Sarcoplasmic reticulum function in determining atrioventricular contractile differences in rat heart

1997 ◽  
Vol 273 (5) ◽  
pp. H2498-H2507 ◽  
Author(s):  
Ave Minajeva ◽  
Allen Kaasik ◽  
Kalju Paju ◽  
Enn Seppet ◽  
Anne-Marie Lompré ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Time Course ◽  
Ventricular Myocardium ◽  
Lower Amount ◽  
Functional Coupling ◽  
Cross Sectional ◽  
Tension Development ◽  
Rest Periods ◽  
Tissue Homogenates ◽  
Tension Transients

The relationships between the contractile characteristics and the sarcoplasmic reticulum (SR) function of rat atrial and ventricular trabeculae were compared. The isometric developed tension (DT) and the rates of contraction (+dT/d t) and relaxation (−dT/d t) normalized to cross-sectional area were 3.7, 2.2, and 1.8 times lower, respectively, in intact atrial strips compared with ventricular strips, whereas +dT/d t and −dT/d t(normalized to DT) were 2.3 and 2.8 times higher, respectively, in atria. Atria exhibited a maximal potentiation of DT after shorter rest periods than ventricles and a lower reversal for prolonged rest periods. Caffeine-induced tension transients in saponin-permeabilized fibers suggested that the Ca2+concentration released in atrial myofibrils reached a lower maximum and decayed more slowly than in ventricular preparations. However, the tension-time integrals indicated an equivalent capacity of sequestrable Ca2+ in SR from both tissues. In atrial, as in ventricular myocardium, the SR Ca2+ uptake was more efficiently supported by ATP produced by the SR-bound MM form of creatine kinase (CK; MM-CK) than by externally added ATP, suggesting a tight functional coupling between the SR Ca2+adenosinetriphosphatase (ATPase) and MM-CK. The maximal rate of oxalate-supported Ca2+ uptake was two times higher in atrial than in ventricular tissue homogenates. The SR Ca2+-ATPase 2a mRNA content normalized to 18S RNA was 38% higher in atria than in ventricles, whereas the amount of mRNA encoding the α-myosin heavy chain, calsequestrin, and the ryanodine receptor was similar in both tissues. Thus a lower amount of readily releasable Ca2+ together with a faster uptake rate may partly account for the shorter time course and lower tension development in intact atrial myocardium compared with ventricular myocardium.

Contraction and sarcoplasmic reticulum Ca2+ content in single myocytes of guinea pig heart: effect of ryanodine

1990 ◽  
Vol 259 (4) ◽  
pp. H1222-H1229 ◽  
Author(s):  
B. Lewartowski ◽  
R. G. Hansford ◽  
G. A. Langer ◽  
E. G. Lakatta
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Time Course ◽  
Ventricular Myocardium ◽  
Short Exposure ◽  
Isolated Cells ◽  
Guinea Pig Heart ◽  
Time To Peak ◽  
The Relationship ◽  
Steady State Amplitude

The relationship between the ability of sarcoplasmic reticulum (SR) to accumulate and retain Ca2+ and the electrically stimulated contractions (ESCs) of isolated cells from guinea pig ventricular myocardium was investigated. Caffeine contractures or rapid cooling contractures were used as a relative measure of the SR Ca2+ content. Depletion of SR Ca2+ by short exposure to caffeine (15 mM) or by prolonged rest resulted in a reduction of the amplitude of the ESCs by 83 +/- 14 and 65 +/- 11% (means +/- SD), respectively. This result points to SR as a major source of the Ca2+ that activates contraction. However, depriving the SR of the ability to retain Ca2+ by means of prolonged (up to 75 min) exposure to 0.1 microM ryanodine (as shown by the absence of contractile response to caffeine or cooling) did not prevent an ESC of nearly normal amplitude (81 +/- 24% control), albeit with a reduced contraction velocity and a time to peak contraction prolonged by 51 +/- 11%. Additionally, while rest decay of ESCs was present after ryanodine treatment, the time for the ESCs to recover their steady-state amplitude was prolonged at least twofold. Thus, in contrast with the normal guinea pig cells, ESCs of the myocytes exposed to ryanodine are controlled by sarcolemmal processes. This change in the state of excitation-contraction coupling results mainly in modification of the time course of the ESCs and of the time course of the response of the cells to the change in the rate of stimulation.

