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Left Ventricular Myocardium (leave + ventricular_myocardium)
Selected AbstractsEffects of right and left vagal stimulation on left ventricular acetylcholine levels in the catACTA PHYSIOLOGICA, Issue 1 2001T. Akiyama To test the effectiveness of, and the interactions between, right and left vagal stimulation on left ventricular acetylcholine (ACh) levels, we applied the dialysis technique to the heart of anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and perfused with Krebs,Henseleit buffer containing eserine. Dialysate ACh content was measured as an index of ACh release from post-ganglionic vagal nerve terminals in the left ventricular myocardium. We electrically stimulated the right and left cervical vagal nerves separately or together and investigated the dialysate ACh response. In two different regions of the left ventricle, substantial dialysate ACh responses were observed by the stimulation (20 Hz) of both right and left cervical vagal nerves. At stimulation frequencies of both 10 and 20 Hz, the dialysate ACh response to the bilateral vagal stimulation was almost algebraically the calculated sum of the individual dialysate ACh responses to unilateral vagal stimulation. In conclusion, ACh levels in the left ventricle are affected by both right and left vagal nerves and show little evidence of interactions between right and left vagal nerves at the level of the cardiac ganglia. [source] Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded heartsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004T. Miyamoto Abstract Background, The peroxisome proliferator-activated receptor (PPAR) , is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPAR, and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. Methods, Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by ,-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPAR, and fatty acid oxidation enzymes were examined by Western blotting. Results, Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0·06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by ,-oxidation was faster than the sham-control hearts (P < 0·05). However, protein levels of PPAR, and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. Conclusions, These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPAR, and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli. [source] Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiographyJOURNAL OF INTERNAL MEDICINE, Issue 5 2002C. M. Sköld Abstract. Sköld CM, Larsen FF, Rasmussen E, Pehrsson SK, Eklund AG (Karolinska Hospital and Institutet, Stockholm, Sweden). Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiography. J Intern Med 2002; 252: 465,471. Objectives. To elucidate whether cardiac magnetic resonance imaging (MRI) could be useful in disclosing structural changes in the myocardium in sarcoidosis patients and to relate echo-Doppler derived indices of left ventricular function to electrocardiogram (ECG) findings. Design. The MRI was performed in 18 consecutive patients with sarcoidosis. Left ventricular ejection fraction (LVEF), i.e. systolic function, was estimated echocardiographically by Simpson's two-dimensional method (n = 16). Diastolic function was estimated by age-corrected Doppler-derived indices: isovolumetric relaxation time (IVRT), deceleration time (DT) and early filling/atrial contraction ratio (E/A ratio). Results. Eleven patients had conduction defects or dysrhythmias (ECG+) whilst seven patients had a normal ECG (ECG,). In two patients, high signalling, contrast-enhanced, isolated regions, suggestive of deposits, were seen in the left ventricular myocardium on MRI. Both these patients had abnormal ECGs and signs of systolic and/or diastolic dysfunction on echocardiography. LVEF was subnormal in seven of 10 of the ECG+ patients and in two of six of the ECG,. Signs of diastolic dysfunction were found in 59% and 56% of the measurements in the ECG+ and ECG, patients, respectively. Conclusion. We conclude (i) that myocardial deposits on MRI in sarcoidosis patients have a high specificity for cardiac involvement but a rather low sensitivity; (ii) that a substantial proportion of sarcoidosis patients with abnormal ECGs have echocardiographic signs of systolic and/or diastolic dysfunction. [source] Manganese ions as intracellular contrast agents: proton relaxation and calcium interactions in rat myocardiumNMR IN BIOMEDICINE, Issue 2 2003Wibeke Nordhųy Abstract Paramagnetic manganese (Mn) ions (Mn2+) are taken up into cardiomyocytes where they are retained for hours. Mn content and relaxation parameters, T1 and T2, were measured in right plus left ventricular myocardium excised from isolated perfused rat hearts. In the experiments 5,min wash-in of MnCl2 were followed by 15,min wash-out to remove extracellular (ec) Mn2+ MnCl2, 25 and 100,µM, elevated tissue Mn content to six and 12 times the level of control (0,µM MnCl2). Variations in perfusate calcium (Ca2+) during wash-in of MnCl2 and experiments