title: Partial ischemia reduces the efficiency of sarcoplasmic reticulum Ca2+ transport in rat EDL.
abstract: To investigate the hypothesis that prolonged partial ischemia would result in a depression in homogenate sarcoplasmic reticulum (SR) Ca2+-sequestering and mechanical properties in muscle, a cuff was placed around the hindlimb of 8 adult Sprague-Dawley rats (267+/-5.8 g; x +/- S.E.) and partially inflated (315 mm Hg) for 2 h. Following occlusion, the EDL was sampled both from the ischemic (I) and contralateral control (C) leg and SR properties compared with the EDL muscles extracted from rats (n = 8) immediately following anaesthetization (CC). Ischemia was indicated by a lower (p < 0.05) concentration (mmol.kg dry wt(-1)) of ATP (19.0+/-0.7 vs. 16.7+/-0.7) and phosphocreatine (58.1+/-5.7 vs. 35.0+/-4.6) in I compared to C. Although Ca2+-ATPase activity (micromol x g protein(-1) x sec(-1)), both maximal and submaximal, was not different between C and I (19.7+/-0.4 vs. 18.5+/-1.3), reductions (p < 0.05) in Ca2+-uptake (mmol x g protein(-1) x sec(-1)) of between 18.2 and 24.7% across a range of submaximal free Ca2+-levels were observed in I compared to C. Lower submaximal Ca2+-ATPase activity and Ca2+-uptake were also observed in the EDL in C compared to CC animals. Time dependent reductions (p < 0.05) were found in peak twitch and maximal tetanic tension in EDL from I but not C. It is concluded that partial ischemia, resulting in modest reductions in energy state in EDL, induces a reduction in Ca2+-uptake independent of changes in Ca2+-ATPase activity. These changes reduce the coupling ratio and the efficiency of Ca2+-transport by SR.
authors.affiliation: Department of Kinesiology, University of Waterloo, Ontario, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Tupling
authors.forename: H
authors.initials: H
authors.lastname: Green
authors.forename: S
authors.initials: S
authors.lastname: Tupling
mesh_terms: D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D004734:Energy Metabolism; D006614:Hindlimb / Q000378:metabolism; D066298:In Vitro Techniques; D017136:Ion Transport; D007511:Ischemia / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012433:Ryanodine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism*; D013997:Time Factors
chemical_list: D010725:Phosphocreatine; D012433:Ryanodine; D019344:Lactic Acid; D000001:Calcimycin; D000252:Calcium-Transporting ATPases; D002118:Calcium