The increase in calcium binding of cardiac plasma membrane lipoprotein caused by general anesthetics and alcohol

1980 ◽  
Vol 58 (5) ◽  
pp. 525-530 ◽  
Author(s):  
S. Tsuyoshi Ohnishi ◽  
David M. Obzansky ◽  
Henry L. Price
Keyword(s):  
Plasma Membrane ◽  
Calcium Binding ◽  
Contractile Force ◽  
General Anesthetics ◽  
Myocardial Depression ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Membrane Lipoprotein

(1) Ca2+-binding lipoprotein was purified from dog heart plasma membrane and the effect of several general anesthetics, ethanol, and acetaldehyde on the Ca2+ binding was studied.(2) These drugs, which are known to cause myocardial depression increased the Ca2+ binding at clinically useful concentrations.(3) These results raise the possibility that these drugs, by increasing the Ca2+ binding to the plasma membrane, limit the availability of superficially located Ca2+ for excitation–contraction coupling and result in depression of myocardial contractile force.

Correlation between myocardial contractile force and cytosolic inorganic phosphate during early ischemia

1997 ◽  
Vol 272 (3) ◽  
pp. H1333-H1341 ◽  
Author(s):  
M. X. He ◽  
S. Wang ◽  
H. F. Downey
Keyword(s):  
Inorganic Phosphate ◽  
Contractile Force ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Rat Hearts ◽  
Initial Control ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Developed Pressure

To test the role of inorganic phosphate (Pi) in downregulation of myocardial contractile force at the onset of ischemia, Pi of rat hearts was determined with 31P nuclear magnetic resonance spectroscopy. Forty cycles of brief hypoperfusion (30% of baseline flow for 33 s) were used to achieve a time resolution of 0.512 s for comparing dynamic changes in Pi and contractile force. Initial control values of left ventricular developed pressure (LVP), heart rate, and oxygen consumption were 136 +/- 11 mmHg, 236 +/- 4 beats/min, and 95 +/- 3 microl O2 x min(-1) x g(-1); these values were unchanged at the end of the experiment. During the first 10 s of hypoperfusion, Pi increased at a rate (percentage of the total observed change) faster than the decrease in LVP; Pi and LVP then changed at the same rate during the remainder of the hypoperfusion. ADP did not change in advance of LVP. Intracellular pH did not change. The results indicate that Pi plays an important role in initiating the downregulation of myocardial contractile force at the onset of ischemia. Perfusion pressure also declined faster than LVP at the onset of ischemia, indicating potential importance of vascular collapse in contractile downregulation during early ischemia.

scholarly journals Local Control Models of Cardiac Excitation–Contraction Coupling

1999 ◽  
Vol 113 (3) ◽  
pp. 469-489 ◽  
Author(s):  
Michael D. Stern ◽  
Long-Sheng Song ◽  
Heping Cheng ◽  
James S.K. Sham ◽  
Huang Tian Yang ◽  
...  
Keyword(s):  
Lipid Bilayers ◽  
Calcium Binding ◽  
Calcium Release ◽  
Stochastic Dynamics ◽  
Single Channel ◽  
Channel Measurements ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Calcium Induced Calcium Release ◽  
Gating Scheme

In cardiac muscle, release of activator calcium from the sarcoplasmic reticulum occurs by calcium- induced calcium release through ryanodine receptors (RyRs), which are clustered in a dense, regular, two-dimensional lattice array at the diad junction. We simulated numerically the stochastic dynamics of RyRs and L-type sarcolemmal calcium channels interacting via calcium nano-domains in the junctional cleft. Four putative RyR gating schemes based on single-channel measurements in lipid bilayers all failed to give stable excitation–contraction coupling, due either to insufficiently strong inactivation to terminate locally regenerative calcium-induced calcium release or insufficient cooperativity to discriminate against RyR activation by background calcium. If the ryanodine receptor was represented, instead, by a phenomenological four-state gating scheme, with channel opening resulting from simultaneous binding of two Ca2+ ions, and either calcium-dependent or activation-linked inactivation, the simulations gave a good semiquantitative accounting for the macroscopic features of excitation–contraction coupling. It was possible to restore stability to a model based on a bilayer-derived gating scheme, by introducing allosteric interactions between nearest-neighbor RyRs so as to stabilize the inactivated state and produce cooperativity among calcium binding sites on different RyRs. Such allosteric coupling between RyRs may be a function of the foot process and lattice array, explaining their conservation during evolution.

scholarly journals Impact of Loss of T-Tubules on Myocardial Contractile Force and Kinetics

2010 ◽  
Vol 98 (3) ◽  
pp. 5a ◽  
Author(s):  
Cecilia Ferrantini ◽  
Raffaele Coppini ◽  
Guo Liang Wang ◽  
Mei Luo Zhang ◽  
Ewout de Vries ◽  
...  
Keyword(s):  
Contractile Force ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
T Tubules
Sign in / Sign up

Export Citation Format

Share Document