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Whole Heart (whole + heart)
Selected AbstractsEffects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic InnervationEXPERIMENTAL PHYSIOLOGY, Issue 3 2001G. André Ng A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source] Mechanisms of exercise-induced improvements in the contractile apparatus of the mammalian myocardiumACTA PHYSIOLOGICA, Issue 4 2010O. J. Kemi Abstract One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction. For instance, myocardial improvements may still be observed after exercise training in post-myocardial infarction heart failure. In both health and disease, it is the changes that occur in the individual cardiomyocytes with respect to their ability to contract that by and large drive the exercise training-induced adaptation to the heart. Here, we review the evidence and the mechanisms by which exercise training induces beneficial changes in the mammalian myocardium, as obtained by means of experimental and clinical studies, and argue that these changes ultimately alter the function of the whole heart and contribute to the changes in whole-body function. [source] Effects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic InnervationEXPERIMENTAL PHYSIOLOGY, Issue 3 2001G. André Ng A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source] Correction for heart rate variability during 3D whole heart MR coronary angiographyJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2008Stijntje D. Roes MD Abstract Purpose To evaluate the effect of a real-time adaptive trigger delay on image quality to correct for heart rate variability in 3D whole-heart coronary MR angiography (MRA). Materials and Methods Twelve healthy adults underwent 3D whole-heart coronary MRA with and without the use of an adaptive trigger delay. The moment of minimal coronary artery motion was visually determined on a high temporal resolution MRI. Throughout the scan performed without adaptive trigger delay, trigger delay was kept constant, whereas during the scan performed with adaptive trigger delay, trigger delay was continuously updated after each RR-interval using physiological modeling. Signal-to-noise, contrast-to-noise, vessel length, vessel sharpness, and subjective image quality were compared in a blinded manner. Results Vessel sharpness improved significantly for the middle segment of the right coronary artery (RCA) with the use of the adaptive trigger delay (52.3 ± 7.1% versus 48.9 ± 7.9%, P = 0.026). Subjective image quality was significantly better in the middle segments of the RCA and left anterior descending artery (LAD) when the scan was performed with adaptive trigger delay compared to constant trigger delay. Conclusion Our results demonstrate that the use of an adaptive trigger delay to correct for heart rate variability improves image quality mainly in the middle segments of the RCA and LAD. J. Magn. Reson. Imaging 2008;27:1046,1053. © 2008 Wiley-Liss, Inc. [source] Whole-heart coronary magnetic resonance angiography at 3 Tesla in 5 minutes with slow infusion of Gd-BOPTA, a high-relaxivity clinical contrast agentMAGNETIC RESONANCE IN MEDICINE, Issue 1 2007Xiaoming Bi Abstract T1 -shortening contrast agents have been used to improve the depiction of coronary arteries with breath-hold magnetic resonance angiography (MRA). The spatial resolution and coverage are limited by the duration of the arterial phase of the contrast media passage. In this study we investigated the feasibility of acquiring free-breathing, whole-heart coronary MRA during slow infusion of the contrast media (0.3 ml/s) for prolonged blood signal enhancement time. Ultrashort TR (3 ms) and parallel data acquisition were used to allow the whole-heart MRA in approximately 5 min. A newly approved gadolinium (Gd)-based high T1 relaxivity contrast agent, gadobenate dimeglumine ([Gd-BOPTA]2,), was used and coronary MRA was performed on a whole-body 3 Tesla (T) system to improve the signal-to-noise ratio (SNR). Results from eight volunteers demonstrate that this coronary MRA method is capable of imaging the whole heart in 4.5 ± 0.6 min. Major coronary arteries are well depicted with high SNR (42.4 ± 12.5) and contrast-to-noise ratio (CNR; 27.1 ± 7.6). Magn Reson Med 58:1,7, 2007. © 2007 Wiley-Liss, Inc. [source] Side-to-side linking of myocardial cells in hypertrophic cardiomyopathy: Whole heart microscopic observation with tangential sectionsPATHOLOGY INTERNATIONAL, Issue 11 2005Hirotake Masuda By cross-section or longitudinal section, it is difficult to investigate longitudinal features of myocardial cells in the whole heart. Here, introducing the use of tangential sections to obtain longitudinal aspect of myocardial cells in any part of myocardium, the authors evaluated myocardium in the left ventricle in 10 normal hearts and four hearts with hypertrophic cardiomyopathy (HCM). Tangential sections were obtained by peeling the superficial layer of myocardium. After peeling the whole surface, secondary deep layer was peeled. These procedures were repeated more than five times through the wall. Intercalated discs (ICD) were observed immunohistochemically with anti-N-cadherin and antidesmoplakin. In normal hearts, myocardial cells were cut longitudinally and ran parallel in tangential sections. They linked end-to-end with simple and regular ICD with average lengths of 120,130 µm and average sarcomere numbers of 56,65. In HCM hearts, many myocardial cells were cut almost longitudinally running approximately parallel in tangential sections. Myocardial cells frequently showed side-to-side linking characterized by skewed ICD, indistinct ICD counterparts, and longitudinally arranged ICD. Two young HCM hearts had circle-shaped ICD and vacuole-like structures highlighted by immunostaining for N-cadherin, which were actually