Sarcoplasmic reticulum-related changes in cytosolic calcium in pressure-overload-induced feline LV hypertrophy

1993 ◽  
Vol 265 (6) ◽  
pp. H2009-H2016 ◽  
Author(s):  
B. A. Bailey ◽  
S. R. Houser
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Time Course ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Cytosolic Calcium ◽  
Left Ventricular ◽  
Heart Weight ◽  
Body Weight Ratio ◽  
Rest Periods ◽  
Premature Beats

Alterations in Ca2+ homeostasis that involve the sarcoplasmic reticulum (SR) were studied in feline left ventricular (LV) myocytes isolated from hearts with LV hypertrophy induced by slow, progressive pressure overload. At death, severe hypertrophy was evidenced by increased heart weight-to-body weight ratio (8.4 +/- 0.6 vs. 4.2 +/- 0.2 g/kg in controls). Steady-state Ca2+ transients (measured as. indo 1 fluorescence at 410 nm/480 nm; I410/I480) in LV hypertrophy (LVH) myocytes had diminished peak amplitudes (I410/I480 2.28 +/- 0.07 vs. 2.53 +/- 0.07 in controls) and prolonged durations (0.75 +/- 0.03 vs. 0.59 +/- 0.02 s in controls). The magnitude of shortening was reduced and the contractile duration was prolonged in LVH myocytes. The idea that changes in SR function are responsible for these alterations in the Ca2+ transient was tested by studying two aspects of SR-related Ca2+ homeostasis. Restitution of releasable SR Ca2+ was studied by measuring indo 1 transients and contractions during premature beats. The time course of restitution of both the indo 1 transient and contraction of hypertrophy myocytes was significantly slower than in controls. These data suggest that restitution of releasable SR Ca2+ is slowed in hypertrophy myocytes. The reduction of the indo 1 transient and contraction in beats following long rest periods (rest decay) was measured to determine the rate of Ca2+ loss from the SR. Rest decay was significantly (P < 0.05) more pronounced in hypertrophy myocytes, suggesting that Ca2+ loss from the SR is accelerated in these myocytes. (ABSTRACT TRUNCATED AT 250 WORDS)

Changes in Striated Muscle Fibres During Contraction and Growth with Particular Reference to Myofibril Splitting

1971 ◽  
Vol 9 (1) ◽  
pp. 123-137
Author(s):  
G. GOLDSPINK
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Actin Filaments ◽  
Sarcomere Length ◽  
Biceps Brachii ◽  
Hexagonal Lattice ◽  
Muscle Fibres ◽  
Cross Sectional ◽  
Tension Development ◽  
Transverse Tubular System ◽  
Myosin Filaments

