Spontaneous mechanical alternans in papillary muscles from atherosclerotic rabbits

1980 ◽  
Vol 239 (5) ◽  
pp. H674-H680
Author(s):  
D. W. Peterson ◽  
C. A. Napolitano ◽  
D. W. Griffith
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Right Ventricular ◽  
Lipid Composition ◽  
Maximum Rate ◽  
Maximum Velocity ◽  
Atherogenic Diet ◽  
Papillary Muscles ◽  
Velocity Of Shortening ◽  
Induced Changes ◽  
Develop Tension

Mechanical alternans developed spontaneously in 5 of 17 right ventricular papillary muscles from atherosclerotic rabbits. The rabbits had eaten an atherogenic diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets for 116-184 days. In one muscle mechanical alternans developed slowly and persisted. When the condition had developed fully, in the weaker contraction the muscle shortened only 20% as far when contracting isotonically and developed only 38% as much tension when contracting isometrically. Added to the superfusate, calcium (5.0 mM) or norepinephrine (1.5 X 10(-5) M) abolished the alternans. In four muscles mechanical alternans was only temporary. Compared with the 12 muscles that did not develop alternans, these 4, when contracting isometrically 12 times/min but not in alternans, had longer latency and required more time to develop tension at the maximum rate and to develop peak tension. Contracting isotonically, they required more time to accelerate to maximum velocity of shortening and to shorten maximally. Raising the contraction frequency to 24/min decreased the differences in performance between the two groups. Norepinephrine (1.5 X 10(-5) M) made the differences smaller still. We think that both the mechanical alternans and the differences in performance between the muscles that developed alteranans and those that did not resulted from a defect in the cardiac cell's handling of calcium. Diet-induced changes in the lipid composition of the sarcoplasmic reticulum or sarcolemma or both seem probable causes.

Effects of sevoflurane on the contractility of ferret ventricular myocardium

2000 ◽  
Vol 89 (5) ◽  
pp. 1778-1786 ◽  
Author(s):  
Anna E. Bartunek ◽  
Philippe R. Housmans
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Right Ventricular ◽  
Ventricular Myocardium ◽  
Papillary Muscles ◽  
Depressant Effect ◽  
Intracellular Ca ◽  
Mild Stimulation ◽  
Equal Amplitude ◽  
Stimulation Of

Isotonic and isometric variables of contractility and relaxation of isolated ferret right ventricular papillary muscles were measured before and during exposure to incremental concentrations of sevoflurane (0–4.9% vol/vol) (30°C) ( n = 9). In a second group of muscles ( n = 8), effects of sevoflurane were compared with those of low [Ca2+]o (0.45–2.25 mM in steps of 0.45 mM). Sevoflurane caused a reversible concentration-dependent decrease in contractility (ED50 of developed force 4.6 ± 0.9% vol/vol). When compared with twitches of equal amplitude in low extracellular Ca2+ concentration, sevoflurane accelerated both isometric and isotonic relaxation. The myocardial depressant effect of sevoflurane is less than that of isoflurane and results mainly from a decrease of intracellular Ca2+ availability. The abbreviated isometric relaxation likely reflects a decrease in Ca2+ sensitivity and the faster isotonic relaxation may reflect a mild stimulation of Ca2+ uptake by the sarcoplasmic reticulum.

Thyroid status and Na(+)-K+ pump current, intracellular sodium, and action potential duration in rabbit heart

1995 ◽  
Vol 268 (5) ◽  
pp. H1838-H1846 ◽  
Author(s):  
M. M. Doohan ◽  
L. C. Hool ◽  
H. H. Rasmussen
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Pump Current ◽  
Rabbit Heart ◽  
Papillary Muscles ◽  
Thyroid Status ◽  
Intracellular Na Activity ◽  
Induced Changes

