scholarly journals Cardiac Morphofunctional Characteristics of Transgenic Rats With Overexpression of the Bradykinin B1 Receptor in the Endothelium

2017 ◽  
pp. 925-932
Author(s):  
R. F. LEVY ◽  
A. J. SERRA ◽  
E. L. ANTONIO ◽  
L. DOS SANTOS ◽  
D. S. BOCALINI ◽  
...  
Keyword(s):  
Papillary Muscle ◽  
Left Ventricular ◽  
Left Ventricular Cavity ◽  
Papillary Muscles ◽  
Sprague Dawley ◽  
Transgenic Rats ◽  
Ventricular Performance ◽  
B1 Receptor ◽  
Bradykinin B1 Receptor

Our aim was to evaluate whether endothelial overexpressing of the bradykinin B1 receptor could be associated with altered left ventricular and myocardial performance. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function in Sprague Dawley transgenic rats overexpressing the endothelial bradykinin B1 receptor (Tie2B1 rats). The myocardial inotropism was evaluated on papillary muscles contracting in vitro. In Tie2B1 animals, an enlarged left ventricular cavity and lower fractional shortening coupled with a lower rate of pressure change values indicated depressed left ventricular performance. Papillary muscle mechanics revealed that both Tie2B1 and wild-type rat groups had the same contractile capacities under basal conditions; however, in transgenic animals, there was accentuated inotropism due to post-pause potentiation. Following treatment with the Arg9-BK agonist, Tie2B1 papillary muscles displayed a reduction in myocardial inotropism. Endothelial B1 receptor overexpression has expanded the LV cavity and worsened its function. There was an exacerbated response of papillary muscle in vitro to a prolonged resting pause, and the use of a B1 receptor agonist impairs myocardial inotropism.

Insights From In-Vitro Flow Visualization Into the Mechanism of Systolic Anterior Motion of the Mitral Valve in Hypertrophic Cardiomyopathy Under Steady Flow Conditions

1992 ◽  
Vol 114 (3) ◽  
pp. 406-413 ◽  
Author(s):  
X. P. Lefebvre ◽  
A. P. Yoganathan ◽  
R. A. Levine
Keyword(s):  
Mitral Valve ◽  
Flow Field ◽  
Flow Visualization ◽  
Papillary Muscle ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Papillary Muscles ◽  
Systolic Anterior Motion ◽  
Septal Hypertrophy

Hypertrophic obstructive cardiomyopathy is a heart disease characterized by a thickened interventricular septum which narrows the left ventricular outflow tract, and by systolic anterior motion (SAM) of the mitral valve which can contact the septum and create dynamic subaortic obstruction. The most common explanation for SAM has been the Venturi mechanism which postulates that septal hypertrophy, by narrowing the outflow tract, produces high velocities and thus low pressure between the mitral valve and the septum, causing the valve leaflets to move anteriorly. This hypothesis, however, fails to explain why SAM often begins early in systole, when outflow tract velocities are low or negligible or why it may occur in the absence of septal hypertrophy. The goal of this study was therefore to investigate an alternative hypothesis in which structural abnormalities of the papillary muscles act as a primary cause of SAM by altering valve restraint and thereby changing the geometry of the closed mitral apparatus and its relationship to the surrounding flow field. In order to test this hypothesis, an in vitro model of the left ventricle which included an explanted human mitral valve with intact chords and papillary muscle apparatus was constructed. Flow visualization was used to observe the ventricular flow field and the mitral valve geometry. Displacing the papillary muscles anteriorly and closer to each other, as observed clinically in patients with cardiomyopathy and obstruction produced SAM in the absence of septal hypertrophy. Flow could be seen impacting on the upstream (posterior) surface of the leaflets; such flow is capable of producing form drag forces which can initiate and maintain SAM. In contrast, increasing septal hypertrophy to narrow the outflow tract and create velocities as high as 3.3 m/s did not produce SAM in the absence of papillary muscle displacement, despite an increase in the calculated lift forces. Therefore, primary abnormalities of the papillary muscle-mitral valve apparatus can alter the relationship of the mitral valve to the surrounding flow field in such a way that SAM is generated, whereas the Venturi mechanism, induced by septal hypertrophy alone, is insufficient to do so with a normally positioned and tethered valve.

