scholarly journals Development of Ischemic Contracture in Isolated Skeletal Muscles: Relation to the Capacity for Anaerobic Glycolysis.

1994 ◽  
Vol 44 (1) ◽  
pp. 105-115 ◽  
Author(s):  
Mehis VIRU
Keyword(s):  
Skeletal Muscles ◽  
Anaerobic Glycolysis ◽  
Ischemic Contracture

Adenosine protects ischemic and reperfused myocardium by receptor-mediated mechanisms

1993 ◽  
Vol 264 (1) ◽  
pp. H163-H170 ◽  
Author(s):  
M. F. Janier ◽  
J. L. Vanoverschelde ◽  
S. R. Bergmann
Keyword(s):  
Protective Action ◽  
Lactate Production ◽  
Low Flow ◽  
Anaerobic Glycolysis ◽  
Ischemia And Reperfusion ◽  
Tissue Necrosis ◽  
Ischemic Contracture ◽  
Developed Pressure ◽  
Stimulation Of

To evaluate the role of adenosine receptors in the mediation of adenosine-induced protection of the heart during ischemia and reperfusion, isolated rabbit hearts were perfused at constant flow with 1 microM adenosine started before low-flow ischemia followed by reperfusion. Adenosine delayed the time of onset of ischemic contracture [to 28 +/- 19 (SD) min compared with 10 +/- 10 min in control hearts] and decreased the amplitude of ischemic contracture (29 +/- 16 vs. 48 +/- 14 mmHg; P<0.05 for each compared with controls). This protection was accompanied by an increase in tissue ATP content (1.72 +/- 0.78 vs. 0.96 +/- 0.23 mumol/g; P < 0.05) and stimulation of anaerobic glycolysis (lactate production of 0.78 +/- 0.28 mumol.g-1 x min-1 compared with 0.53 +/- 0.23 mumol.g-1 x min-1; P < 0.05). Functional recovery during reperfusion was enhanced by adenosine (developed pressure 88 +/- 16% compared with 57 +/- 23% of baseline; P < 0.05), and tissue necrosis, assessed by creatine kinase release, was decreased. The potent, nonselective adenosine receptor blocker 8-phenyltheophylline (10 microM) blocked all of the salutary effects of adenosine. Adenosine given only at reperfusion modestly attenuated reperfusion-induced contracture. The results suggest that exogenous adenosine attenuates ischemic injury by receptor-mediated stimulation of anaerobic glycolysis. During reperfusion its protective action is related to vasodilation.

Ischemic contracture begins when anaerobic glycolysis stops: a 31P-NMR study of isolated rat hearts

1991 ◽  
Vol 261 (2) ◽  
pp. H469-H478 ◽  
Author(s):  
P. B. Kingsley ◽  
E. Y. Sako ◽  
M. Q. Yang ◽  
S. D. Zimmer ◽  
K. Ugurbil ◽  
...  
Keyword(s):  
Intracellular Ph ◽  
Left Ventricular ◽  
Atp Depletion ◽  
Resonance Spectroscopy ◽  
Anaerobic Glycolysis ◽  
Ischemic Contracture ◽  
Atp Levels ◽  
Nmr Study ◽  
Rat Hearts ◽  
Glycolytic Atp

The relationships among myocardial ATP, intracellular pH, and ischemic contracture in Langendorff-perfused rat hearts were investigated by 31P nuclear magnetic resonance spectroscopy during total global normothermic ischemia while the left ventricular pressure was recorded continuously via an intraventricular balloon. Glucose-perfused hearts (n = 63) were divided into five groups based on the time of onset of contracture (TOC), and three other groups of hearts were treated to vary the ischemic glycogen availability. ATP levels, which showed no evidence of accelerated ATP depletion during contracture, were significant and variable at TOC. Intracellular pH initially declined and then leveled off at TOC, with lower final pH in hearts with later TOC. We conclude that contracture began when anaerobic glycolysis (and thus glycolytic ATP synthesis) stopped. These results, though consistent with the concept that ischemic contracture in normal hearts results from rigor bond formation due to low ATP levels at the myofibrils, suggest that TOC is more closely related to glycolytic ATP production than to total cellular ATP content, thus providing evidence of some degree of subcellular compartmentation or metabolite channeling. In glycolytically inhibited hearts, the quite early contracture may have a Ca2+ component.