Thyroid status influences the abundance of Na(+)-K+ pumps in the heart. To evaluate whether this phenomenon may contribute to a dependence of the action potential duration (APD) on thyroid status, we induced hypothyroidism in a group of New Zealand White rabbits. Another group was treated similarly but also received triiodothyronine (T3). Right ventricular myocytes were isolated and voltage clamped at -40 mV. We identified Na(+)-K+ pump current (Ipump) as a ouabain-induced shift in holding current. Mean Ipump, measured using patch pipettes containing 10 mM Na+, was 0.24 +/- 0.02 pA/pF in 9 cells from 4 hypothyroid rabbits and 0.48 +/- 0.05 in 10 cells from 4 rabbits treated with T3 (P < 0.001). Because thyroid status influences Na+ influx, we measured intracellular Na+ activity (aiNa) in right ventricular papillary muscles. We found that aiNa was 5.20 +/- 0.42 mM in nine papillary muscles from seven hypothyroid rabbits and 7.62 +/- 0.69 mM in nine papillary muscles from six rabbits treated with T3 (P < 0.01). The effect of thyroid-induced changes in Ipump and aiNa on APD was stimulated with a computer model. The simulations predicted that thyroid-induced changes in Ipump can influence APD. The predicted changes were similar to changes in APD measured in isolated papillary muscles.

Mechanisms contributing to pulsus alternans in pressure-overload cardiac hypertrophy

1996 ◽  
Vol 271 (6) ◽  
pp. H2490-H2500 ◽  
Author(s):  
G. Kotsanas ◽  
S. M. Holroyd ◽  
R. Young ◽  
C. L. Gibbs
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Right Ventricular ◽  
Time Course ◽  
Pressure Overload ◽  
Papillary Muscles ◽  
Postextrasystolic Potentiation ◽  
Cycling Rate ◽  
Simultaneous Measurements ◽  
Pulsus Alternans

The mechanisms underlying pulsus alternans in pressure-over-load (POL) cardiac hypertrophy were investigated. Simultaneous measurements of force and intracellular Ca2+ (using fura 2) in right ventricular papillary muscles under conditions that produced mechanical alternans, revealed alternation of the amplitude of the Ca2+ transient together with alternation of force in some POL muscles. Instances when alternation of force occurred without any apparent alternation of the Ca2+ transient were also observed. Exposure of muscles to 5 microM ryanodine significantly attenuated mechanical alternans, thereby implicating a role for the sarcoplasmic reticulum (SR) in this process. The time course of restitution of force and the intracellular Ca2+ transient were, however, unchanged in POL hearts, indicating that SR Ca2+ cycling was not appreciably slowed. The fraction of Ca2+ recirculated intracellularly was derived from studies of postextrasystolic potentiation and was significantly reduced in the POL hearts, suggesting additional differences in cellular Ca2+ regulation. We conclude that changes in Ca2+ handling play an important role in the onset of mechanical alternans in POL hypertrophy, but that additional factors, most likely a slowing of crossbridge cycling rate, are also likely to be important.

scholarly journals Anti-phospholamban and protein kinase A alter the Ca2+ sensitivity and maximum velocity of Ca2+ uptake by the cardiac sarcoplasmic reticulum

1998 ◽  
Vol 331 (1) ◽  
pp. 245-249 ◽  
Author(s):  
Margaret E. KARGACIN ◽  
Zenobia ALI ◽  
Gary J. KARGACIN
Keyword(s):  
Protein Kinase ◽  
Sarcoplasmic Reticulum ◽  
Maximum Velocity ◽  
Functional Effect ◽  
Dependent Protein Kinase ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Dependent Protein ◽  
Uptake Velocity ◽  
Phospholamban Phosphorylation ◽  
Kinase A

The activity of the SERCA2a Ca2+ pump in the sarcoplasmic reticulum (SR) of cardiac muscle is inhibited by phospholamban. When phospholamban is phosphorylated by cyclic-AMP-dependent protein kinase (PKA) this inhibition is relieved. It is generally agreed that this results in an increase in the Ca2+ sensitivity of the SR Ca2+ pump; however, some investigators have also reported an increase in the maximum velocity of the pump. We have used a sensitive fluorescence method to measure net Ca2+ uptake by native cardiac SR vesicles and compared the effects of a constitutively active subunit of PKA (cPKA) with those of a monoclonal antibody (A1) that binds to phospholamban and is thought to mimic the effect of phosphorylation. Both the Ca2+ sensitivity and the maximum velocity of uptake were increased by cPKA and by A1. The effects of cPKA and A1 on uptake velocity were only slightly additive. No changes in uptake were detected with denatured cPKA or denatured A1. These results indicate that the functional effect of phospholamban phosphorylation is to increase both the Ca2+ sensitivity and the maximum velocity of net Ca2+ uptake into the SR.

