Sequential ischemia/reperfusion results in contralateral skeletal muscle salvage

1996 ◽  
Vol 270 (4) ◽  
pp. H1407-H1413 ◽  
Author(s):  
S. K. Liauw ◽  
B. B. Rubin ◽  
T. F. Lindsay ◽  
A. D. Romaschin ◽  
P. M. Walker
Keyword(s):  
Skeletal Muscle ◽  
Preliminary Analysis ◽  
Adenine Nucleotides ◽  
Ischemia Reperfusion ◽  
Gracilis Muscle ◽  
Muscle Group ◽  
Muscle Ischemia ◽  
Muscle Necrosis ◽  
Shock Proteins

Sequential ischemia/reperfusion in a paired canine gracilis muscle model resulted in significant muscle salvage. In this model, one randomly chosen gracilis muscle was subjected to 5 h of ischemia followed by 48 h of in vivo reperfusion. The contralateral (second) muscle was then made ischemic and reperfused using the same protocol. Muscle necrosis was determined at the end of 48 h of reperfusion. A mean 60% reduction in muscle necrosis was observed in the second group of muscles. Analysis of tissue adenine nucleotides indicated that significant sparing of ATP utilization occurred in the second muscle group during ischemia. Preliminary analysis of tissue heat shock proteins (HSP) showed that the second group of muscles had a different pattern of HSP expression before the onset of ischemia. The results suggest that reduced ATP utilization and altered HSP expression in the second muscle play a role in the tissue salvage observed in this sequential muscle ischemia model.

Therapeutic Metabolic Inhibition: Hydrogen Sulfide Significantly Mitigates Skeletal Muscle Ischemia Reperfusion Injury In Vitro and In Vivo

2010 ◽  
Vol 126 (6) ◽  
pp. 1890-1898 ◽  
Author(s):  
Peter W. Henderson ◽  
Sunil P. Singh ◽  
Andrew L. Weinstein ◽  
Vijay Nagineni ◽  
Daniel C. Rafii ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Metabolic Inhibition ◽  
Muscle Ischemia

Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle

1992 ◽  
Vol 262 (5) ◽  
pp. H1538-H1547 ◽  
Author(s):  
B. B. Rubin ◽  
S. Liauw ◽  
J. Tittley ◽  
A. D. Romaschin ◽  
P. M. Walker
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Time Course ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Prolonged Release ◽  
Intracellular Acidosis ◽  
Edema Formation ◽  
Muscle Necrosis

Skeletal muscle ischemia results in energy depletion and intracellular acidosis. Reperfusion is associated with impaired adenine nucleotide resynthesis, edema formation, and myocyte necrosis. The purpose of these studies was to define the time course of cellular injury and adenine nucleotide depletion and resynthesis in postischemic skeletal muscle during prolonged reperfusion in vivo. The isolated canine gracilis muscle model was used. After 5 h of ischemia, muscles were reperfused for either 1 or 48 h. Lactate and creatine phosphokinase (CPK) release during reperfusion was calculated from arteriovenous differences and blood flow. Adenine nucleotides, nucleosides, bases, and creatine phosphate were quantified by high-performance liquid chromatography, and muscle necrosis was assessed by nitroblue tetrazolium staining. Reperfusion resulted in a rapid release of lactate, which paralleled the increase in blood flow, and a delayed but prolonged release of CPK. Edema formation and muscle necrosis increased between 1 and 48 h of reperfusion (P less than 0.05). Recovery of energy stores during reperfusion was related to the extent of postischemic necrosis, which correlated with the extent of nucleotide dephosphorylation during ischemia (r = 0.88, P less than 0.001). These results suggest that both adenine nucleotide resynthesis and myocyte necrosis, which are protracted processes in reperfusing skeletal muscle, are related to the extent of nucleotide dephosphorylation during ischemia.

