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Ventricular Muscle (ventricular + muscle)
Selected AbstractsDesign of an Artificial Left Ventricular Muscle: An Innovative Way to Actuate Blood Pumps?ARTIFICIAL ORGANS, Issue 6 2009Benjamin Van Der Smissen Abstract Blood pumps assist or take over the pump function of a failing heart. They are essentially activated by a pusher plate, a pneumatic compression of collapsible sacs, or they are driven by centrifugal pumps. Blood pumps relying upon one of these actuator mechanisms do not account for realistic wall deformation. In this study, we propose an innovative design of a blood pump actuator device which should be able to mimic fairly well global left ventricular (LV) wall deformation patterns in terms of circumferential and longitudinal contraction, as well as torsion. In order to reproduce these basic wall deformation patterns in our actuator device, we designed a novel kind of artificial LV "muscle" composed of multiple actively contracting cells. Its contraction is based on a mechanism by which pressurized air, inside such a cell, causes contraction in one direction and expansion perpendicular to this direction. The organization and geometry of the contractile cells within one artificial LV muscle, the applied pressure in the cells, and the governing LV loading conditions (preload and afterload) together determine the global deformation of the LV wall. Starting from a simple plastic bag, an experimental model based on the abovementioned principle was built and connected to a lumped hydraulic model of the vascular system (including compliance and resistance). The wall deformation pattern of this device was validated visually and its pump performance was studied in terms of LV volume and pressure and heart rate. Our experimental results revealed (i) a global LV motion resembling a real LV, and (ii) a close correlation between our model and a real LV in terms of end-systolic volume and pressure, end-diastolic volume and pressure, stroke volume, ejection fraction and pressure-volume relationship. Our proposed model appears promising and it can be considered as a step forward when compared to currently applied actuator mechanisms, as it will likely result in more physiological intracavity blood flow patterns. [source] Epsilon-Like Electrocardiographic Pattern in a Patient with Brugada SyndromeANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009Ozcan Ozeke M.D. Both Brugada syndrome (BrS) and arrhythmogenic right ventricle dysplasia/cardiomyopathy (ARVD/C) can cause repolarization abnormalities in right precordial leads and predispose to sudden cardiac death (SCD) due to ventricular arrhythmias. Although there is controversy over whether BrS is distinct from ARVD/C, it is believed that both are different clinical entities with respect to both the clinical presentation and the genetic predisposition. The coexistence of these two relatively rare clinical entities is also reported, but, some hypothesized that it is more possible that disease of the right ventricular muscle might accentuate the Brugada electrocardiographic pattern. In clinic practice, there may be cases where the dividing line is not so clear. We report a 33-year-old male presenting with recurrent syncope, who has a peculiar pattern of coved-type ST-segment elevation (ST-SE) with epsilon-like wave in right precordial leads. [source] Different sensitivity of isoprenaline-induced responses in ventricular muscle to sodium nitroprusside in normotensive and spontaneously hypertensive rats 1AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2000A. M. Manso 1 The aim of the present work was to study the possible modulatory role of nitric oxide (NO) on the positive inotropic effect induced by the ,-adrenoceptor agonist isoprenaline in myocardial contractility, and whether this modulation is altered by hypertension. 2 The study was performed using right ventricular strips from the hearts of 6-month-old male Wistar,Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The contractile force of electrically-stimulated ventricular strips was measured by a force-displacement transducer. 3 Isoprenaline (from 10 nmol l,1 to 10 ,mol l,1) induced a concentration-dependent increase in cardiac contractility in strips from both rat strains. This positive inotropic effect to isoprenaline was reduced by the NO donor sodium nitroprusside (SNP, 0.1 mmol l,1) in muscles from WKY rats and slightly increased in those from SHR. The SNP-induced increase in strips from SHR was abolished by superoxide dismutase (100 U ml,1). 