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Relevant bibliographies by topics / Rat Ventricular

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Academic literature on the topic 'Rat Ventricular'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "Rat Ventricular"

1

Zhao, Guiling, and W. Jonathan Lederer. "STIM1 in Rat Ventricular Myocytes." Biophysical Journal 100, no. 3 (February 2011): 196a. http://dx.doi.org/10.1016/j.bpj.2010.12.1288.

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Rossi, Stefano, Silvana Baruffi, Andrea Bertuzzi, Michele Miragoli, Domenico Corradi, Roberta Maestri, Rossella Alinovi, et al. "Ventricular activation is impaired in aged rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (December 2008): H2336—H2347. http://dx.doi.org/10.1152/ajpheart.00517.2008.

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Ventricular arrhythmias are frequently observed in the elderly population secondary to alterations of electrophysiological properties that occur with the normal aging process of the heart. However, the underlying mechanisms remain poorly understood. The aim of the present study was to determine specific age-related changes in electrophysiological properties and myocardial structure in the ventricles that can be related to a structural-functional arrhythmogenic substrate. Multiple unipolar electrograms were recorded in vivo on the anterior ventricular surface of four control and seven aged rats during normal sinus rhythm and ventricular pacing. Electrical data were related to morphometric and immunohistochemical parameters of the underlying ventricular myocardium. In aged hearts total ventricular activation time was significantly delayed (QRS duration: +69%), while ventricular conduction velocity did not change significantly compared with control hearts. Moreover, ventricular activation patterns displayed variable numbers of epicardial breakthrough points whose appearance could change with time. Morphological analysis in aged rats revealed that heart weight and myocyte transverse diameter increased significantly, scattered microfoci of interstitial fibrosis were mostly present in the ventricular subendocardium, and gap junction connexin expression decreased significantly in ventricular myocardium compared with control rats. Our results show that in aged hearts delayed total ventricular activation time and abnormal activation patterns are not due to delayed myocardial conduction and suggest the occurrence of impaired impulse propagation through the conduction system leading to uncoordinated myocardial excitation. Impaired interaction between the conduction system and ventricular myocardium might create a potential reentry substrate, contributing to a higher incidence of ventricular arrhythmias in the elderly population.

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GUIDERI, G., C. HEALY, L. KORCEK, and W. GUTSTEIN. "Ventricular fibrillation and the Brattleboro rat." Journal of Molecular and Cellular Cardiology 17, no. 7 (July 1985): 717–20. http://dx.doi.org/10.1016/s0022-2828(85)80071-7.

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NANASI, P. P., C. PANKUCSI, T. BANYASZ, P. SZIGLIGETI, J. Gy PAPP, and A. VARRO. "Electrical restitution in rat ventricular muscle." Acta Physiologica Scandinavica 158, no. 2 (October 1996): 143–53. http://dx.doi.org/10.1046/j.1365-201x.1996.541304000.x.

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5

Krishna, Abhilash, Miguel Valderrabano, Philip T. Palade, and John W. Clark. "Ca2+ Signaling in Rat Ventricular Myocytes." Biophysical Journal 102, no. 3 (January 2012): 509a. http://dx.doi.org/10.1016/j.bpj.2011.11.2790.

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Weber dos Santos, Rodrigo, Anders Nygren, Fernando Otaviano Campos, Hans Koch, and Wayne R. Giles. "Experimental and theoretical ventricular electrograms and their relation to electrophysiological gradients in the adult rat heart." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (October 2009): H1521—H1534. http://dx.doi.org/10.1152/ajpheart.01066.2008.

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The electrical activity of adult mouse and rat hearts has been analyzed extensively, often as a prerequisite for genetic engineering studies or for the development of rodent models of human diseases. Some aspects of the initiation and conduction of the cardiac action potential in rodents closely resemble those in large mammals. However, rodents have a much higher heart rate and their ventricular action potential is triangular and very short. As a consequence, an interpretation of the electrocardiogram in the mouse and rat remains difficult and controversial. In this study, optical mapping techniques have been applied to an in vitro left ventricular adult rat preparation to obtain patterns of conduction and action potential duration measurements from the epicardial surface. This information has been combined with previously published mathematical models of the rat ventricular myocyte to develop a bidomain model for action potential propagation and electrogram formation in the rat left ventricle. Important insights into the basis for the repolarization waveform in the ventricular electrogram of the adult rat have been obtained. Notably, our model demonstrated that the biphasic shape of the rat ventricular repolarization wave can be explained in terms of the transmural and apex-to-base gradients in action potential duration that exist in the rat left ventricle.

