The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle

Yasumitsu Mizobata, Derek Prechek, Jan D. Rounds, Vickye Robinson, Douglas W. Wilmore, Danny O. Jacobs

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Sepsis increases phosphocreatine (PCr) breakdown and reduces PCr stores in skeletal muscle. To determine if systemic infection impairs mitochondrial function, in vivo 13P magnetic resonance spectroscopy (31P MRS) studies of the gastrocnemius muscle were performed in virus-free male Wistar rats 24 or 48 hr after cecal ligation and 18-gauge needle single puncture (24°CLP, n = 16; 48°CLP, n = 15) or sham operation (24°SHAM, n = 18; 48°SHAM, n = 13). Physiologic saline (6 ml/100 g body wt) was injected intraperitoneally for fluid resuscitation. Water but no food was allowed in all animals. High resolution (8.45 Tesla) 31P MRS spectra, obtained at rest and during exercise using a 1.4-cm surface coil, were used to calculate PCr/ATP, PCr/Pi ratios, and intracellular pH. Steady-state muscle exercise was induced by supramaximal sciatic nerve stimulation at 10 Hz for 10 min. Recovery of PCr/(PCr + Pi) ratios after exercise was fitted to a monoexponential curve. The resultant function was used to calculate the half time for PCr recovery, the initial PCr resynthesis rate, and the maximal oxidative ATP synthesis rate, which reflect the rephosphorylation of ADP and are therefore measures of mitochondrial oxidative capacity. PCr/ATP ratios decreased by 12 and 11%, 24 and 48 hr after CLP, respectively. The PCr/Pi ratios decreased incrementally (7% in 24°CLP vs 23% in 48°CLP animals). Twenty-four hours after operation the half time for PCr recovery was shortened while the initial PCr resynthesis rate and maximal oxidative ATP synthesis rate were accelerated in CLP animals compared to controls. By 48 hr these indices of mitochondrial function were significantly slowed. Intracellular pH was well maintained in resting skeletal muscle in all animals. These data demonstrate that the reduction in high energy phosphate (PCr) stores observed during early sepsis are not secondary to mitochondrial dysfunction; in fact, the organelles' ability to rephosphorylate ADP is enhanced.

Original languageEnglish (US)
Pages (from-to)165-173
Number of pages9
JournalJournal of Surgical Research
Volume59
Issue number1
DOIs
StatePublished - Jul 1995
Externally publishedYes

Fingerprint

Phosphocreatine
Skeletal Muscle
Infection
Adenosine Triphosphate
Adenosine Diphosphate
Sepsis
Sciatic Nerve
Punctures
Resuscitation
Organelles
Needles
Ligation
Wistar Rats
Magnetic Resonance Spectroscopy

ASJC Scopus subject areas

  • Surgery

Cite this

Mizobata, Y., Prechek, D., Rounds, J. D., Robinson, V., Wilmore, D. W., & Jacobs, D. O. (1995). The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle. Journal of Surgical Research, 59(1), 165-173. https://doi.org/10.1006/jsre.1995.1149

The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle. / Mizobata, Yasumitsu; Prechek, Derek; Rounds, Jan D.; Robinson, Vickye; Wilmore, Douglas W.; Jacobs, Danny O.

In: Journal of Surgical Research, Vol. 59, No. 1, 07.1995, p. 165-173.

Research output: Contribution to journalArticle

Mizobata, Y, Prechek, D, Rounds, JD, Robinson, V, Wilmore, DW & Jacobs, DO 1995, 'The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle', Journal of Surgical Research, vol. 59, no. 1, pp. 165-173. https://doi.org/10.1006/jsre.1995.1149
Mizobata, Yasumitsu ; Prechek, Derek ; Rounds, Jan D. ; Robinson, Vickye ; Wilmore, Douglas W. ; Jacobs, Danny O. / The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle. In: Journal of Surgical Research. 1995 ; Vol. 59, No. 1. pp. 165-173.
@article{9751850e1f704395974670124040aa8c,
title = "The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle",
abstract = "Sepsis increases phosphocreatine (PCr) breakdown and reduces PCr stores in skeletal muscle. To determine if systemic infection impairs mitochondrial function, in vivo 13P magnetic resonance spectroscopy (31P MRS) studies of the gastrocnemius muscle were performed in virus-free male Wistar rats 24 or 48 hr after cecal ligation and 18-gauge needle single puncture (24°CLP, n = 16; 48°CLP, n = 15) or sham operation (24°SHAM, n = 18; 48°SHAM, n = 13). Physiologic saline (6 ml/100 g body wt) was injected intraperitoneally for fluid resuscitation. Water but no food was allowed in all animals. High resolution (8.45 Tesla) 31P MRS spectra, obtained at rest and during exercise using a 1.4-cm surface coil, were used to calculate PCr/ATP, PCr/Pi ratios, and intracellular pH. Steady-state muscle exercise was induced by supramaximal sciatic nerve stimulation at 10 Hz for 10 min. Recovery of PCr/(PCr + Pi) ratios after exercise was fitted to a monoexponential curve. The resultant function was used to calculate the half time for PCr recovery, the initial PCr resynthesis rate, and the maximal oxidative ATP synthesis rate, which reflect the rephosphorylation of ADP and are therefore measures of mitochondrial oxidative capacity. PCr/ATP ratios decreased by 12 and 11{\%}, 24 and 48 hr after CLP, respectively. The PCr/Pi ratios decreased incrementally (7{\%} in 24°CLP vs 23{\%} in 48°CLP animals). Twenty-four hours after operation the half time for PCr recovery was shortened while the initial PCr resynthesis rate and maximal oxidative ATP synthesis rate were accelerated in CLP animals compared to controls. By 48 hr these indices of mitochondrial function were significantly slowed. Intracellular pH was well maintained in resting skeletal muscle in all animals. These data demonstrate that the reduction in high energy phosphate (PCr) stores observed during early sepsis are not secondary to mitochondrial dysfunction; in fact, the organelles' ability to rephosphorylate ADP is enhanced.",
author = "Yasumitsu Mizobata and Derek Prechek and Rounds, {Jan D.} and Vickye Robinson and Wilmore, {Douglas W.} and Jacobs, {Danny O.}",
year = "1995",
month = "7",
doi = "10.1006/jsre.1995.1149",
language = "English (US)",
volume = "59",
pages = "165--173",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - The Duration of Infection Modifies Mitochondrial Oxidative Capacity in Rat Skeletal Muscle

