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Pulmonary Trunk (pulmonary + trunk)
Selected AbstractsCongenital Atresia of the Ostium of Left Main Coronary Artery: A Rare Coronary Anomaly, Diagnostic Difficulty and Successful Surgical RevascularizationCONGENITAL HEART DISEASE, Issue 5 2007Philip Varghese MRCS ABSTRACT We report the case of an 8-month-old infant who was referred for mechanical circulatory support (extracorporeal membrane oxygenation). Aortogram was compatible with the diagnosis of anomalous origin of left coronary artery to pulmonary trunk. A definitive diagnosis of atresia of the left coronary ostium was only established intraoperatively. Patient underwent successful surgical angioplasty with an autologous pericardial patch. [source] Development of lymphatic vessels in mouse embryonic and early postnatal heartsDEVELOPMENTAL DYNAMICS, Issue 10 2008Juszy, Micha Abstract We aimed to study the spatiotemporal pattern of lymphatic system formation in the embryonic and early postnatal mouse hearts. The first sign of the development of lymphatics are Lyve-1,positive cells located on the subepicardial area. Strands of Lyve-1,positive cells occur first along the atrioventricular sulcus of the diaphragmatic surface and then along the great arteries. Lumenized tubules appear, arranged in rows or in a lattice. They are more conspicuous in dorsal atrioventricular junction, along the major venous and coronary artery branches and at the base of the aorta and the pulmonary trunk extending toward the heart apex. At later stages, some segments of the lymphatic vessels are partially surrounded by smooth muscle cells. Possible mechanisms of lymphangiogenesis are: addition of Lyve-1,positive cells to the existing tubules, elongation of the lymphatic lattice, sprouting and coalescence of tubules. We discuss the existence of various subpopulations of endothelial cells among the Lyve-1,positive cells. Developmental Dynamics 237:2973,2986, 2008. © 2008 Wiley-Liss, Inc. [source] Functional morphology and patterns of blood flow in the heart of Python regius,JOURNAL OF MORPHOLOGY, Issue 6 2009J. Matthias Starck Abstract Brightness-modulated ultrasonography, continuous-wave Doppler, and pulsed-wave Doppler-echocardiography were used to analyze the functional morphology of the undisturbed heart of ball pythons. In particular, the action of the muscular ridge and the atrio-ventricular valves are key features to understand how patterns of blood flow emerge from structures directing blood into the various chambers of the heart. A step-by-step image analysis of echocardiographs shows that during ventricular diastole, the atrio-ventricular valves block the interventricular canals so that blood from the right atrium first fills the cavum venosum, and blood from the left atrium fills the cavum arteriosum. During diastole, blood from the cavum venosum crosses the muscular ridge into the cavum pulmonale. During middle to late systole the muscular ridge closes, thus prohibiting further blood flow into the cavum pulmonale. At the same time, the atrio-ventricular valves open the interventricular canal and allow blood from the cavum arteriosum to flow into the cavum venosum. In the late phase of ventricular systole, all blood from the cavum pulmonale is pressed into the pulmonary trunk; all blood from the cavum venosum is pressed into both aortas. Quantitative measures of blood flow volume showed that resting snakes bypass the pulmonary circulation and shunt about twice the blood volume into the systemic circulation as into the pulmonary circulation. When digesting, the oxygen demand of snakes increased tremendously. This is associated with shunting more blood into the pulmonary circulation. The results of this study allow the presentation of a detailed functional model of the python heart. They are also the basis for a functional hypothesis of how shunting is achieved. Further, it was shown that shunting is an active regulation process in response to changing demands of the organism (here, oxygen demand). Finally, the results of this study support earlier reports about a dual pressure circulation in Python regius. J. Morphol., 2009. © 2008 Wiley-Liss, Inc. [source] Intravascular ultrasound imaging of the pulmonary arteries in primary pulmonary hypertensionRESPIROLOGY, Issue 1 2000Takaaki Nakamoto Objective: Intravascular ultrasound has the unique ability to provide cross-sectional images of the arterial wall. This study examined intravascular ultrasound (IVUS) images of the proximal pulmonary arteries in primary pulmonary hypertension (PPH). Methodology: Study 1: Specimens from four patients who had died of PPH (in vitro PPH group) were compared with those of three patients who had died of subarachnoid haemorrhage but had no evidence of cardiopulmonary disease (in vitro control group). Three-centimetre segments of the following levels were examined by IVUS: pulmonary trunk, eight secondary branch arteries of the upper, middle, and lower lobes of both lungs, and the thoracic descending aorta. Study 2: Four patients with PPH (in vivo PPH group) and five patients without