4 NG-nitro-arginine-methyl ester (L-NAME, 0.1 mmol l,1) and 1H-[1,2,4]oxadiazolo[4,3]quinoxalin-1-one (ODQ, 10 ,mol l,1), respective inhibitors of NO synthase and guanylate cyclase, increased the response to isoprenaline in muscles from WKY rats, whereas it was unaltered in strips from SHR. 5 In strips from WKY rats, the combination of ODQ and SNP produced an increase in the response elicited by isoprenaline, which was similar to that observed with ODQ or L-NAME. 8-Br-cyclicGMP (8-Br-cGMP, 0.1 mmol l,1), a permeable and structural cGMP analogue, decreased the effect induced by isoprenaline only in muscles from WKY rats. 6 These results suggest that the positive inotropic response to isoprenaline in ventricular strips from WKY rats is negatively modulated by NO, and positively by superoxide anions in those from SHR. The lack of a modulatory response to NO in ventricular strips from SHR is probably a result of an alteration of mechanisms in NO-signalling pathway downstream of cGMP formation in SHR hearts. [source] Inhibition of cardiac Na+ current by primaquineBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2002Gerardo Orta-Salazar The electrophysiological effects of the anti-malarial drug primaquine on cardiac Na+ channels were examined in isolated rat ventricular muscle and myocytes. In isolated ventricular muscle, primaquine produced a dose-dependent and reversible depression of dV/dt during the upstroke of the action potential. In ventricular myocytes, primaquine blocked INa+ in a dose-dependent manner, with a Kd of 8.2 ,M. Primaquine (i) increased the time to peak current, (ii) depressed the slow time constant of INa+ inactivation, and (iii) slowed the fast component for recovery of INa+ from inactivation. Primaquine had no effect on: (i) the shape of the I , V curve, (ii) the reversal potential for Na+, (iii) the steady-state inactivation and gNa+ curves, (iv) the fast time constant of inactivation of INa+, and (v) the slow component of recovery from inactivation. Block of INa+ by primaquine was use-dependent. Data obtained using a post-rest stimulation protocol suggested that there was no closed channel block of Na+ channels by primaquine. These results suggest that primaquine blocks cardiac Na+ channels by binding to open channels and unbinding either when channels move between inactivated states or from an inactivated state to a closed state. Cardiotoxicity observed in patients undergoing malaria therapy with aminoquinolines may therefore be due to block of Na+ channels, with subsequent disturbances of impulse conductance and contractility. British Journal of Pharmacology (2002) 135, 751,763; doi:10.1038/sj.bjp.0704460 [source] Lack of Effect of Conduction Direction on Action Potential Durations in Anisotropic Ventricular Strips of Pig HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2002GUILLERMO BERTRAN B.Sc. Anisotropy and Repolarization.Introduction: The influence of activation sequence on the rate of rise of the depolarization phase of action potentials in atrial or ventricular muscles has been well established. However, whether myocardial fiber orientation is important in modulating the repolarization process is unclear. Methods and Results: We examined the influence of activation sequence on the repolarization phase of action potentials in epicardial tissues from the right and left ventricles of domestic pigs. Whereas cells from the right ventricle exhibited direction-dependent differences in action potential duration at 30%, 50%, and 90% of full repolarization (190.6 ± 31.1 msec vs 181.8 ± 32.8 msec, 240.3 ± 23.5 msec vs 236.7 ± 25.4 msec, and 291.3 ± 23.7 msec vs 287.4 ± 25.1 msec for longitudinal and transverse propagation, respectively; P < 0.001), a similar duration of repolarization during both directions of propagation was observed in cells from the left ventricle at 50% and 90% of full repolarization (241.4 ± 39.4 msec and 285.5 ± 39.5 msec vs 240.4 ± 38.9 msec and 284.9 ± 39.6 msec for longitudinal and transverse propagation respectively; P = NS). A slight but significant difference was found at 30% of full repolarization in cells from the left ventricle (190.4 ± 39.0 msec vs 187.0 ± 38.0 msec for longitudinal and transverse propagation, respectively; P < 0.05). In the left ventricle, the duration of repolarization did not change as the distance between the recording site and stimulation site increased. Conclusion: The direction of wavefront propagation with respect to fiber orientation may not play an important role in modulating the duration of repolarization in epicardial cells from the left ventricle. [source] | |||||||||||||||||||