Distribution of c-protein isoforms in sarcomeres of developing chick skeletal muscle

1988 ◽  
Vol 46 ◽  
pp. 226-227
Author(s):  
D. A. Fischman ◽  
J. E. Dennis ◽  
T. Obinata ◽  
H. Takano-Ohmuro
Keyword(s):  
Skeletal Muscles ◽  
Thick Filament ◽  
Protein Isoforms ◽  
Actin Binding ◽  
Striated Muscles ◽  
C Protein ◽  
Sarcomeric Protein ◽  
Thick Filaments ◽  
Cross Bridges ◽  
Bridge Bearing

C-protein is a 150 kDa protein found within the A bands of all vertebrate cross-striated muscles. By immunoelectron microscopy, it has been demonstrated that C-protein is distributed along a series of 7-9 transverse stripes in the medial, cross-bridge bearing zone of each A band. This zone is now termed the C-zone of the sarcomere. Interest in this protein has been sparked by its striking distribution in the sarcomere: the transverse repeat between C-protein stripes is 43 nm, almost exactly 3 times the 14.3 nm axial repeat of myosin cross-bridges along the thick filaments. The precise packing of C-protein in the thick filament is still unknown. It is the only sarcomeric protein which binds to both myosin and actin, and the actin-binding is Ca-sensitive. In cardiac and slow, but not fast, skeletal muscles C-protein is phosphorylated. Amino acid composition suggests a protein of little or no αhelical content. Variant forms (isoforms) of C-protein have been identified in cardiac, slow and embryonic muscles.

The effect of ionophore A23178 on the α-actinin crosslinks in the z-band of frog skeletal muscle: An EM study

1986 ◽  
Vol 44 ◽  
pp. 154-155
Author(s):  
F.T. Llados ◽  
V. Krlho ◽  
G.D. Pappas
Keyword(s):  
Muscle Damage ◽  
Transmitter Release ◽  
Skeletal Muscles ◽  
Calcium Uptake ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Ach Release ◽  
Sustained Action ◽  
Calcium Deposits ◽  
Intense Stimulation

It Is known that Ca++ enters the muscle fiber at the junctional area during the action of the neurotransmitter, acetylcholine (ACh). Pappas and Rose demonstrated that following Intense stimulation, calcium deposits are found In the postsynaptic muscle membrane, Indicating the existence of calcium uptake In the postsynaptic area following ACh release. In addition to this calcium uptake, when mammal Ian skeletal muscles are exposed to a sustained action of the neurotransmitter, muscle damage develops. These same effects, l.e., Increased transmitter release, calcium uptake and finally muscle damage, can be obtained by Incubating the muscle with lonophore A23178.

Comparative Morphology of Skeletal Muscles in Man and Macaque

1993 ◽  
Vol 5 (2) ◽  
pp. 137-146
Author(s):  
Seiichiro INOKUCHI ◽  
Tadanao KIMURA ◽  
Masataka SUZUKI ◽  
Junji ITO ◽  
Hiroo KUMAKURA
Keyword(s):  
Skeletal Muscles ◽  
Comparative Morphology

2482-PUB: Circadian Clock Regulates Fuel Metabolism in Skeletal Muscles

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2482-PUB
Author(s):  
JIDONG LIU ◽  
ZHENG SUN
Keyword(s):  
Circadian Clock ◽  
Skeletal Muscles ◽  
Fuel Metabolism

Diabetes decreases Na+-K+ pump concentration in skeletal muscles, heart ventricular muscle, and peripheral nerves of rat

Diabetes ◽  
1987 ◽  
Vol 36 (7) ◽  
pp. 842-848 ◽  
Author(s):  
K. Kjeldsen ◽  
H. Braendgaard ◽  
P. Sidenius ◽  
J. S. Larsen ◽  
A. Norgaard
Keyword(s):  
Peripheral Nerves ◽  
Skeletal Muscles ◽  
Ventricular Muscle
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