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 ◽  
...  
1997 ◽  
Vol 272 (3) ◽  
pp. H1333-H1341 ◽  
Author(s):  
M. X. He ◽  
S. Wang ◽  
H. F. Downey

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.


1980 ◽  
Vol 58 (5) ◽  
pp. 525-530 ◽  
Author(s):  
S. Tsuyoshi Ohnishi ◽  
David M. Obzansky ◽  
Henry L. Price

(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.


1980 ◽  
Vol 238 (3) ◽  
pp. H406-H413 ◽  
Author(s):  
D. E. Euler

In adult dogs anesthetized with pentobarbital sodium, ventricular fibrillation thresholds determined by scanning the vulnerable period with a train of 14 pulses (4 ms, 100 Hz) were significantly less (P less than 0.01) than fibrillation thresholds determined by scanning the vulnerable period with a single 10-ms stimulus. Following beta-adrenergic blockade with propranolol, the relative increase in the fibrillation thresholds measured with trains was about seven times greater than the relative increase in the single-stimulus threshold (P less than 0.01). In a group of animals subjected to chronic cardiac denervation, fibrillation thresholds measured with trains were about three times greater than in a group of shamthoracotomized animals (P less than 0.01). Furthermore, the train fibrillation thresholds of the catecholamine-depleted hearts were not significantly different from the train thresholds of beta-blocked innervated hearts. These data, coupled with the finding that trains of stimuli produced a marked augmentation in local myocardial contractile force, suggest that locally released norepinephrine during a fibrillation-threshold determination may exert a profound influence on the level of current necessary to evoke fibrillation.


1975 ◽  
Vol 148 (2) ◽  
pp. 578-583 ◽  
Author(s):  
R. A. Brace ◽  
J. B. Scott ◽  
W.-T. Chen ◽  
D. K. Anderson ◽  
F. J. Haddy

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