Relation between contractile function and regulatory cardiac proteins in hypertrophied hearts

1996 ◽  
Vol 270 (6) ◽  
pp. H2021-H2028 ◽  
Author(s):  
B. Stein ◽  
S. Bartel ◽  
U. Kirchhefer ◽  
S. Kokott ◽  
E. G. Krause ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Troponin I ◽  
Contractile Function ◽  
Papillary Muscles ◽  
Camp Accumulation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
C Protein ◽  
Camp Formation ◽  
Phosphate Incorporation

The aim of this study was to examine the mechanism(s) underlying the reduced isoproterenol-induced positive inotropic and lusitropic effects in hypertrophied hearts. Chronic beta-adrenergic stimulation (2.4 mg isoproterenol.kg-1. day-1 for 4 days) induced cardiac hypertrophy by 33 +/- 2% in rats. A parallel downregulation of phospholamban (PLB) and sarcoplasmic reticulum Ca2(+)-ATPase (SERCA2) protein expression by 49 and 40%, respectively, was observed, whereas troponin I (TNI) and C protein remained unchanged. In papillary muscles from chronically beta-adrenergically stimulated rats, the isoproterenol-induced positive inotropic and lusitropic effects, as well as adenosine 3',5'-cyclic monophosphate (cAMP) accumulation, were attenuated compared with those in control animals. Acute exposure to isoproterenol induced phosphate incorporation into PLB, TNI, and C protein of 48 +/- 4.6, 55 +/- 5.0, and 27 +/- 4.9 pmol/mg homogenate protein, respectively, in control animals. In the hypertrophied hearts, phosphate incorporation into PLB was reduced by 76%, whereas phosphate incorporation into TNI or C protein remained unchanged. In conclusion, chronic beta-adrenergic stimulation reduced the isoproterenol-stimulated positive inotropic and lusitropic effects in papillary muscles, which were accompanied by 1) diminished cAMP formation, 2) attenuation of cAMP-mediated PLB phosphorylation, and 3) downregulation of PLB and SERCA2 protein.

Comparative force-velocity relation and analyses of myosin of dog atria and ventricles

1982 ◽  
Vol 243 (3) ◽  
pp. H391-H397 ◽  
Author(s):  
J. Wikman-Coffelt ◽  
H. Refsum ◽  
G. Hollosi ◽  
L. Rouleau ◽  
L. Chuck ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Calcium Concentration ◽  
Maximum Velocity ◽  
Calcium Sensitivity ◽  
Myofibrillar Proteins ◽  
Maximal Velocity ◽  
Velocity Of Shortening ◽  
Force Velocity ◽  
Normal Calcium ◽  
Actin Concentration

The isolated muscle and purified myofibrillar proteins of canine atria and ventricles were compared relative to force-velocity relations and rate of adenosine 5'-triphosphatase (ATPase) activity as a function of calcium concentrations. The maximal stress development of isolated trabeculae of canine atria was similar to that of canine right ventricular papillary muscles when analyzed at saturating calcium concentrations (7.5 mM); however, stress was less in the atria when studied at normal calcium concentrations (2.5 mM). The maximal velocity of shortening of atrial trabeculae was about 2.3 times higher than that of ventricular muscle. Regulated actomyosin characterized from the myofibrillar proteins of the two tissues gave directionally similar calcium sensitivity. The maximum velocity of shortening for actin-activated atrial myosin of the dog was approximately 1.8 times higher when the latter was analyzed as a function of actin concentration. Both maximal tension of isolated muscle and regulated actomyosin ATPase activity were dependent on calcium concentration.

Positive inotropic responses in cardiac muscles: influence of stimulation frequency and species

1982 ◽  
Vol 60 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Peter K. S. Siegl ◽  
John H. McNeill
Keyword(s):  
Right Ventricular ◽  
Species Difference ◽  
Extracellular Calcium ◽  
Stimulation Frequency ◽  
Force Frequency ◽  
Papillary Muscles ◽  
Drug Induced ◽  
Cardiac Muscles ◽  
Inotropic Responses ◽  
Isolated Rat