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von Planta, I., M. H. Weil, M. von Planta, J. Bisera, S. Bruno, R. J. Gazmuri, and E. C. Rackow. "Cardiopulmonary resuscitation in the rat." Journal of Applied Physiology 65, no. 6 (December 1, 1988): 2641–47. http://dx.doi.org/10.1152/jappl.1988.65.6.2641.

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A standardized method of cardiopulmonary resuscitation in rodents has been developed for anesthetized, mechanically ventilated rats. Ventricular fibrillation was induced and maintained by an alternating current delivered to the right ventricular endocardium. After 4 min of ventricular fibrillation, the chest was compressed with a pneumatic piston device. Eight of 14 animals were successfully resuscitated with DC countershock after 6 min of cardiac arrest. In confirmation of earlier studies from our laboratories in dogs, pigs, and human patients, this rodent model of cardiopulmonary resuscitation demonstrated large venoarterial [H+] and PCO2 gradients associated with reduced pulmonary excretion of CO2 during the low-flow state. Mean aortic pressure, coronary perfusion pressure, and end-tidal CO2 during chest compression were predictive of successful resuscitation.

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Fang, Xiangshao, Wanchun Tang, Shijie Sun, Lei Huang, Yun-Te Chang, Zitong Huang, and Max Harry Weil. "Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia." Journal of Applied Physiology 101, no. 4 (October 2006): 1091–96. http://dx.doi.org/10.1152/japplphysiol.01487.2005.

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Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

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Springhorn, J. P., and W. C. Claycomb. "Translation of heart preproenkephalin mRNA and secretion of enkephalin peptides from cultured cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 5 (November 1, 1992): H1560—H1566. http://dx.doi.org/10.1152/ajpheart.1992.263.5.h1560.

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Rat ventricular cardiac muscle has previously been shown to contain exceptionally high levels of preproenkephalin mRNA (ppEnk mRNA). We have recently determined that the level of ppEnk mRNA is developmentally and hormonally regulated in rat ventricular cardiac muscle tissue and in cultured myocytes (J. P. Springhorn and W. C. Claycomb. Biochem. J. 258: 73-77, 1989). We demonstrate in the current study that heart ppEnk mRNA is structurally identical at the 5' end to brain ppEnk mRNA using a ribonuclease protection assay and that heart ppEnk mRNA can be translated in vitro using a rabbit reticulocyte lysate system. In vitro synthesized preproenkephalin peptides were immunoprecipitated with a polyclonal antibody directed to the carboxy-terminal seven amino acids of preproenkephalin. We have also established by radioimmunoassay that enkephalin-containing peptides are secreted from cultured neonatal and adult rat ventricular cardiac muscle cells. This secretion is linear with respect to time and can be stimulated by phorbol 12-myristate 13-acetate (PMA) and adenosine 3',5'-cyclic monophosphate (cAMP). It was determined by column chromatography that cAMP induced neonatal rat ventricular cardiac muscle cells to secrete Met5-enkephalin-Arg6-Phe7, whereas PMA plus 3-isobutyl-1-methylxanthine induced adult rat ventricular cardiac muscle cells to secrete Met5-enkephalin. These studies establish that ventricular heart muscle ppEnk mRNA can be translated and that enkephalin peptides are secreted from ventricular cardiac muscle cells.

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Weikert, C. "Cellular engineering of ventricular adult rat cardiomyocytes." Cardiovascular Research 59, no. 4 (October 1, 2003): 874–82. http://dx.doi.org/10.1016/s0008-6363(03)00508-x.

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Dissertations / Theses on the topic "Rat Ventricular"

1

Anwar, Attia. "Functional role of NFAT in ventricular cardiomyocytes of rat." Giessen VVB Laufersweiler, 2006. http://geb.uni-giessen.de/geb/volltexte/2006/3817/index.html.

