Ventricular Tissue (ventricular + tissue)

Distribution by Scientific Domains

Selected Abstracts

Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Simulation Study Using a Dynamic Mechanoelectric Model of Ventricular Tissue

SATOKO HIRABAYASHI master of environment
Introduction: To investigate the mechanisms underlying the increased prevalence of ventricular fibrillation (VF) in the mechanically compromised heart, we developed a fully coupled electromechanical model of the human ventricular myocardium. Methods and Results: The model formulated the biophysics of specific ionic currents, excitation,contraction coupling, anisotropic nonlinear deformation of the myocardium, and mechanoelectric feedback (MEF) through stretch-activated channels. Our model suggests that sustained stretches shorten the action potential duration (APD) and flatten the electrical restitution curve, whereas stretches applied at the wavefront prolong the APD. Using this model, we examined the effects of mechanical stresses on the dynamics of spiral reentry. The strain distribution during spiral reentry was complex, and a high strain-gradient region was located in the core of the spiral wave. The wavefront around the core was highly stretched, even at lower pressures, resulting in prolongation of the APD and extension of the refractory area in the wavetail. As the left ventricular pressure increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated the wave breakup and meandering of tips through interactions between the wavefront and wavetail. Conclusions: This simulation study indicates that mechanical loading promotes meandering and wave breaks of spiral reentry through MEF. Mechanical loading under pathological conditions may contribute to the maintenance of VF through these mechanisms. [source]

Comparison of effects of acetylcholine on electromechanical characteristics in guinea-pig atrium and ventricle

W. J. Zang
The direct negative effects of acetylcholine (ACh) on guinea-pig atria and ventricles were investigated using standard microelectrodes, a force transducer and a video edge-detection system. It was found that: (1) ACh (at 0.001,100 ,m) decreased the force of contraction and shortened the action potential duration (APD) in both atria and ventricles in a concentration-dependent manner, and that the atria were more sensitive to ACh than the ventricles; and (2) the direct negative inotropic effect of ACh (1 ,m) on an isolated cardiac cell was similar to that on the isolated myocardium. But this effect was not present in all isolated ventricular cells, while all the atrial cells responded to ACh. In conclusion, ACh had direct inhibitory effects on both atrial and ventricular tissue and myocytes, although the effects were greater in atria than in ventricles; and the negative inotropic effect of ACh was closely related to the shortening of the APD. [source]

Effect of sodium houttuyfonate on myocardial hypertrophy in mice and rats

Jian Ping Gao
Abstract Objectives The aim of the study was to determine the effect of sodium houttuyfonate on myocardial hypertrophy and its mechanism of action in mice and rats. Methods A mouse model of myocardial hypertrophy was established by subcutaneous injection with isoproterenol. Mice were randomly divided into five groups: normal control; isoproterenol control; isoproterenol plus metoprolol; isoproterenol plus low- and high-dose sodium houttuyfonate. A rat model of myocardial hypertrophy was established by intraperitoneal injection with l -thyroxine. Rats were randomly divided into five groups: normal control; l -thyroxine control; l -thyroxine plus captopril; l -thyroxine plus low- and high-dose sodium houttuyfonate. At the end of the experiments, the left ventricular weight index and heart weight index were determined in mice and rats, the size of cardiomyocytes was measured in rats and the concentrations of cAMP in plasma and angiotensin II in ventricular tissue of mice were detected by radioimmunoassay. The endothelin-1 concentration was measured by radioimmunoassay and the hydroxyproline content was measured by a digestive method in ventricular tissue of rats. Key findings After 7,9 days of treatment, sodium houttuyfonate significantly reduced the left ventricular weight index and heart weight index in mice and rats with myocardial hypertrophy, decreased the size of cardiomyocytes in rats, and reduced the content of cAMP and angiotensin II in mice with myocardial hypertrophy. It also decreased the endothelin-1 concentration and the hydroxyproline content in ventricular tissue in rats. Conclusions Sodium houttuyfonate can inhibit myocardial hypertrophy in mouse and rat models by restricting the activity of the sympathetic nervous system and decreasing the levels of angiotensin II and endothelin-1 in ventricular tissue. [source]