Ultrastructural measurements were carried out on the mouse biceps brachii and soleus muscles fixed at different states of contraction and stretch. At a sarcomere length of 2.7-2.9 µm the more peripheral actin filaments ran slightly obliquely from the Z-disk to the A-band. This is due to a mismatch between the rhombic actin lattice at the Z-disk and the hexagonal lattice at the M-line. For a perfect transformation of a rhombic lattice into a hexagonal lattice the ratio of the lattice spacings has to be 1:1.51. However, at this sarcomere length the ratio is about 1:2.0 (Z:M). During contraction the angle of the peripheral actin filaments remains approximately the same because the expansion of the M lattice is compensated for, partly by an increase in the Z-lattice spacing and partly by the bowing of the peripheral myosin filaments. When the sarcomeres are stretched beyond 3.0 µm the myosin filaments straighten out and the Z:M ratio decreases. The ratio of 1:1.51 is almost attained when there is no overlap of the actin and myosin filaments. Ultrastructural measurements were also carried out on biceps brachii muscles of different ages. The lattice spacings for a standard sarcomere length did not change during the post-natal growth period. The amount of myofibrillar material and sarcoplasmic reticulum plus transverse tubular system were estimated using linear analysis for muscles at 3 different stages of growth. It was found that the myofibrillar cross-sectional area in an individual muscle fibre may increase 40-fold during growth and that the transverse tubular and sarcoplasmic reticulum systems increase at about the same rate. In both the biceps brachii and the soleus muscles the myosin and actin filaments are not built into a continuous mass but they are divided into numerous discrete myofibrils. Subdivision of the myofibril mass occurs because the myofibrils split once they attain a certain size. The evidence presented in this paper supports the suggestion that the longitudinal splitting of the myofibrils occurs by the ripping of the Z-disks. When tension is rapidly developed by 2 adjacent sarcomeres a stress is produced at the centre of the Z-disk resulting from the oblique pull of the actin filaments. This causes some of the Z-disk filaments to rip and the rip then extends across the disk with the direction of the weave of the lattice. Evidence for the mechanism includes electron-micrographs showing Z-disks that are apparently just commencing to split; in these cases a hole can be seen in the centre of the disk. A model experiment is described which demonstrates the importance of the rate of tension development in causing myofibril splitting. Rapid tension development produces a snatch effect which causes the Z-disk filaments to break more readily. This may explain why the myofibrils in fast muscles tend to be small and discrete whilst those in slow muscles are larger and more irregular in shape.

Decline of contractility during ischemia-reperfusion injury: actin glutathionylation and its effect on allosteric interaction with tropomyosin

2006 ◽  
Vol 290 (3) ◽  
pp. C719-C727 ◽  
Author(s):  
Frank C. Chen ◽  
Ozgur Ogut
Keyword(s):  
Reperfusion Injury ◽  
Posttranslational Modifications ◽  
Actin Polymerization ◽  
Time Course ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Concentration ◽  
Cross Sectional ◽  
The Impact

The severity and duration of ischemia-reperfusion injury is hypothesized to play an important role in the ability of the heart subsequently to recover contractility. Permeabilized trabeculae were prepared from a rat model of ischemia-reperfusion injury to examine the impact on force generation. Compared with the control perfused condition, the maximum force (Fmax) per cross-sectional area and the rate of tension redevelopment of Ca2+-activated trabeculae fell by 71% and 44%, respectively, during ischemia despite the availability of a high concentration of ATP. The reduction in Fmax with ischemia was accompanied by a decline in fiber stiffness, implying a drop in the absolute number of attached cross bridges. However, the declines during ischemia were largely recovered after reperfusion, leading to the hypothesis that intrinsic, reversible posttranslational modifications to proteins of the contractile filaments occur during ischemia-reperfusion injury. Examination of thin-filament proteins from ischemic or ischemia-reperfused hearts did not reveal proteolysis of troponin I or T. However, actin was found to be glutathionylated with ischemia. Light-scattering experiments demonstrated that glutathionylated G-actin did not polymerize as efficiently as native G-actin. Although tropomyosin accelerated the time course of native and glutathionylated G-actin polymerization, the polymerization of glutathionylated G-actin still lagged native G-actin at all concentrations of tropomyosin tested. Furthermore, cosedimentation experiments demonstrated that tropomyosin bound glutathionylated F-actin with significantly reduced cooperativity. Therefore, glutathionylated actin may be a novel contributor to the diverse set of posttranslational modifications that define the function of the contractile filaments during ischemia-reperfusion injury.