scholarly journals The Violin Heart

2010 ◽  
Vol 4 ◽  
pp. 117954681000400 ◽  
Author(s):  
James Ker
Keyword(s):  
Case Report ◽  
Papillary Muscle ◽  
Interventricular Septum ◽  
Lateral Wall ◽  
Left Ventricular ◽  
Left Ventricular Cavity ◽  
Papillary Muscles ◽  
Musical Note ◽  
Bundle Of His

Left ventricular false tendons are thin, fibromuscular structures which traverse the left ventricular cavity. They are thought to be intracavitary radiations of the bundle of His. Usually these tendons span between the interventricular septum and the lateral wall or a papillary muscle. They have been known to be a source of innocent and musical murmurs. In this case report a peculiar left ventricular false tendon is shown—one extending between the two papillary muscles, giving the appearance of a musical note. During ventricular diastole the tendon is pulled taut between the two heads of the papillary muscles and during ventricular systole the tendon relaxes. The echocardiographic characteristics and possible long term implications are discussed.

Myocardial mechanics predict hemodynamic performance during normal function and alcohol-induced dysfunction in rats

1991 ◽  
Vol 261 (6) ◽  
pp. H1880-H1888
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
P. Anversa
Keyword(s):  
Pressure Rise ◽  
Normal Function ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Least Squares Regression ◽  
Tension Development ◽  
Myocardial Mechanics

To determine whether mechanical evaluation of muscle tissue removed from the myocardium can be employed as a direct indicator of cardiac contractile performance in situ, isometric and isotonic parameters of muscle mechanics in vitro were correlated with in vivo global functional characteristics of the same heart. Twelve-month-old animals maintained on standard food and water were employed as representative of normal cardiac function. Animals of identical age with left ventricular (LV) dysfunction induced by oral alcohol (30%) ingestion from 4 to 12 mo were utilized to represent depressed cardiac performance. Accordingly, 24 h after the establishment of the hemodynamic profile for a control or experimental heart, the LV posterior papillary muscle was removed from the same heart and examined isometrically and isotonically. Least squares regression analysis was employed to establish a correlation coefficient and P values between various in vitro and in vivo parameters. Hemodynamic measurements were performed under chloral hydrate anesthesia and LV pump performance was evaluated with respect to aortic and ventricular pressures and the rates of rise and decay of the LV pressure trace. Papillary muscles were evaluated with respect to timing parameters of the isometric and isotonic twitch, the first derivative of isometric tension development, and the speed of muscle shortening at increasing physiologic loads. LV peak rate of pressure rise and decay were then correlated with the various isometric and isotonic properties. Myocardial mechanics and hemodynamics revealed depressed function in the papillary muscles and hearts from alcoholic rats. Moreover, significant correlations were found between the LV rate of pressure change (peak +dP/dt and -dP/dt) and both isometric and isotonic twitch measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Studies to Elucidate the Mechanism of Cardio Protective and Hypotensive Activities of Anogeissus acuminata (Roxb. ex DC.) in Rodents

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3471
Author(s):  
Fatima Saqib ◽  
Muhammad Arif Aslam ◽  
Khizra Mujahid ◽  
Luigi Marceanu ◽  
Marius Moga ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Ex Vivo ◽  
Inflammatory Cells ◽  
Left Ventricular ◽  
Guanosine Monophosphate ◽  
Sprague Dawley ◽  
Positive Effects ◽  
Creatine Kinase Mb