AU - Mizobata, Yasumitsu

AU - Prechek, Derek

AU - Rounds, Jan D.

AU - Robinson, Vickye

AU - Wilmore, Douglas W.

AU - Jacobs, Danny O.

PY - 1995/7

Y1 - 1995/7

N2 - Sepsis increases phosphocreatine (PCr) breakdown and reduces PCr stores in skeletal muscle. To determine if systemic infection impairs mitochondrial function, in vivo 13P magnetic resonance spectroscopy (31P MRS) studies of the gastrocnemius muscle were performed in virus-free male Wistar rats 24 or 48 hr after cecal ligation and 18-gauge needle single puncture (24°CLP, n = 16; 48°CLP, n = 15) or sham operation (24°SHAM, n = 18; 48°SHAM, n = 13). Physiologic saline (6 ml/100 g body wt) was injected intraperitoneally for fluid resuscitation. Water but no food was allowed in all animals. High resolution (8.45 Tesla) 31P MRS spectra, obtained at rest and during exercise using a 1.4-cm surface coil, were used to calculate PCr/ATP, PCr/Pi ratios, and intracellular pH. Steady-state muscle exercise was induced by supramaximal sciatic nerve stimulation at 10 Hz for 10 min. Recovery of PCr/(PCr + Pi) ratios after exercise was fitted to a monoexponential curve. The resultant function was used to calculate the half time for PCr recovery, the initial PCr resynthesis rate, and the maximal oxidative ATP synthesis rate, which reflect the rephosphorylation of ADP and are therefore measures of mitochondrial oxidative capacity. PCr/ATP ratios decreased by 12 and 11%, 24 and 48 hr after CLP, respectively. The PCr/Pi ratios decreased incrementally (7% in 24°CLP vs 23% in 48°CLP animals). Twenty-four hours after operation the half time for PCr recovery was shortened while the initial PCr resynthesis rate and maximal oxidative ATP synthesis rate were accelerated in CLP animals compared to controls. By 48 hr these indices of mitochondrial function were significantly slowed. Intracellular pH was well maintained in resting skeletal muscle in all animals. These data demonstrate that the reduction in high energy phosphate (PCr) stores observed during early sepsis are not secondary to mitochondrial dysfunction; in fact, the organelles' ability to rephosphorylate ADP is enhanced.

AB - Sepsis increases phosphocreatine (PCr) breakdown and reduces PCr stores in skeletal muscle. To determine if systemic infection impairs mitochondrial function, in vivo 13P magnetic resonance spectroscopy (31P MRS) studies of the gastrocnemius muscle were performed in virus-free male Wistar rats 24 or 48 hr after cecal ligation and 18-gauge needle single puncture (24°CLP, n = 16; 48°CLP, n = 15) or sham operation (24°SHAM, n = 18; 48°SHAM, n = 13). Physiologic saline (6 ml/100 g body wt) was injected intraperitoneally for fluid resuscitation. Water but no food was allowed in all animals. High resolution (8.45 Tesla) 31P MRS spectra, obtained at rest and during exercise using a 1.4-cm surface coil, were used to calculate PCr/ATP, PCr/Pi ratios, and intracellular pH. Steady-state muscle exercise was induced by supramaximal sciatic nerve stimulation at 10 Hz for 10 min. Recovery of PCr/(PCr + Pi) ratios after exercise was fitted to a monoexponential curve. The resultant function was used to calculate the half time for PCr recovery, the initial PCr resynthesis rate, and the maximal oxidative ATP synthesis rate, which reflect the rephosphorylation of ADP and are therefore measures of mitochondrial oxidative capacity. PCr/ATP ratios decreased by 12 and 11%, 24 and 48 hr after CLP, respectively. The PCr/Pi ratios decreased incrementally (7% in 24°CLP vs 23% in 48°CLP animals). Twenty-four hours after operation the half time for PCr recovery was shortened while the initial PCr resynthesis rate and maximal oxidative ATP synthesis rate were accelerated in CLP animals compared to controls. By 48 hr these indices of mitochondrial function were significantly slowed. Intracellular pH was well maintained in resting skeletal muscle in all animals. These data demonstrate that the reduction in high energy phosphate (PCr) stores observed during early sepsis are not secondary to mitochondrial dysfunction; in fact, the organelles' ability to rephosphorylate ADP is enhanced.

UR - http://www.scopus.com/inward/record.url?scp=0029102095&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029102095&partnerID=8YFLogxK

U2 - 10.1006/jsre.1995.1149

DO - 10.1006/jsre.1995.1149

M3 - Article

C2 - 7630122

AN - SCOPUS:0029102095

VL - 59

SP - 165

EP - 173

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 1

ER -