Application of magnetic resonance neurography in the evaluation of patients with peripheral nerve pathology

1996 ◽  
Vol 85 (2) ◽  
pp. 299-309 ◽  
Author(s):  
Aaron G. Filler ◽  
Michel Kliot ◽  
Franklyn A. Howe ◽  
Cecil E. Hayes ◽  
Dawn E. Saunders ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Time Course ◽  
Spin Echo ◽  
Fast Spin Echo ◽  
Mr Neurography ◽  
Magnetic Resonance Neurography ◽  
Cross Sectional ◽  
Content Type ◽  
Direct Nerve ◽  
Fine Print

✓ Currently, diagnosis and management of disorders involving nerves are generally undertaken without images of the nerves themselves. The authors evaluated whether direct nerve images obtained using the new technique of magnetic resonance (MR) neurography could be used to make clinically important diagnostic distinctions that cannot be readily accomplished using existing methods. The authors obtained T2-weighted fast spin—echo fat-suppressed (chemical shift selection or inversion recovery) and T1-weighted images with planes parallel or transverse to the long axis of nerves using standard or phased-array coils in healthy volunteers and referred patients in 242 sessions. Longitudinal and cross-sectional fascicular images readily distinguished perineural from intraneural masses, thus predicting both resectability and requirement for intraoperative electrophysiological monitoring. Fascicle pattern and longitudinal anatomy firmly identified nerves and thus improved the safety of image-guided procedures. In severe trauma, MR neurography identified nerve discontinuity at the fascicular level preoperatively, thus verifying the need for surgical repair. Direct images readily demonstrated increased diameter in injured nerves and showed the linear extent and time course of image hyperintensity associated with nerve injury. These findings confirm and precisely localize focal nerve compressions, thus avoiding some exploratory surgery and allowing for smaller targeted exposures when surgery is indicated. Direct nerve imaging can demonstrate nerve continuity, distinguish intraneural from perineural masses, and localize nerve compressions prior to surgical exploration. Magnetic resonance neurography can add clinically useful diagnostic information in many situations in which physical examinations, electrodiagnostic tests, and existing image techniques are inconclusive.

Structures of Physiological Interest in the Frog Heart Ventricle

1972 ◽  
Vol 11 (1) ◽  
pp. 179-203
Author(s):  
SALLY G. PAGE ◽  
R. NIEDERGERKE
Keyword(s):  
Endothelial Cell ◽  
Sarcoplasmic Reticulum ◽  
Volume Ratio ◽  
Frog Heart ◽  
Geometrical Parameters ◽  
Cross Sectional ◽  
Small Surface ◽  
Endothelial Cell Layer ◽  
Ionic Size ◽  
Line Level

Two structures of physiological interest in frog heart ventricles have been examined in detail: (a) the layer of endothelial cells which encloses each bundle of heart fibres, and (b) the sarcoplasmic reticulum (SR) inside the heart fibres. Some additional observations on fibre sizes and types have been made. Movement across the endothelial cell layer of molecules (molecular or ionic size ≤ 12.5 nm) occurs through narrow clefts separating each endothelial cell from its neighbour. This conclusion results from experiments made with the extracellular markers ferritin and horseradish peroxidase. A diffusion equation describing the movement of solutes into and out of the fibre bundle has been derived using several geometrical parameters, such as the length and width of the clefts and the size of the extracellular aqueous space inside the bundle, all of which were determined from electron micrographs of the tissue. The theoretical solution for a stepwise change of external calcium concentration gives a halftime of 2.3 s (± 0.8 s, S.D. of 13 bundles) for diffusion equilibrium at the surface of the heart fibres; this value, however, is likely to be an overestimate, by some 20-30 %, on account of several systematic errors which are described. The sarcoplasmic reticulum in heart fibres consists of a network of thin tubules which partially encircle the myofibrils at Z-line level and also form occasional longitudinal connexions. Branches extend to peripheral regions of the cell and terminate in close apposition to the inner surface of the cell membrane. The volume of the SR is estimated to be approximately 0.5% of the myofibrillar volume of the cells. Cross-sectional areas of heart fibres (and also their shapes) vary considerably, from less than 2 to more than 100 µm2 (average 17.4 µm2).Fibres of large size and small surface/volume ratio contain many fewer myofibrils and more glycogen granules than fibres of the same size but larger surface/volume ratio. Physiological implications of these results are discussed.