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Bhagatte, Yusuf. "Characterisation of temperature preconditioning of adult rat ventricular myocytes." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/28244.

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Temperature preconditioning is a relatively novel cardioprotective intervention, demonstrated to protect ex vivo isolated rat hearts against ischaemia- reperfusion injury. For the first time, the effect of temperature preconditioning on isolated ventricular myocytes was investigated in this study. This was followed by characterisation of the molecular mechanisms involved in temperature preconditioning. Temperature preconditioning (16°C) was found to be cardioprotective in isolated adult rat ventricular myocytes enhancing contractile recovery and preventing calcium dysregulation after metabolic inhibition and re-energisation (simulated ischaemia-reperfusion). Temperature preconditioning also preserved mitochondrial function by delaying the pathological opening of the mitochondrial permeability transition pore (mPTP) in a model of reperfusion injury. For the first time, reactive oxygen species (ROS) are shown to be released from the mitochondria exclusively during the hypothermic episodes of the temperature preconditioning protocol. This was characterised using a mitochondrially targeted ROS biosensor and ROS release was observed during the brief bursts to 16°C during temperature preconditioning. A ROS scavenger (MPG) significantly attenuated ROS accumulation during temperature preconditioning and consequently abolished the temperature preconditioning-induced protective delay in mPTP opening. Western blot analysis revealed temperature preconditioning phosphorylation of the pro-survival kinase ERK1/2. ERK1/2 activation was shown to be downstream of ROS release as the presence of a ROS scavenger during temperature preconditioning completely blocked ERK1/2 activation. The cardioprotective effects of temperature preconditioning on mPTP opening were completely lost by inhibiting ERK1/2 activation. Thus mitochondrial ROS release and ERK1/2 activation are both necessary to signal the cardioprotective effects of temperature preconditioning in cardiac myocytes.

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Fujimura, Atsushi. "Fluid shear-induced hypertrophy in neonatal rat ventricular myocytes." Diss., [La Jolla, Calif.] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1462110.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed April 1, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 51-55).

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Qu, Jihong. "The sodium background currents in cultured neonatal rat ventricular myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq26394.pdf.

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Collins, Helen Elizabeth. "Diurnal variation in excitation-contraction coupling in rat ventricular myocytes." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/29009.

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Diurnal variation has been reported in many cardiovascular haemodynamics parameters such as heart rate and blood pressure and the cardiac action potential. This variation may result from the diurnal variation in sympathetic activity or in cardiac gene expression. However, it is unknown whether these time-of-day dependent changes impact on excitation-contraction (EC) coupling. There is also a morning peak in the onset of ventricular arrhythmias and associated sudden cardiac death in man, which appear linked to the increase in sympathetic activity. Therefore, the aims of this investigation were to determine whether there was a time-of-day dependent variation in EC-coupling and its modulation by sympathetic stimulation. Left ventricular myocytes were isolated during either the resting period (ZT3) or the active period (ZT15) o f the adult Wistar rat. [Ca[superscript 2+]][subscript i] was determined using Fura-2 and contraction strength was determined using cell-edge detection in response to electrical field stimulation, and gene expression was determined using quantitative real-time RT-PCR. To determine the effects of hypertension-induced hypertrophy, myocytes were isolated from pre- and post-hypertensive spontaneously hypertensive rats (SHR). The basal Ca[superscript 2+] transient, contraction strength and SR Ca[superscript 2+] content were significantly greater in resting period (ZT3) myocytes than active period (ZT15) myocytes. Systolic [Ca[superscript 2+]], amplitude of Ca[superscript 2+] transient and SR Ca[superscript 2+] content in response to isoproterenol (> 3nM) were significantly greater in resting period (ZT3) myocytes. The percentage of myocytes developing arrhythmic activity in response to isoproterenol was greater in resting period (ZT3) myocytes. Nitric oxide synthase (NOS) inhibition using L-NNA significantly increased systolic [Ca[superscript 2+]], amplitude of Ca[superscript 2+] transient, SR Ca[superscript 2+] content and the percentage of myocytes developing arrhythmic activity in active period (ZT15) myocytes thereby depressing time-of-day dependent variation in these parameters. In addition, expression of NOS1 was significantly greater in active period (ZT15) myocytes. Diurnal variation in the Ca[superscript 2+] transient and its responsiveness to isoproterenol were depressed in adult SHR, however, this did not reflect a depression of diurnal cycling in NOS1 expression. This shows for the first time a time-of-day dependent variation in the Ca[superscript 2+]-transient and resulting contraction strength, reflecting levels of SR Ca[superscript 2+]-loading, due to a NOS-signalling pathway. There was also a reduction in sympathetic-induced arrhythmic activity in active period (ZT15) myocytes which was associated with increased NOS activity. Therefore, variation in NOS may be a means of protecting against arrhythmias during severe sympathetic stimulation. Loss of protection through disruption to the circadian clock resulting from cardiomyopathies such as hypertension-induced hypertrophy may result in a decreased threshold for sympathetic-induced arrhythmias, however; this requires further work to elucidate the underlying molecular mechanisms.