Anogeissus acuminata (Roxb. ex DC.) is a folkloric medicinal plant in Asia; including Pakistan; used as a traditional remedy for cardiovascular disorders. This study was planned to establish a pharmacological basis for the trivial uses of Anogeissus acuminata in certain medical conditions related to cardiovascular systems and to explore the underlying mechanisms. Mechanistic studies suggested that crude extract of Anogeissus acuminata (Aa.Cr) produced in vitro cardio-relaxant and vasorelaxant effects in isolated paired atria and aorta coupled with in vivo decrease in blood pressure by invasive method; using pressure and force transducers connected to Power Lab Data Acquisition System. Moreover; Aa.Cr showed positive effects in left ventricular hypertrophy in Sprague Dawley rats observed hemodynamically by a decrease in cardiac cell size and fibrosis; along with absence of inflammatory cells; coupled with reduced levels of angiotensin converting enzyme (ACE) and renin concentration along with increased concentrations of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP). In Acute Myocardial Infarction (AMI) model; creatine kinase (CK), creatine kinase-MB (CK-MB) and lactic acid dehydrogenase (LDH levels) were found to be decreased; along with decreased necrosis; edema and recruitment of inflammatory cells histologically. In vivo and ex vivo studies of Anogeissus acuminata provided evidence of vasorelaxant; hypotensive and cardioprotective properties facilitated through blockage of voltage-gated Ca++ ion channel; validating its use in cardiovascular diseases

Discovery of dehydro-oxopiperazine acetamides as novel bradykinin B1 receptor antagonists with enhanced in vitro potency

2012 ◽  
Vol 22 (2) ◽  
pp. 1061-1067 ◽  
Author(s):  
Wenyuan Qian ◽  
Jian Jeffrey Chen ◽  
Jason Human ◽  
Toshihiro Aya ◽  
Jiawang Zhu ◽  
...  
Keyword(s):  
Receptor Antagonists ◽  
B1 Receptor ◽  
Bradykinin B1 Receptor

Afterload as a primary determinant of ventricular performance

1963 ◽  
Vol 204 (4) ◽  
pp. 604-610 ◽  
Author(s):  
Edmund H. Sonnenblick ◽  
S. Evans Downing
Keyword(s):  
Blood Pressure ◽  
Stroke Volume ◽  
Papillary Muscle ◽  
Work Performance ◽  
Diastolic Pressure ◽  
Muscle Length ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Inotropic State ◽  
Primary Determinant

The importance of aortic blood pressure as a determinant of left ventricular performance was systematically evaluated in the intact cat heart, and compared with the effects of afterloading on work performed by the isotonically contracting isolated cat papillary muscle. In the papillary muscle, at any one muscle length and state of contractility, work was determined by the afterload with which the muscle shortened. In the intact heart, blood pressure (BP) may be considered a gross approximation of the afterload encountered by the contracting ventricle. It was found that at any given initial left ventricular end-diastolic pressure (LVEDP), work performed was a function of the BP. At a constant BP, norepinephrine increased the work performed at any LVEDP by augmenting stroke volume. This work could be further increased by a concomitant increase of BP. Over a broad range, stroke volume was independent of the BP. The state of contractility of the myocardium sets the limits of work; however, work performance remains largely dependent on the BP (afterload). Thus, ventricular performance at a given constant inotropic state is the product of two largely independent variables, the preload (establishing initial muscle length) and the afterload.

In Vitro Measurement of the Coaptation Force Distribution in Normal and Functional Regurgitant Porcine Mitral Valves

2015 ◽  
Vol 137 (7) ◽  
Author(s):  
John Adams ◽  
Malachy J. O'Rourke
Keyword(s):  
Mitral Valve ◽  
Myocardial Ischemia ◽  
Papillary Muscle ◽  
Force Distribution ◽  
Papillary Muscles ◽  
Flow Loop ◽  
Static Tests ◽  
Mitral Valves ◽  
Static Conditions