pulmonary hypertension and no evidence of cardiopulmonary disease (in vivo control group) were examined. The IVUS images of the apical segmental artery of the right upper lobe and the descending branch of the right pulmonary artery were studied. Results: Echographic examination of formalin-fixed preparations of secondary branch sections of the pulmonary artery failed to show a clear three-layer structure in the in vitro control group (24 preparations), but a distinct three-layer structure and increased vessel wall thickness were observed in the in vitro PPH group (32 preparations). Similar findings were obtained in the in vivo study. The mean echo density of the proximal pulmonary arterial wall correlated well with the mean pulmonary arterial pressure (mPA) in the in vitro PPH, and also correlated with the mPA in the in vivo study (r = 0.960, P < 0.0001). The echo intensity of secondary branch sections of the pulmonary artery was higher in the in vitro PPH group than in the in vitro control group (180.5 ± 27.0 vs 132.5 ± 26.7 counts, P < 0.001); similar results were obtained in the in vivo study (144.7 ± 23.4 vs 85.0 ± 14.3 counts, P < 0.01). Conclusions: These results suggest that the histological changes detected in the pulmonary artery walls in the PPH group were responsible for the increased echo intensity. [source] Expression of Lymphatic Markers During Avian and Mouse CardiogenesisTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 2 2010Ganga Karunamuni Abstract The adult heart has been reported to have an extensive lymphatic system, yet the development of this important system during cardiogenesis is still largely unexplored. The nuclear-localized transcription factor Prox-1 identified a sheet of Prox-1-positive cells on the developing aorta and pulmonary trunk in avian and murine embryos just before septation of the four heart chambers. The cells coalesced into a branching lymphatic network that spread within the epicardium to cover the heart. These vessels eventually expressed the lymphatic markers LYVE-1, VEGFR-3, and podoplanin. Before the Prox-1-positive cells were detected in the mouse epicardium, LYVE-1, a homologue of the CD44 glycoprotein, was primarily expressed in individual epicardial cells. Similar staining patterns were observed for CD44 in avian embryos. The proximity of these LYVE-1/CD44-positive mesenchymal cells to Prox-1-positive vessels suggests that they may become incorporated into the lymphatics. Unexpectedly, we detected LYVE-1/PECAM/VEGFR-3-positive vessels within the embryonic and adult myocardium, which remained Prox-1/podoplanin-negative. Lymphatic markers were surprisingly found in adult rat and embryonic mouse epicardial cell lines, with Prox-1 also exhibiting nuclear-localized expression in primary cultures of embryonic avian epicardial cells. Our data identified three types of cells in the embryonic heart expressing lymphatic markers: (1) Prox-1-positive cells from an extracardiac source that migrate within the serosa of the outflow tract into the epicardium of the developing heart, (2) individual LYVE-1-positive cells in the epicardium that may be incorporated into the Prox-1-positive lymphatic vasculature, and (3) LYVE-1-positive cells/vessels in the myocardium that do not become Prox-1-positive even in the adult heart. Anat Rec, 2010. © 2009 Wiley-Liss, Inc. [source] Angioarchitecture of the venous and capillary system in heart defects induced by retinoic acid in mice,BIRTH DEFECTS RESEARCH, Issue 7 2009Anna Ratajska Abstract BACKGROUND: Corrosion casting and immunohistochemical staining with anti-alpha smooth muscle actin and anti-CD34 was utilized to demonstrate the capillary plexus and venous system in control and malformed mouse hearts. METHODS: Outflow tract malformations (e.g., double outlet right ventricle, transposition of the great arteries, and common truncus arteriosus) were induced in progeny of pregnant mice by retinoic acid administration at day 8.5 of pregnancy. RESULTS: Although control hearts exhibited areas in which capillaries tended to be oriented in parallel arrays, the orientation of capillaries in the respective areas of malformed hearts was chaotic and disorganized. The major branch of a conal vein in control hearts runs usually from the left side of the conus to its right side at the root of the pulmonary trunk and opens to the right atrium below the right auricle; thus, it has a curved course. On the other hand, a conal vein in malformed hearts courses from the left side or from the anterior side of the conus and tends to traverse straight upwards along the dextroposed aorta or along the aortopulmonary groove with its proximal part located outside of the heart. Other cardiac veins in outflow tract malformations are positioned in the same locations as in control hearts. CONCLUSIONS: We postulate that the changed location of the conal vein and disorganized capillary plexus result from malformed morphogenesis of the outflow tract and/or a disturbed regulation of angiogenic growth factor release from the adjacent environment. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||