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Vongvatcharanon, Uraporn. "Postnatal ventricular modelling in the (mRen-2) 27 transgenic rat." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326673.

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Sarai, Nobuaki. "Nonuniformity of sarcomere shortenings in the isolated rat ventricular myocyte." Kyoto University, 2003. http://hdl.handle.net/2433/148482.

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Latcham, Shena L. "Effects of treprostinil sodium in a monocrotaline-induced rat model of pulmonary hypertension." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4288.

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Thesis (M.S.)--University of Missouri-Columbia, 2005.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2005" Includes bibliographical references.

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Nagasawa, Atsushi. "Basic fibroblast growth factor attenuates left-ventricular remodeling following surgical ventricular restoration in a rat ischemic cardiomyopathy model." Kyoto University, 2020. http://hdl.handle.net/2433/259712.

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Anwar, Attia [Verfasser]. "Functional role of NFAT in ventricular cardiomyocytes of rat / by Attia Anwar." Giessen : VVB Laufersweiler, 2006. http://d-nb.info/98866108X/34.

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Books on the topic "Rat Ventricular"

1

Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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5

Kassiri, Zamaneh. Reduction of transient outward K+ current and hypertrophy in neonatal rat ventricular myocytes: Role of calcium-dependent signaling pathways. 2002.

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Jones, Michael, Norman Qureshi, and Kim Rajappan. Ventricular tachyarrhythmias: Ventricular tachycardia and ventricular fibrillation. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0118.

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Ventricular tachyarrhythmias are abnormal patterns of electrical activity arising from the ventricular tissue (myocardium and conduction tissue). Ventricular tachycardia (VT) is an abnormal rapid heart rhythm originating from the ventricles. The rhythm may arise from the ventricular myocardium and/or from the distal conduction system. The normal heart rate is usually regular, between 60 and 100 bpm, and there is synchronized atrial and ventricular contraction. In VT, the ventricles contract at a rate greater than 120 bpm and typically from 150 to 300 bpm, and are no longer coordinated with the atria. There is still organized contraction of the ventricles in VT, with discrete QRS complexes. It is a potentially life-threatening arrhythmia, with the risk of degenerating into ventricular fibrillation and resulting in sudden cardiac death. It is characterized by a broad-complex tachycardia on ECG.

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Padmanabhan, Rajagopala, and Penny Sappington. Ventricular Assist Devices (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0021.

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Ventricular assist devices (VADs) have become a cornerstone of therapy in the management of end-stage heart failure, both as a means of bridging to cardiac transplantation and as destination therapy for long-term quality of life improvement. Responding to medical emergencies in patients with VADs poses numerous challenges to rapid response team (RRT) providers. Managing these patients requires basic understanding of VAD function and physiology and the multitude of complications that follow their implantation. Most healthcare professionals lack exposure to VADs, and although it may seem daunting, this chapter will provide a systematic approach of how to identify, troubleshoot, diagnose, and manage VAD-associated complications and provide emergency care for the VAD patient.

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Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrial fibrillation. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0116.