Closure of the left atrioventricular orifice is achieved when the anterior and posterior leaflets of the mitral valve press together to form a coaptation zone along the free edge of the leaflets. This coaptation zone is critical to valve competency and is maintained by the support of the mitral annulus, chordae tendinae, and papillary muscles. Myocardial ischemia can lead to an altered performance of this mitral complex generating suboptimal mitral leaflet coaptation and a resultant regurgitant orifice. This paper reports on a two-part experiment undertaken to measure the dependence of coaptation force distribution on papillary muscle position in normal and functional regurgitant porcine mitral heart valves. Using a novel load sensor, the local coaptation force was measured in vitro at three locations (A1–P1, A2–P2, and A3–P3) along the coaptation zone. In part 1, the coaptation force was measured under static conditions in ten whole hearts. In part 2, the coaptation force was measured in four explanted mitral valves operating in a flow loop under physiological flow conditions. Here, two series of tests were undertaken corresponding to the normal and functional regurgitant state as determined by the position of the papillary muscles relative to the mitral valve annulus. The functional regurgitant state corresponded to grade 1. The static tests in part 1 revealed that the local force was directly proportional to the transmitral pressure and was nonuniformly distributed across the coaptation zone, been strongest at A1–P1. In part 2, tests of the valve in a normal state showed that the local force was again directly proportional to the transmitral pressure and was again nonuniform across the coaptation zone, been strongest at A1–P1 and weakest at A2–P2. Further tests performed on the same valves in a functional regurgitant state showed that the local force measured in the coaptation zone was directly proportional to the transmitral pressure. However, the force was now observed to be weakest at A1–P1 and strongest at A2–P2. Movement of the anterolateral papillary muscle (APM) away from both the annular and anterior–posterior (AP) planes was seen to contribute significantly to the altered force distribution in the coaptation zone. It was concluded that papillary muscle displacement typical of myocardial ischemia changes the coaptation force locally within the coaptation zone.

A three-component force vector cell for in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall

1997 ◽  
Vol 30 (10) ◽  
pp. 1071-1075 ◽  
Author(s):  
Shehab R. Hashim ◽  
Arnold Fontaine ◽  
Shengqiu He ◽  
Robert A. Levine ◽  
Ajit P. Yoganathan
Keyword(s):  
Papillary Muscle ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Force Vector ◽  
Component Force

Mechanism of prolonged electromechanical delay in late activated myocardium during left bundle branch block

2011 ◽  
Vol 301 (6) ◽  
pp. H2334-H2343 ◽  
Author(s):  
Kristoffer Russell ◽  
Otto A. Smiseth ◽  
Ola Gjesdal ◽  
Eirik Qvigstad ◽  
Per Andreas Norseng ◽  
...  
Keyword(s):  
Papillary Muscle ◽  
Left Bundle Branch Block ◽  
Biventricular Pacing ◽  
Lateral Wall ◽  
Mechanical Dyssynchrony ◽  
Left Ventricular ◽  
Electromechanical Delay ◽  
Bundle Branch Block ◽  
Experimental Findings

During left bundle branch block (LBBB), electromechanical delay (EMD), defined as time from regional electrical activation (REA) to onset shortening, is prolonged in the late-activated left ventricular lateral wall compared with the septum. This leads to greater mechanical relative to electrical dyssynchrony. The aim of this study was to determine the mechanism of the prolonged EMD. We investigated this phenomenon in an experimental LBBB dog model ( n = 7), in patients ( n = 9) with biventricular pacing devices, in an in vitro papillary muscle study ( n = 6), and a mathematical simulation model. Pressures, myocardial deformation, and REA were assessed. In the dogs, there was a greater mechanical than electrical delay (82 ± 12 vs. 54 ± 8 ms, P = 0.002) due to prolonged EMD in the lateral wall vs. septum (39 ± 8 vs.11 ± 9 ms, P = 0.002). The prolonged EMD in later activated myocardium could not be explained by increased excitation-contraction coupling time or increased pressure at the time of REA but was strongly related to dP/d t at the time of REA ( r = 0.88). Results in humans were consistent with experimental findings. The papillary muscle study and mathematical model showed that EMD was prolonged at higher dP/d t because it took longer for the segment to generate active force at a rate superior to the load rise, which is a requirement for shortening. We conclude that, during LBBB, prolonged EMD in late-activated myocardium is caused by a higher dP/d t at the time of activation, resulting in aggravated mechanical relative to electrical dyssynchrony. These findings suggest that LV contractility may modify mechanical dyssynchrony.

scholarly journals Unusual Anomalous Single Papillary Muscle Causing Symptomatic Mid-left Ventricular Cavity Obstruction: Octopus Papillary Muscle

2006 ◽  
Vol 19 (7) ◽  
pp. 939.e9-939.e11 ◽  
Author(s):  
Ajay S. Shah ◽  
Atul Kukar ◽  
Farooq A. Chaudhry ◽  
Mark V. Sherrid
Keyword(s):  
Papillary Muscle ◽  
Left Ventricular ◽  
Left Ventricular Cavity ◽  
Ventricular Cavity
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