Altered calcium (Ca2+) mobilization after burn trauma

Beneficial effects of calcium antagonist dantrolene

D. Maass, J. W. Horton, D. J. White, M. Thompson, B. Giroir, G. Arteaga

Research output: Contribution to journalArticle

Abstract

Numerous studies have shown that elevated intracellular calcium concentration [Ca2+]i occurs in several cell types after stress related injury. However, the mechanism responsible for the increased [Ca2+]i (that is, altered Ca2+ release or uptake from intracellular organelles such as the sarcoplasmic reticulum, SR, versus altered Ca2+ influx) remains unclear. This study examined the contribution of SR dysfunction to postburn Ca2+ dyshomeostasis in burn injury. Rats were given a 3° burn over 43% TBSA and fluid treated for 24 hours (n=18); sham burns were included for controls (n=19). Hearts were harvested 24 hrs postburn and Ca2+ uptake was measured in myocardial homogenates and normalized for protein concentration. Compared to shams, maximal Ca2+ uptake capacity (350±10 nmoles/ng protein) and Ca2+ uptake velocity (58±2 nmole/mg/min) were reduced after burn trauma (292±15, p<0.01 and 49±1, p<0.01 respectively). In additional studies, burned rats (n=9) received dantrolene a drug which blocks Ca2+ release from the SR (10 mg/kg, IV, 30 min, 8 hrs, and 20 hrs postburn); shams received vehicle. Myocytes were isolated (collagenase digestion) 24 hrs postburn. Fura-2 loaded cells (1×105/ml) were excited at wavelengths of 340/380 nm (Hitachi spectrofluorometer) and [Ca2+]i was calculated from fura-2 ratios. Burn trauma increased myocyte [Ca2+]i compared to shams (152±6 vs 307±29 nm, p<0.05); dantrolene reduced the postburn rise in [Ca2+] , (164±22 nm, p<0.05). The ability of dantrolene to normalize myocyte [Ca2+]i coupled with abnormalities in SR Ca2+ transport suggest that postburn Ca2+ dyshomeostasis is related to the defects in up take/release of Ca2+ from the SR.

Original languageEnglish (US)
JournalFASEB Journal
Volume11
Issue number3
StatePublished - 1997
Externally publishedYes

Fingerprint

Dantrolene
antagonists
Muscle Cells
Calcium
calcium
Rats
Wounds and Injuries
Fura-2
Collagenases
Sarcoplasmic Reticulum
Proteins
Burns
Organelles
Digestion
Wavelength
Defects
Fluids
myocytes
Pharmaceutical Preparations
uptake mechanisms

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Maass, D., Horton, J. W., White, D. J., Thompson, M., Giroir, B., & Arteaga, G. (1997). Altered calcium (Ca2+) mobilization after burn trauma: Beneficial effects of calcium antagonist dantrolene. FASEB Journal, 11(3).

Altered calcium (Ca2+) mobilization after burn trauma : Beneficial effects of calcium antagonist dantrolene. / Maass, D.; Horton, J. W.; White, D. J.; Thompson, M.; Giroir, B.; Arteaga, G.

In: FASEB Journal, Vol. 11, No. 3, 1997.

Research output: Contribution to journalArticle

Maass, D, Horton, JW, White, DJ, Thompson, M, Giroir, B & Arteaga, G 1997, 'Altered calcium (Ca2+) mobilization after burn trauma: Beneficial effects of calcium antagonist dantrolene', FASEB Journal, vol. 11, no. 3.
Maass, D. ; Horton, J. W. ; White, D. J. ; Thompson, M. ; Giroir, B. ; Arteaga, G. / Altered calcium (Ca2+) mobilization after burn trauma : Beneficial effects of calcium antagonist dantrolene. In: FASEB Journal. 1997 ; Vol. 11, No. 3.
@article{a86d7c24c3c3407bb7568c646420c244,
title = "Altered calcium (Ca2+) mobilization after burn trauma: Beneficial effects of calcium antagonist dantrolene",
abstract = "Numerous studies have shown that elevated intracellular calcium concentration [Ca2+]i occurs in several cell types after stress related injury. However, the mechanism responsible for the increased [Ca2+]i (that is, altered Ca2+ release or uptake from intracellular organelles such as the sarcoplasmic reticulum, SR, versus altered Ca2+ influx) remains unclear. This study examined the contribution of SR dysfunction to postburn Ca2+ dyshomeostasis in burn injury. Rats were given a 3° burn over 43{\%} TBSA and fluid treated for 24 hours (n=18); sham burns were included for controls (n=19). Hearts were harvested 24 hrs postburn and Ca2+ uptake was measured in myocardial homogenates and normalized for protein concentration. Compared to shams, maximal Ca2+ uptake capacity (350±10 nmoles/ng protein) and Ca2+ uptake velocity (58±2 nmole/mg/min) were reduced after burn trauma (292±15, p<0.01 and 49±1, p<0.01 respectively). In additional studies, burned rats (n=9) received dantrolene a drug which blocks Ca2+ release from the SR (10 mg/kg, IV, 30 min, 8 hrs, and 20 hrs postburn); shams received vehicle. Myocytes were isolated (collagenase digestion) 24 hrs postburn. Fura-2 loaded cells (1×105/ml) were excited at wavelengths of 340/380 nm (Hitachi spectrofluorometer) and [Ca2+]i was calculated from fura-2 ratios. Burn trauma increased myocyte [Ca2+]i compared to shams (152±6 vs 307±29 nm, p<0.05); dantrolene reduced the postburn rise in [Ca2+] , (164±22 nm, p<0.05). The ability of dantrolene to normalize myocyte [Ca2+]i coupled with abnormalities in SR Ca2+ transport suggest that postburn Ca2+ dyshomeostasis is related to the defects in up take/release of Ca2+ from the SR.",
author = "D. Maass and Horton, {J. W.} and White, {D. J.} and M. Thompson and B. Giroir and G. Arteaga",
year = "1997",
language = "English (US)",
volume = "11",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "3",