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

1994 ◽  
Vol 266 (1) ◽  
pp. H68-H78 ◽  
Author(s):  
C. R. Cory ◽  
R. W. Grange ◽  
M. E. Houston
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Pressure Overload ◽  
Fold Increase ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Tension Development ◽  
Sequestration Potential

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

Reduced information processing speed as primum movens for cognitive decline in MS

2014 ◽  
Vol 21 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Jeroen Van Schependom ◽  
Marie B D’hooghe ◽  
Krista Cleynhens ◽  
Mieke D’hooge ◽  
Marie-Claire Haelewyck ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Information Processing ◽  
Processing Speed ◽  
Time Course ◽  
Age At Onset ◽  
Memory Task ◽  
Cognitive Domain ◽  
Information Processing Speed ◽  
Survival Curves ◽  
Cross Sectional

Background: Cognitive impairment affects half of the multiple sclerosis (MS) patient population and is an important contributor to patients’ daily activities. Most cognitive impairment studies in MS are, however, cross-sectional or/and focused on the early disease stages. Objective: We aim to assess the time course of decline of different cognitive domains. Methods: We collected neuropsychological data on 514 MS patients to construct Kaplan-Meier survival curves of the tests included in the Neuropsychological Screening Battery for MS (NSBMS) and the Symbol Digit Modalities Test (SDMT). Cox-proportional hazard models were constructed to examine the influence of MS onset type, age at onset, gender, depression and level of education on the time course, expressed as age or disease. Results: Survival curves of tests focusing on information processing speed (IPS) declined significantly faster than tests with less specific demands of IPS. Median age for pathological decline was 56.2 years (95% CI: 54.4–58.2) on the SDMT and 63.9 years (95% CI: 60–66.9) on the CLTR, a memory task. Conclusion: In conclusion, IPS is the cognitive domain not only most widely affected by MS but it is also the first cognitive deficit to emerge in MS.

scholarly journals Relationship between five Epigenetic Clocks, Telomere Length and Functional Capacity assessed in Older Adults: Cross-sectional and Longitudinal Analyses

2021 ◽  
Author(s):  
Valentin Max Vetter ◽  
Christian Humberto Kalies ◽  
Yasmine Sommerer ◽  
Dominik Spira ◽  
Johanna Drewelies ◽  
...  
Keyword(s):  
Telomere Length ◽  
Time Course ◽  
Nutritional Assessment ◽  
Depression Scale ◽  
Mini Nutritional Assessment ◽  
Epigenetic Clock ◽  
Cross Sectional ◽  
Biomarkers Of Aging ◽  
Functional Assessments

AbstractDNA methylation age acceleration (DNAmAA, derived from an epigenetic clock) and relative leukocyte telomere length (rLTL) are widely accepted biomarkers of aging. Nevertheless, it is still unclear which aspects of aging they represent best. Here we evaluated longitudinal associations between baseline rLTL and DNAmAA (estimated with 7-CpG clock) and functional assessments covering different domains of aging. Additionally, we made use of cross-sectional data on these assessments and examined their association with DNAmAA estimated by five different DNAm age measures.Two-wave longitudinal data was available for 1,083 participants of the Berlin Aging Study II (BASE-II) who were re-examined on average 7.4 years after baseline as part of the GendAge study. Functional outcomes were assessed with Fried’s frailty score, Tinetti mobility test, falls in the past 12 months (yes/no), Finger-floor distance, Mini Mental State Examination (MMSE), Center for Epidemiologic Studies Depression Scale (CES-D), Activities of Daily Living (ADL), Instrumented ADL (IADL) and Mini Nutritional Assessment (MNA).Overall, we found no evidence for an association between the molecular biomarkers measured at baseline, rLTL and DNAmAA (7-CpG clock), and functional assessments assessed at follow-up. Similarly, a cross-sectional analyses of follow-up data did also not show evidence for associations of the various DNAmAA measures (7-CpG clock, Horvath’s clock, Hannum’s clock PhenoAge, and GrimAge) with functional assessments.In conclusion, neither rLTL nor 7-CpG DNAmAA were able to predict impairment in the analyzed assessments over a ∼7 year time-course. Similarly, DNAmAA as estimated by five epigenetic clocks was not a good cross-sectional marker of health deterioration either.

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