Mechanism of Early Contractile Failure During Ischemia

1994 ◽  
pp. 71-84
Author(s):  
Hideo Kusuoka ◽  
Yukihiro Koretsune ◽  
Mary C. Corretti ◽  
Eduardo Marban
Keyword(s):  
Contractile Failure

1039: Substrate Depletion is Central to Contractile Failure in a Model of Ischaemic Priapism

2005 ◽  
Vol 173 (4S) ◽  
pp. 282-282
Author(s):  
Pardeep Kumar ◽  
S. Minhas ◽  
C.Y. Li ◽  
P. Kell ◽  
D.J. Ralph ◽  
...  
Keyword(s):  
Contractile Failure

scholarly journals Metabolic changes during ischaemia and their role in contractile failure in isolated ferret hearts.

1992 ◽  
Vol 454 (1) ◽  
pp. 467-490 ◽  
Author(s):  
A C Elliott ◽  
G L Smith ◽  
D A Eisner ◽  
D G Allen
Keyword(s):  
Metabolic Changes ◽  
Contractile Failure

Time course of structure, function, and metabolic changes due to an exogenous source of oxygen metabolites in rat heart

1989 ◽  
Vol 67 (12) ◽  
pp. 1549-1559 ◽  
Author(s):  
Madhu Gupta ◽  
Pawan K. Singal
Keyword(s):  
Time Course ◽  
Active Oxygen Species ◽  
Lipid Peroxide ◽  
High Energy ◽  
Active Oxygen ◽  
High Energy Phosphates ◽  
Oxygen Species ◽  
Peroxide Content ◽  
Resting Tension ◽  
Contractile Failure

Effects of xanthine (2 mM) and xanthine oxidase (10 U/L) perfusion on myocardial function, lipid peroxide content, high-energy phosphates and their metabolites, and ultrastructure were examined in isolated perfused rat hearts to define the time course of myocardial injury due to exogenous supply of active oxygen species. Peak-developed force and dF/dt showed a decline within 5 min and complete contractile failure was seen at 20 min. Resting tension was higher at 10 min and reached a maximum value of 400% at 40 min. These changes in contractile parameters were reduced by superoxide dismutase (1.2 × 105 U/L), catalase (2 and 4 × 104 U/L), and mannitol (10 and 20 mM). Lipid peroxide content was significantly higher at 5 min and rose continuously with xanthine – xanthine oxidase (X–XO) perfusion. A close correlation was noted (r = 0.935) between increased lipid peroxide content and a decrease in peak-developed force. Creatine phosphate and adensoine triphosphate (ATP) showed a time-dependent decrease due to X–XO perfusion. Loss of ATP also correlated (r = 0.819) with the contractile failure. Adenosine diphosphate showed an increase at 5 min followed by a decrease at 20 and 40 min. Adenosine monophosphate, adenosine, and creatine content increased with X–XO perfusion. In a semiquantitative morphometric study, significant myocardial and vascular changes became apparent only after 10 min of X–XO perfusion. When a 5-min perfusion with X–XO was followed by a control perfusion, a recovery of developed force and normal structure was noted at 40 min. These data show that X–XO induced contractile failure involves partially reduced forms of oxygen such as superoxide, hydroxyl radicals, and hydrogen peroxide. The negative inotropic effect of a vascular supply of these active oxygen species may be related to increased lipid peroxidation as well as the loss of high-energy phosphates. Structural damage to myocytes and blood vessels and a rise in resting tension were delayed events requiring a continuous and longer exposure to radical species.Key words: myocardial failure, oxygen radicals, lipid peroxidation, myocardial high-energy phosphates, myocardial cell damage, antioxidant protection.

scholarly journals Mechanism of early contractile failure during hypoxia in intact ferret heart: evidence for modulation of maximal Ca2+-activated force by inorganic phosphate.

1986 ◽  
Vol 59 (3) ◽  
pp. 270-282 ◽  
Author(s):  
H Kusuoka ◽  
M L Weisfeldt ◽  
J L Zweier ◽  
W E Jacobus ◽  
E Marban
Keyword(s):  
Inorganic Phosphate ◽  
Ferret Heart ◽  
Contractile Failure

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of α-fodrin

2001 ◽  
Vol 281 (3) ◽  
pp. H1286-H1294 ◽  
Author(s):  
Tsuyoshi Tsuji ◽  
Yoshimi Ohga ◽  
Yoshiro Yoshikawa ◽  
Susumu Sakata ◽  
Takehisa Abe ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Calpain Inhibitor ◽  
Contractile Dysfunction ◽  
Area Index ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Total Mechanical Energy ◽  
Cardiac Contractile Dysfunction ◽  
Contractile Failure

The aim of the present study was to examine the mechanisms of Ca2+ overload-induced contractile dysfunction in rat hearts independent of ischemia and acidosis. Experiments were performed on 30 excised cross-circulated rat heart preparations. After hearts were exposed to high Ca2+, there was a contractile failure associated with a parallel downward shift of the linear relation between myocardial O2 consumption per beat and systolic pressure-volume area (index of a total mechanical energy per beat) in left ventricles from all seven hearts that underwent the protocol. This result suggested a decrease in O2consumption for total Ca2+ handling in excitation-contraction coupling. In the hearts that underwent the high Ca2+ protocol and had contractile failure, we found marked proteolysis of a cytoskeleton protein, α-fodrin, whereas other proteins were unaffected. A calpain inhibitor suppressed the contractile failure by high Ca2+, the decrease in O2 consumption for total Ca2+ handling, and membrane α-fodrin degradation. We conclude that the exposure to high Ca2+ may induce contractile dysfunction possibly by suppressing total Ca2+ handling in excitation-contraction coupling and degradation of membrane α-fodrin via activation of calpain.

Glucose uptake in rat soleus: effect of acute unloading and subsequent reloading

1988 ◽  
Vol 64 (4) ◽  
pp. 1428-1432 ◽  
Author(s):  
E. J. Henriksen ◽  
M. E. Tischler
Keyword(s):  
Maximum Voluntary Contraction ◽  
Lactate Concentration ◽  
Creatine Phosphate ◽  
Voluntary Contraction ◽  
Gradual Decline ◽  
Muscle Lactate ◽  
Generating Capacity ◽  
Target Force ◽  
Muscle Biopsies ◽  
Contractile Failure

Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.

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