Mechanisms of postischemic injury in skeletal muscle: intervention strategies

1996 ◽  
Vol 80 (2) ◽  
pp. 369-387 ◽  
Author(s):  
B. B. Rubin ◽  
A. Romaschin ◽  
P. M. Walker ◽  
D. C. Gute ◽  
R. J. Korthuis
Keyword(s):  
Skeletal Muscle ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Microvascular Dysfunction ◽  
Intervention Strategies ◽  
Atp Production ◽  
Proinflammatory Mediators ◽  
Muscle Ischemia ◽  
Nitric Oxide Metabolism ◽  
Muscle Necrosis

Reperfusion of ischemic skeletal muscle leads to adverse local and systemic effects. These detrimental effects may be attenuated by interfering with or modulating the pathophysiological processes that are set in motion during ischemia and/or reperfusion. The purpose of this paper is to review the different intervention strategies that have been employed in an attempt to elucidate the mechanisms involved in the pathogenesis of skeletal muscle ischemia-reperfusion injury. The results of these studies indicate that the postischemic injury processes that lead to cell dysfunction and death are multifactorial in nature and include oxidant generation, elaboration of proinflammatory mediators, infiltration of leukocytes, Ca2+ overload, phospholipid peroxidation and depletion, impaired nitric oxide metabolism, and reduced ATP production. Although the etiopathogenesis of skeletal muscle ischemia-reperfusion is complex, careful delineation of the mechanisms that contribute to postischemic microvascular dysfunction and muscle necrosis has progressed to the point where rational intervention strategies may be proposed and implemented as potential treatments for skeletal muscle dysfunction associated with ischemia-reperfusion.

Neutrophils as mediators of human skeletal muscle ischemia-reperfusion syndrome

1992 ◽  
Vol 23 (6) ◽  
pp. 627-634 ◽  
Author(s):  
Lucia Formigli ◽  
Lola Domenici Lombardo ◽  
Chiara Adembri ◽  
Sandra Brunelleschi ◽  
Enrico Ferrari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Ischemia

Mechanisms of Pi regulation of the skeletal muscle SR Ca2+ release channel

2000 ◽  
Vol 278 (3) ◽  
pp. C601-C611 ◽  
Author(s):  
Edward M. Balog ◽  
Bradley R. Fruen ◽  
Patricia K. Kane ◽  
Charles F. Louis
Keyword(s):  
Skeletal Muscle ◽  
Single Channel ◽  
Adenine Nucleotides ◽  
Muscle Fibers ◽  
Open Probability ◽  
Release Channel ◽  
High Concentrations ◽  
Channel Open Time ◽  
Stimulation Of

Inorganic phosphate (Pi) accumulates in the fibers of actively working muscle where it acts at various sites to modulate contraction. To characterize the role of Pi as a regulator of the sarcoplasmic reticulum (SR) calcium (Ca2+) release channel, we examined the action of Pi on purified SR Ca2+ release channels, isolated SR vesicles, and skinned skeletal muscle fibers. In single channel studies, addition of Pi to the cis chamber increased single channel open probability ( P o; 0.079 ± 0.020 in 0 Pi, 0.157 ± 0.034 in 20 mM Pi) by decreasing mean channel closed time; mean channel open times were unaffected. In contrast, the ATP analog, β,γ-methyleneadenosine 5′-triphosphate (AMP-PCP), enhanced P o by increasing single channel open time and decreasing channel closed time. Pi stimulation of [3H]ryanodine binding by SR vesicles was similar at all concentrations of AMP-PCP, suggesting Pi and adenine nucleotides act via independent sites. In skinned muscle fibers, 40 mM Pi enhanced Ca2+-induced Ca2+ release, suggesting an in situ stimulation of the release channel by high concentrations of Pi. Our results support the hypothesis that Pi may be an important endogenous modulator of the skeletal muscle SR Ca2+ release channel under fatiguing conditions in vivo, acting via a mechanism distinct from adenine nucleotides.

Ischemia/reperfusion-induced changes in intracellular free Ca2+ levels in rat skeletal muscle fibers – an in vivo study

2000 ◽  
Vol 440 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Tamás Ivanics ◽  
Zsuzsa Miklós ◽  
Zoltán Ruttner ◽  
Sándor Bátkai ◽  
Dick W. Slaaf ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
In Vivo Study ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Induced Changes
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