including nifedipine showed that myocardial slow Ca2+ channels are the main pathway for Mn2+ uptake and that Mn2+ acts as a pure Ca2+ competitor and a preferred substrate for slow Ca2+ channel entry. Inversion recovery analysis at 20,MHz revealed two components for longitudinal relaxation: a short T1,,,1 and a longer T1,,,2. Approximate values for control and Mn-treated hearts were in the range 600,125,ms for T1,,,1 and 2200,750,ms for T1,,,2. The population fractions were about 59 and 41% for the short and the long component, respectively. The intracellular (ic) R1,,,1 and R2,,,1 correlated best with tissue Mn content. Applying two-site exchange analyses on the obtained T1 data yielded results in parallel to, but also differing from, results reported with an ec contrast agent. The calculated lifetime of ic water (,ic) of about 10,s is compatible with a slow water exchange in the present excised cardiac tissue. The longitudinal relaxivity of Mn ions in ic water [60 (s mM),1] was about one order of magnitude higher than that of MnCl2 in water in vitro [6.9 (s mM),1], indicating that ic Mn-protein binding is an important potentiating factor in relaxation enhancement. Copyright © 2003 John Wiley & Sons, Ltd. [source] X-linked fetal cardiomyopathy caused by a novel mutation in the TAZ genePRENATAL DIAGNOSIS, Issue 5 2006April N. Brady Abstract Objectives Mutations in the tafazzin (TAZ) gene at chromosomal locus Xq28 are responsible for Barth syndrome (BTHS), X-linked endocardial fibroelastosis (EFE), X-linked fatal infantile dilated cardiomyopathy (CMD3A), and familial isolated noncompaction of left ventricular myocardium (INVM). This evaluation was performed to determine if a known familial TAZ gene mutation might present with abnormal fetal cardiac pathology findings as early as the second trimester of pregnancy. Methods Prenatal diagnosis revealed that a male fetus was positive for a known familial arg94his TAZ gene mutation. An elective termination with subsequent fetal pathology examination was performed at 18 weeks' gestation. Results Fetal examination revealed cardiomegaly, EFE, and subendocardial vacuolization of the myocytes. Conclusion Characteristic cardiac pathology findings of a TAZ gene mutation are seen in a fetus at 18 weeks' gestation. To our knowledge, this case provides the earliest fetal pathologic description of a TAZ cardiomyopathy. Copyright © 2006 John Wiley & Sons, Ltd. [source] Three-dimensional architecture of the left ventricular myocardiumTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2006Paul P. Lunkenheimer Abstract Concepts for ventricular function tend to assume that the majority of the myocardial cells are aligned with their long axes parallel to the epicardial ventricular surface. We aimed to validate the existence of aggregates of myocardial cells orientated with their long axis intruding obliquely between the ventricular epicardial and endocardial surfaces and to quantitate their amount and angulation. To compensate for the changing angle of the long axis of the myocytes relative to the equatorial plane of the ventricles with varying depths within the ventricular walls, the so-called helical angle, we used pairs of cylindrical knives of different diameters to punch semicircular slices from the left ventricular wall of pigs, the slices extending from the epicardium to the endocardium. The slices were pinned flat, fixed in formaldehyde, embedded in paraffin, sectioned, stained with azan or hematoxilin and eosin, and analyzed by a new semiautomatic procedure. We made use of new techniques in informatics to determine the number and angulation of the aggregates of myocardial cells cut in their long axis. The alignment of the myocytes cut longitudinally varied markedly between the epicardium and the endocardium. Populations of myocytes, arranged in strands, diverge by varying angles from the epicardial surface. When paired knives of decreasing diameter were used to cut the slices, the inclination of the diagonal created by the arrays increases, while the lengths of the array of cells cut axially decreases. The visualization of the size, shape, and alignment of the myocytic arrays at any side of the ventricular wall is determined by the radius of the knives used, the range of helical angles subtended by the alignment of the myocytes throughout the thickness of the wall, and their angulation relative to the epicardial surface. Far from the majority of the ventricular myocytes being aligned at angles more or less tangential to the epicardial lining, we found that three-fifths of the myocardial cells had their long axes diverging at angles between 7.5 and 37.5° from an alignment parallel to the epicardium. This arrangement, with the individual myocytes supported by connective tissue, might control the cyclic rearrangement of the myocardial fibers. This could serve as an important control of both ventricular mural thickening and intracavitary shape. Anat Rec Part A 288A:565,578, 2006. © 2006 Wiley-Liss, Inc. [source] | |||||||||||||