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Atrial fibrillation is a tachycardia arising in the atria, with atrial electrical activity occurring chaotically and continuously, without any effective atrial contraction occurring. The effects of this are an irregular ventricular rate, loss of the atrial contribution to ventricular filling, and the pooling of blood in the atria, thus increasing the risk of thrombus formation. The ventricular rate may be fast, slow, or of normal speed, depending on the state of the patient’s atrioventricular conduction. Atrial fibrillation is classified as paroxysmal (self-terminating within 7 days), persistent (lasting longer than 1 week, or requiring cardioversion to terminate) or permanent (cardioversion unable to terminate durably to sinus rhythm).

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Bauer, Robert, and Raghavan Murugan. Portable Monitor and Defibrillators (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0031.

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Portable monitors with the capability of defibrillation, synchronized cardioversion, and transcutaneous pacing are frequently used by the rapid response teams (RRTs) in several acute care facilities to provide quick information and to treat lethal arrhythmias in critically ill and unstable patients. Portable monitors are used on lethal arrhythmias such as ventricular fibrillation (VF), monomorphic ventricular tachycardia (VT), or polymorphic ventricular tachycardia, also known as Torsades de pointes (TdP). Properly identifying lethal arrhythmias and knowing how to use the portable monitor/defibrillator is essential to positive patient outcomes. In this chapter, we review the use of portable monitors for monitoring and detection of cardiac arrhythmias as well as outline the procedure for defibrillation, synchronized cardioversion, and transcutaneous pacing in the setting of RRT activation.

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Schneider, Antoine, and Rinaldo Bellomo. Atrial Fibrillation and Other Cardiac Arrhythmias (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0005.

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Cardiac arrhythmias are common in hospitalized patients, with their incidence increasing in older patients and those with comorbidities. Cardiac arrhythmias represent a trigger for approximately 10% of rapid response team (RRT) activations. Of those, atrial fibrillation (AF) is the most commonly observed. Other common cardiac arrhythmias in the in-hospital setting include supraventricular tachycardia, atrial flutter, ventricular tachycardia, and bradycardias. Members of the RRT should be skilled in the diagnosis and management of these common arrhythmias. This chapter presents an overview of cardiac arrhythmias that RRT members are likely to encounter, discussing their incidence and significance, as well as their immediate management.

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Book chapters on the topic "Rat Ventricular"

1

Piper, H. M., A. Volz, and P. Schwartz. "Adult Ventricular Rat Heart Muscle Cells." In Cell Culture Techniques in Heart and Vessel Research, 36–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75262-9_3.

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Kharche, S., H. Zhang, R. C. Clayton, and Arun V. Holden. "Hypertrophy in Rat Virtual Left Ventricular Cells and Tissue." In Functional Imaging and Modeling of the Heart, 153–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11494621_16.

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Liu, Q. Y., E. Karpinski, C. G. Benishin, and P. K. T. Pang. "GTPγS Activates Calcium Channels in Neonatal Rat Ventricular Cells." In Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, 341–42. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7_32.

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Ventura-Clapier, R., H. Mekhfi, V. Saks, and G. Vassort. "Creatine Kinase and Mechanical Properties of Rat Ventricular Muscle." In Developments in Cardiovascular Medicine, 397–406. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2053-1_26.

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Scamps, F., E. Mayoux, D. Charlemagne, and G. Vassort. "Calcium Current in Normal and Hypertrophied Isolated Rat Ventricular Myocytes." In Developments in Cardiovascular Medicine, 55–67. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1513-1_4.

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Cleeman, Lars, Wei Wang, and Martin Morad. "Rapid Confocal Measurements of Ca2+ Sparks in Rat Ventricular Myocytes." In Calcium and Cellular Metabolism, 25–36. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9555-4_3.

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Bulysheva, A. A., B. Hargrave, N. Burcus, C. G. Lundberg, L. Murray, and R. Heller. "Gene Electro Transfer to Left Ventricular Myocardium in Rat and Porcine Models." In 1st World Congress on Electroporation and Pulsed Electric Fields in Biology, Medicine and Food & Environmental Technologies, 395–98. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-287-817-5_86.

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Meij, Johanna T. A., and Jos M. J. Lamers. "Alpha-1-adrenergic stimulation of phosphoinositide breakdown in cultured neonatal rat ventricular myocytes." In Lipid Metabolism in Normoxic and Ischemic Heart, 73–75. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4_11.