Inotropic responses to cumulative additions of methoxaminc (10−7 to 3 × 10−4 M), isoproterenol (10−9 to 10−5 M), or calcium (2 to 32 mM) were measured in isolated rat left atria and papillary muscles and rabbit right ventricular papillary muscles at three stimulation frequencies. Cardiac muscles were incubated in oxygenated Chenoweth–Koelle solution (2 mM calcium) at 37 °C. The basal developed force (BDF) before and maximum developed force (MDF) after challenge with methoxamine and isoproterenol were inversely related to stimulation frequency in rat preparations. BDF was directly related to stimulation rate in rabbit papillary muscles while MDF was independent of the rate. Drug-induced increases in force (MDF – BDF) were independent of stimulation frequency in rat and inversely related to stimulation frequency in rabbit. Responses to calcium were similar to the observed adrenergic responses. Also, force–frequency relationships of the rat and rabbit preparations were not similar in the absence and presence of these agonists. These data show that inotropic responses by rat and rabbit hearts are not affected similarly by stimulation frequency and this may reflect a species difference in the utilization of extracellular calcium for contraction.

scholarly journals Tricuspid Valve Dysplasia in a Dog

2019 ◽  
Vol 47 ◽  
Author(s):  
Gabriela De Carvalho Cid ◽  
Luciano Da Silva Alonso ◽  
Ana Paula De Castro Pires ◽  
Mariana Siqueira d'Avila Taïna Gonçalves ◽  
Taïna Gonçalves ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Tricuspid Valve ◽  
Right Atrial ◽  
Pulmonary Insufficiency ◽  
Papillary Muscles ◽  
Ventricular Enlargement ◽  
Pathological Findings ◽  
Chordae Tendineae ◽  
Clinicopathological Findings ◽  
The Right

Background: Congenital cardiac diseases are a common cause of death in puppies. Tricuspid valve dysplasia is characterized by thickening and displacement of the leaflets of the tricuspid valve, agenesis of the valves, and incomplete separation of valve components. Papillary muscles may fuse and display shortened or absent chordae tendineae that contribute to tricuspid regurgitation. Diagnostic features of tricuspid valve dysplasia include cardiomegaly with massive right atrium enlargement on thoracic radiography and tricuspid insufficiency on an ultrasound. We aimed to describe clinicopathological findings in a dog (Canis familiaris) with tricuspid dysplasia.Case: We aimed to describe tricuspid valve dysplasia in a dog referred for necropsy at the Anatomical Pathology Sector of The Rural Federal University of Rio de Janeiro, Brazil, with a clinical history of abdominal swelling, dyspnea, cyanosis, ascites, and prostration. Echocardiography and abdominal ultrasound revealed right ventricular enlargement, hepatomegaly, and splenomegaly. Examination of the heart showed prominent enlargement, thickening and dilation of the right chambers, thickening of the tricuspid leaflets, and moderately shortened chordae tendineae. The liver was enlarged, with a nutmeg pattern, and foci of clotting and fibrin adhesions in the lateral right lobule.Discussion: Epidemiological, clinical, and pathological findings were consistent with tricuspid valve dysplasia. Although structural abnormalities of the tricuspid and mitral valves are well known in fetuses and neonates, congenital and secondary tricuspid malformations are rare in dogs. The survival rate is associated with the severity of heart lesions. Tricuspid valve dysplasia is mostly observed in large-breed dogs (>20 kg), particularly in Labrador Retrievers, Boxers, and German Shepherds. Regardless, most dogs with tricuspid valve dysplasia are of a pure-breed, which differs from our findings because our dog was a mongrel. Our dog displayed signs of dyspnea, cyanosis, abdominal swelling, prostration, and enlarged liver and spleen on ultrasound examination. Tricuspid valve dysplasia led to heart enlargement and right congestive heart failure, with consequent ascites, abdominal swelling, weakness, lethargy, jugular venous distension, and hepatomegaly. Overall, the heart showed prominent enlargement, thickening and dilation of the right chambers, thickening of the tricuspid leaflets, and moderately shortened chordae tendineae. The liver had a nutmeg pattern. Tricuspid valve dysplasia is characterized by malformation of the tricuspid valve leaflets, chord tendineae, or papillary muscles. Malformed tricuspid valves are known to result in variable degrees of regurgitation, leading to right atrial overflow and ventricular eccentric hypertrophy. Differential diagnosis includes myocarditis, tricuspid valve endocarditis, tricuspid endocardiosis, tricuspid valve prolapse and right ventricular dysplasia, right ventricular enlargement with tricuspidal regurgitation due to pulmonary insufficiency, and arrhythmogenic right ventricular cardiomyopathy. Signs of heart murmurs (irregular sounds of the heart) on clinical examination may indicate an irregular blood flow pattern, and imaging tests may be necessary for assessing the presence and severity of any lesions. The epidemiologic, clinical, and pathological findings were consistent with those of tricuspid valve dysplasia. 

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