extracellular structures comparable with irregular side-to-side linking. It is considered that side-to-side linking of myocardial cells is a characteristic microscopic feature in HCM rather than myocardial disarray. [source] Nondestructive optical determination of fiber organization in intact myocardial wallMICROSCOPY RESEARCH AND TECHNIQUE, Issue 7 2008Rebecca M. Smith Abstract Mapping the myocardial fiber organization is important for assessing the electrical and mechanical properties of normal and diseased hearts. Current methods to determine the fiber organization have several limitations: histological sectioning mechanically distorts the tissue and is labor-intensive, while diffusion tensor imaging has low spatial resolution and requires expensive MRI scanners. Here, we utilized optical clearing, a fluorescent dye, and confocal microscopy to create three-dimensional reconstructions of the myocardial fiber organization of guinea pig and mouse hearts. We have optimized the staining and clearing procedure to allow for the nondestructive imaging of whole hearts with a thickness up to 3.5 mm. Myocardial fibers could clearly be identified at all depths in all preparations. We determined the change of fiber orientation across strips of guinea pig left ventricular wall. Our study confirms the qualitative result that there is a steady counterclockwise fiber rotation across the ventricular wall. Quantitatively, we found a total fiber rotation of 105.7 ± 14.9° (mean ± standard error of the mean); this value lies within the range reported by previous studies. These results show that optical clearing, in combination with a fluorescent dye and confocal microscopy, is a practical and accurate method for determining myocardial fiber organization. Microsc. Res. Tech., 2008. © 2008 Wiley-Liss, Inc. [source] Differential expression of cardiac mitochondrial proteinsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 3 2008Julia R. Smith Abstract Mitochondria were isolated from whole hearts of Dahl salt sensitive (SS) and chromosome 13 consomic control (SS.13BN/Mcwi) rats using a mechanical homogenization process followed by density centrifugation. The proteins present in the two mitochondria preparations were quantified; equal amounts of protein from each sample were taken and trypsinized in the presence of either 16O or 18O before pooling. Incorporation of one or two 18O atoms at the C-terminus of the peptide cleaved by trypsin allows the distinction between the two samples. The proteins were identified by automated MS/MS sequencing and relative amounts of each protein assessed by comparison of the intensities of the constituent peptides. Relative quantification was performed using the ZoomQuant (v1.24) software. Nine proteins were found to be differentially expressed. Electron transfer flavoprotein alpha (P13803, ETFA) protein expression was two-fold lower in the SS compared to the SS.13BN. This was confirmed by Western blot and 2-DE gel quantification. Potential functional implications of this differential expression include an impaired capacity of the heart to oxidize fatty acids in the SS strain compared to the control. Mathematical modeling of mitochondrial electron transport predicted that the observed change in ETFA expression may result in decreased activity of the electron transport chain. [source] EPIGALLOCATECHIN-3-GALLATE ATTENUATES CARDIAC HYPERTROPHY IN HYPERTENSIVE RATS IN PART BY MODULATION OF MITOGEN-ACTIVATED PROTEIN KINASE SIGNALSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2009Dan-Dan Chen SUMMARY 1It has been demonstrated that epigallocatechin-3-gallate (EGCG) inhibits cardiac hypertrophy through its antihypertensive and anti-oxidant effects. However, the underlying molecular mechanism is not clear. 2In the present study, we tested the hypothesis that EGCG attenuates transaortic abdominal aortic constriction (TAC)-induced ventricular hypertrophy by regulating mitogen-activated protein kinase (MAPK) signal pathways in hypertensive rats. Four groups of rats were used: (i) a sham-operated control group; (ii) an EGCG-treated (50 mg/kg per day, i.p., for 21 days) sham-operated group; (iii) a TAC group; and (iv) an EGCG-treated TAC group. Histological analysis of whole hearts and biochemical analyses of left ventricular (LV) tissue were used to investigate the effects of EGCG. 3The results showed that the LV myocyte diameter and the expression of atrial natriuretic peptide, brain natriuretic peptide and ,-myocardial heavy chain were significantly decreased in the EGCG-treated (50 mg/kg per day, i.p.) TAC group. Levels of reactive oxygen species and malondialdehyde in the lV were significantly reduced by EGCG in the TAC group. Total superoxide dismutase, catalase and glutathione peroxidase activities were decreased in the TAC group, and this decrease was significantly restored by EGCG treatment. Phosphorylation of extracellular signal-regulated kinase 2, p38 and c-Jun N-terminal kinase 1 was significantly reversed in the LV of EGCG-treated TAC rats (40%, 53% and 52%vs TAC, respectively), accompanied by significant inhibition of nuclear factor-,B and activator protein-1. Transaortic abdominal aortic constriction significantly upregulated LV expression of matrix metalloproteinase-9 from 32 ± 6 to 100 ± 12% and this increase was inhibited by EGCG treatment (from 100 ± 12 to 50 ± 15%). In addition, TAC decreased mitochondrial DNA copy number and the activity of respiratory chain complexes I (from 100 ± 7 to 68 ± 5%), III (from 100 ± 4 to 2 ± 5%) and IV (from 766 ± 2 to 100 ± 5%); this decrease was reversed by EGCG treatment to levels seen in sham-operated rats. 4In conclusion, EGCG attenuates TAC-induced ventricular hypertrophy in hypertensive rats in part by suppression of anti-oxidant enzymes and regulation of MAPK signals. [source] |