Intracellular Calcium Modulators for Cardiac Muscle in Pathological Conditions.

1996 ◽  
Vol 37 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Nobumasa ISHIDE
Keyword(s):  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Pathological Conditions ◽  
Calcium Modulators

Interrelating of ventricular pressure and intracellular calcium in intact hearts

1997 ◽  
Vol 273 (3) ◽  
pp. H1509-H1522 ◽  
Author(s):  
D. Baran ◽  
K. Ogino ◽  
R. Stennett ◽  
M. Schnellbacher ◽  
D. Zwas ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Heart Function ◽  
Strong Support ◽  
Force Production ◽  
Muscle Length ◽  
Calcium Transient ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Critical Examination

Although the mechanistic link between variations in intracellular calcium and its effects on myofilament regulatory proteins and subsequent impact on cardiac muscle force production have been known for some time, characterization of cardiac contractile properties are predominantly confined to phenomenological descriptions of the relationship between either muscle length and force or ventricular pressure and volume. However, as recognition of the limitations of these theories grow, investigators have begun to look toward more fundamental theories of cardiac contraction to explain whole heart function. The goal of the present study was first to explore, on a theoretical level, the degree of complexity required in a biochemical model necessary to adequately explain both equilibrium and twitch contraction behavior of cardiac muscle. Central to this analysis was a critical examination of the evidence for and against the importance of a calcium-free, force-generating state. Next, we determined whether such theories can actually account for the interrelationships between the experimentally measured time courses of pressure generation and the calcium transient measured from intact ventricles during both normal twitches as well as during complex contraction sequences. The results of this analysis provide strong support for a four-state model, including the calcium-free, force-generating state. These results will help guide the continuing quest for a mechanistic theory of ventricular function.

Effects of Sevoflurane on the Intracellular Ca2+Transient in Ferret Cardiac Muscle

2000 ◽  
Vol 93 (6) ◽  
pp. 1500-1508 ◽  
Author(s):  
Anna E. Bartunek ◽  
Philippe R. Housmans
Keyword(s):  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Negative Inotropic Effect ◽  
Calcium Transient ◽  
Ventricular Myocardium ◽  
Peak Force ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Intracellular Calcium Transient

Background Sevoflurane depresses myocardial contractility by decreasing transsarcolemmal Ca2+ influx. In skinned muscle fibers, sevoflurane affects actin-myosin cross-bridge cycling, which might contribute to the negative inotropic effect. It is uncertain to what extent decreases in Ca2+ sensitivity of the contractile proteins play a role in the negative inotropic effect of sevoflurane in intact cardiac muscle tissue. The aim of this study was to assess whether sevoflurane decreases myofibrillar Ca2+ sensitivity in intact living cardiac fibers and to quantify the relative importance of changes in myofibrillar Ca2+ sensitivity versus changes in myoplasmic Ca2+ availability by sevoflurane. Methods The effects of sevoflurane 0-4.05% vol/vol (0-1.5 minimum alveolar concentration [MAC]) on isometric and isotonic variables of contractility and on the intracellular calcium transient were assessed in isolated ferret right ventricular papillary muscles microinjected with the Ca2+-regulated photoprotein aequorin. The intracellular calcium transient was analyzed in the context of a multicompartment model of intracellular Ca2+ buffers in mammalian ventricular myocardium. Results Sevoflurane decreased contractility, time to peak force, time to half isometric relaxation, and the [Ca2+]i transient in a reversible, concentration-dependent manner. Increasing [Ca2+]o in the presence of sevoflurane to produce peak force equal to control increased intracellular Ca2+ transient higher than control. Conclusions Sevoflurane decreases myoplasmic Ca2+ availability and myofibrillar Ca2+ sensitivity in equal proportions except at 4.05% vol/vol (1.5 MAC), where Ca2+ availability is decreased more. These changes are at the basis of the negative inotropic effect of sevoflurane in mammalian ventricular myocardium.

scholarly journals The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum–Plasma Membrane Junctions in Striated Muscle

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 109
Author(s):  
Stefano Perni
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Structure Prediction ◽  
Calcium Release ◽  
Striated Muscle ◽  
Short Review ◽  
Published Data ◽  
Intracellular Calcium Release

Contraction of striated muscle is triggered by a massive release of calcium from the sarcoplasmic reticulum (SR) into the cytoplasm. This intracellular calcium release is initiated by membrane depolarization, which is sensed by voltage-gated calcium channels CaV1.1 (in skeletal muscle) and CaV1.2 (in cardiac muscle) in the plasma membrane (PM), which in turn activate the calcium-releasing channel ryanodine receptor (RyR) embedded in the SR membrane. This cross-communication between channels in the PM and in the SR happens at specialized regions, the SR-PM junctions, where these two compartments come in close proximity. Junctophilin1 and Junctophilin2 are responsible for the formation and stabilization of SR-PM junctions in striated muscle and actively participate in the recruitment of the two essential players in intracellular calcium release, CaV and RyR. This short review focuses on the roles of junctophilins1 and 2 in the formation and organization of SR-PM junctions in skeletal and cardiac muscle and on the functional consequences of the absence or malfunction of these proteins in striated muscle in light of recently published data and recent advancements in protein structure prediction.

Electron Probe Analysis and Cryoultramicrotomy of Cardiac Muscle: Mitochondrial Granules

1975 ◽  
Vol 33 ◽  
pp. 532-533 ◽  
Author(s):  
Avril V. Somlyo ◽  
J. Silcox ◽  
A.P. Somlyo
Keyword(s):  
Cardiac Muscle ◽  
Papillary Muscle ◽  
Electron Probe ◽  
Ventricular Myocardium ◽  
Cytoplasmic Calcium ◽  
Electron Probe Analysis ◽  
Thin Sections ◽  
Pathological Conditions ◽  
Carbon Coated ◽  
Morphological Detail

The contribution of mitochondria to the regulation of cytoplasmic calcium levels in the heart is an unsettled question. In certain pathological conditions, mitochondrial granules thought to contain calcium have been found in fixed myocardium.Mouse ventricular myocardium, papillary muscle and trabeculae, unfixed and without cryoprotectants, were quick-frozen in Freon 22 cooled in liquid N2 or in liquid N2 slush. Sections were cut with glass knives at -100-120° C, placed on Cu or carbon coated nylon grids, and dried on a cold block at l0-2-10-5 Torr. Some sections were vapor stained with crystalline Os under vacuum, but the analyses reported are of unstained sections. Even 5 minute “pre-fixation” with glutaraldehyde, before cryoultramicrotomy, or staining of unfixed frozen thin sections with NH4 molybdate removed elements of interest (e.g.: K).The morphological detail detectable by inherent contrast or Os vapor staining varied in different preparations and even in different regions of the same sections. In fortuitous examples (Fig. 1) the filament lattice could be clearly demonstrated.

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