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Makiguchi, M., H. Kawaguchi, H. Yasuda, and M. Tamura. "The Effect of Intracellular Oxygen Concentration on Ventricular Fibrillation in Perfused Rat Heart." In Oxygen Transport to Tissue IX, 305–8. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-7433-6_35.

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Hagler, Herbert K., Alan C. Morris, and L. Maximilian Buja. "X-Ray Microanalysis and Free Calcium Measurements in Cultured Neonatal Rat Ventricular Myocytes." In Electron Probe Microanalysis, 181–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74477-8_14.

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Conference papers on the topic "Rat Ventricular"

1

Demir, S. S. "Simulating Cardiac Ventricular Action Potentials in Rat and Mouse." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616359.

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Zhang, F., D. H. Ren, Z. You, S. W. Anderson, and X. Zhang. "Neonatal rat ventricular myocytes force mapping using double-sided micropillar arrays." In TRANSDUCERS 2015 - 2015 18th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2015. http://dx.doi.org/10.1109/transducers.2015.7180938.

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Farrar, G. E., G. T. Gullberg, and A. I. Veress. "Full Cardiac Cycle Strain Measurement Using Hyperelastic Warping, Application to Detecting Myocardial Dysfunction in Rat microPET Images." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53654.

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Assessments of regional heart wall deformation (wall motion, thickening, strain) are commonly used to evaluate left ventricular wall function in the clinical setting. Nuclear based imaging modalities such as PET and SPECT are commonly used to localize ischemic myocardial disease, and can identify impairment of cardiac function due to hypertrophic or dilated cardiomyopathies. Regional wall motion analysis in conjunction with global left ventricular (LV) ejection fraction is commonly used to assess systolic and diastolic function. The quantification of ventricular strains throughout the entire cardiac cycle provides valuable information that could be used to more effectively differentiate between diastolic and systolic dysfunction, as well as a more complete picture of overall cardiac performance.

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Hongxia, Sun, and Yu Chunyan. "Experiment of taishinone on rat ventricular fibroblasts proliferation and its underlying mechanisms." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027981.

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Rashid, S., M. E. Wagshul, M. Yu, H. Benveniste, J. Li, and J. P. McAllister. "Development of ventricular expansion and increased pulsatile CSF flow in a rat model." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413296.

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Frede, W., R. Medert, M. Freichel, M. Gorenflo, and S. Uhl. "Cardiac Role of the Ion Channel TRPM4 under Right Ventricular Pressure Load in Rat." In 50th Annual Meeting of the German Society for Pediatric Cardiology (DGPK). Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1628318.

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Siamwala, J. H., A. Zhao, C. Mantsounga, A. Morrison, G. Choudhary, S. I. S. Rounds, and E. O. Harrington. "Interleukin-1 Beta Modulates Rat and Human Ventricular Cardiac Fibroblast Proliferation and Collagen Secretion." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3831.

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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176422.

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Abstract:

The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.

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Li, Min, Todd Horn, Brittney A. McKeon, Robbert D. Brown, Maria Frid, Nnamdi Nelson, Timothy McKinsey, and Kurt Stenmark. "Rat Genetic Strain Differences In Right Ventricular Remodeling In Response To Hypoxia-Induced Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4756.

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Witzenburg, Colleen, Sarah Vanderheiden, Tina M. Nagel, Stefan M. Kren, Doris A. Taylor, and Victor H. Barocas. "Sex Differences in the Mechanical Behavior of the Decellularized Rat Left Ventricle." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80654.

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Abstract:

There are fundamental differences in the size and performance of male and female hearts. Even after adjustments for height and body surface area, the left ventricle of a healthy male is larger in both volume and mass [1]. There are differences in contractile performance between papillary muscle from male and female rats with male rats showing slower responses in both isometric and isotonic tests [2]. It is less clear, however, whether the underlying structure or mechanical properties vary between sexes as well. Of particular interest to us is the extracellular matrix (ECM) of the ventricular wall, which provides structural stability to the heart. This matrix can be isolated by perfusion decellularization [3].

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