects of Sildenafil on Pulmonary Vascular RemodelingCARDIOVASCULAR THERAPEUTICS, Issue 1 2010Zhen Zeng Pulmonary hypertension is a group of diseases comprising vascular constriction and obstructive changes of the pulmonary vasculature. Phosphodiesterase type 5 inhibitors, for example, sildenafil, can alleviate vascular remodeling in the monocrotaline pulmonary hypertension model in rats. We investigate the mechanisms of sildenafil on the pulmonary vascular remodeling of pulmonary hypertension induced by monocrotaline (MCT) in rats. Thirty Sprague-Dawley rats (weighing 200,220 g) were administered with MCT abdominal cavity injection or equivalent volume of normal saline (NS) (which were treated as C group n = 10) to induce pulmonary hypertension model. Fourteen days later, 20 MCT treated rats were randomly fed with sildenafil (25mg/kg/day) or placebo as S, P group (10 rats for each group), respectively. Another 6 weeks later, mean pulmonary artery pressure (mPAP), index of right ventricular hypertrophy (RV/LV+S) of all animals were measured under general anesthesia. Pulmonary tissue was collected to investigate pathological features of pulmonary arteries and to measure protein expression of ERK1/ERK2 and MKP1. After 6 weeks, there were significant elevated mPAP and RV/LV+S in both P and S groups. The ratio of wall thickness to vessel diameter in pulmonary arteries with diameters <200 ,m were increased in both P and S groups. But the ratio of wall thickness to vessel diameter was smaller in S group than that in P group. The phosphorylation level of ERK1/ERK2 were elevated in both P and S groups, but the level of phosphorlation ERK1/ERK2 were lower in S group than that in P group. Intriguingly, the expression level of MKP1 was significantly increased in both S and P groups, while it was higher in S group than that in P group. The Sildenafil can decrease mPAP and inhibit the progress of pulmonary vascular remodeling in pulmonary hypertension rats. The ERK-MAP kinase signaling pathway might play a role during this process. [source] | ||||||||||