The Effect of Ablation Electrode Length and Catheter Tip to Endocardial Orientation on Radiofrequency Lesion Size in the Canine Right Atrium

CHAN, R.C., et al.: The Effect of Ablation Electrode Length and Catheter Tip to Endocardial Orientation on Radiofrequency Lesion Size in the Canine Right Atrium. Although the determinants of radiofrequency lesion size have been characterized in vitro and in ventricular tissue in situ, the effects of catheter tip length and endocardial surface orientation on lesion generation in atrial tissue have not been studied. Therefore, the dimensions of radiofrequency lesions produced with 4-, 6-, 8-, 10-, and 12-mm distal electrode lengths were characterized in 26 closed-chested dogs. The impact of parallel versus perpendicular catheter tip/endocardial surface orientation, established by biplane fluoroscopy and/or intracardiac echocardiography, on lesion dimensions was also assessed. Radiofrequency voltage was titrated to maintain a steady catheter tip temperature of 75C for 60 seconds. With a perpendicular catheter tip/tissue orientation, the lesion area increased from 29 7 mm2 with a 4-mm tip to 42 12 mm2 with the 10-mm tip, but decreased to 29 8 mm2 with ablation via a 12-mm tip. With a parallel distal tip/endocardial surface orientation, lesion areas were significantly greater: 54 22 mm2 with a 4-mm tip, 96 28 mm2 with a 10- mm tip and 68 24 mm2 with a 12-mm tip (all P < 0.001 vs perpendicular orientation). Lesion lengths and apparent volumes were larger with parallel, compared to perpendicular tip/tissue orientations, although lesion depth was independent of catheter tip length with both catheter tip/tissue orientations. Electrode edge effects were not observed with any tip length. Direct visualization using intracardiac ultrasound guidance was subjectively helpful in insuring an appropriate catheter tip/tissue interface needed to maximize lesion size. Although atrial lesion size is critically dependent on catheter tip length, it is more influenced by the catheter orientation to the endocardial surface. This information may also be helpful in designing electrode arrays for the creation of continuous linear lesions for the elimination of complex atrial tachyarrhythmias. [source]

Phosphodiesterase inhibition by naloxone augments the inotropic actions of ,-adrenergic stimulation

Background: In a shock state, naloxone generates the cardiovascular pressor effect by displacing the endogenous opiate-like peptide ,-endorphin, resulting in restoration of the normal response to catecholamines. In addition to this opioid antagonistic effect, the non-opiate receptor-mediated effect has also been proposed. The aim of this study was to define the mechanism of non-opiate receptor-mediated action of naloxone. Methods: In guinea-pig ventricular tissues, cumulative concentration,response curves for isoproterenol as well as for forskolin and 3-isobutylmethylxanthine (IBMX) were obtained by increasing the concentration stepwise. To assess the effect on the phosphodiesterase (PDE), the effects of naloxone on contractile forces induced by isoproterenol (0.05 ,M) in the presence of IBMX, cilostamide (a PDE III inhibitor), or rolipram (a PDE IV inhibitor) were observed. Naloxone-induced changes in cAMP production by isoproterenol both in the absence and in the presence of IBMX were measured. Naloxone-induced changes in cAMP production by forskolin in the presence of IBMX were also measured. Results: Naloxone (30 ,M) produced a leftward shift of the isoproterenol concentration,response curve (0.01,2 ,M) without changing the maximal response. Forskolin (0.5,10 ,M) produced a concentration-dependent increase in contractile forces. Naloxone increased the maximal inotropic response of forskolin. Naloxone showed no effect on the IBMX concentration,response curve. In the presence of IBMX (200 ,M), naloxone did not alter the contractions evoked by isoproterenol or forskolin. Whereas naloxone increased contractile forces significantly (approximately 25%) more than that of isoproterenol in the presence of rolipram, no alteration of contractile forces in the cilostamide-incubated muscles was observed. Naloxone caused a concentration-related increase of cAMP in the absence of IBMX, but caused no change in its presence. Conclusions: The enhancement of myocardial contractility by naloxone in the presence of stimulation of adenylyl cyclase activity appears to be mediated by inhibition of PDE, specifically PDE III. [source]