}

TY - JOUR

T1 - Altered calcium (Ca2+) mobilization after burn trauma

T2 - Beneficial effects of calcium antagonist dantrolene

AU - Maass, D.

AU - Horton, J. W.

AU - White, D. J.

AU - Thompson, M.

AU - Giroir, B.

AU - Arteaga, G.

PY - 1997

Y1 - 1997

N2 - Numerous studies have shown that elevated intracellular calcium concentration [Ca2+]i occurs in several cell types after stress related injury. However, the mechanism responsible for the increased [Ca2+]i (that is, altered Ca2+ release or uptake from intracellular organelles such as the sarcoplasmic reticulum, SR, versus altered Ca2+ influx) remains unclear. This study examined the contribution of SR dysfunction to postburn Ca2+ dyshomeostasis in burn injury. Rats were given a 3° burn over 43% TBSA and fluid treated for 24 hours (n=18); sham burns were included for controls (n=19). Hearts were harvested 24 hrs postburn and Ca2+ uptake was measured in myocardial homogenates and normalized for protein concentration. Compared to shams, maximal Ca2+ uptake capacity (350±10 nmoles/ng protein) and Ca2+ uptake velocity (58±2 nmole/mg/min) were reduced after burn trauma (292±15, p<0.01 and 49±1, p<0.01 respectively). In additional studies, burned rats (n=9) received dantrolene a drug which blocks Ca2+ release from the SR (10 mg/kg, IV, 30 min, 8 hrs, and 20 hrs postburn); shams received vehicle. Myocytes were isolated (collagenase digestion) 24 hrs postburn. Fura-2 loaded cells (1×105/ml) were excited at wavelengths of 340/380 nm (Hitachi spectrofluorometer) and [Ca2+]i was calculated from fura-2 ratios. Burn trauma increased myocyte [Ca2+]i compared to shams (152±6 vs 307±29 nm, p<0.05); dantrolene reduced the postburn rise in [Ca2+] , (164±22 nm, p<0.05). The ability of dantrolene to normalize myocyte [Ca2+]i coupled with abnormalities in SR Ca2+ transport suggest that postburn Ca2+ dyshomeostasis is related to the defects in up take/release of Ca2+ from the SR.

AB - Numerous studies have shown that elevated intracellular calcium concentration [Ca2+]i occurs in several cell types after stress related injury. However, the mechanism responsible for the increased [Ca2+]i (that is, altered Ca2+ release or uptake from intracellular organelles such as the sarcoplasmic reticulum, SR, versus altered Ca2+ influx) remains unclear. This study examined the contribution of SR dysfunction to postburn Ca2+ dyshomeostasis in burn injury. Rats were given a 3° burn over 43% TBSA and fluid treated for 24 hours (n=18); sham burns were included for controls (n=19). Hearts were harvested 24 hrs postburn and Ca2+ uptake was measured in myocardial homogenates and normalized for protein concentration. Compared to shams, maximal Ca2+ uptake capacity (350±10 nmoles/ng protein) and Ca2+ uptake velocity (58±2 nmole/mg/min) were reduced after burn trauma (292±15, p<0.01 and 49±1, p<0.01 respectively). In additional studies, burned rats (n=9) received dantrolene a drug which blocks Ca2+ release from the SR (10 mg/kg, IV, 30 min, 8 hrs, and 20 hrs postburn); shams received vehicle. Myocytes were isolated (collagenase digestion) 24 hrs postburn. Fura-2 loaded cells (1×105/ml) were excited at wavelengths of 340/380 nm (Hitachi spectrofluorometer) and [Ca2+]i was calculated from fura-2 ratios. Burn trauma increased myocyte [Ca2+]i compared to shams (152±6 vs 307±29 nm, p<0.05); dantrolene reduced the postburn rise in [Ca2+] , (164±22 nm, p<0.05). The ability of dantrolene to normalize myocyte [Ca2+]i coupled with abnormalities in SR Ca2+ transport suggest that postburn Ca2+ dyshomeostasis is related to the defects in up take/release of Ca2+ from the SR.

UR - http://www.scopus.com/inward/record.url?scp=33750198855&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750198855&partnerID=8YFLogxK

M3 - Article

VL - 11

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 3

ER -