title: Relationship between energetic, ionic, and functional status in the perfused rat heart following thermal injury: a 31P and 23Na NMR study.
abstract: To test the hypothesis that energy deficits and intracellular ion derangements may be the cellular basis for intrinsic myocardial dysfunction in rats after burn trauma, we examined ATP metabolism, intracellular pH, sodium, and mechanical performance simultaneously in perfused beating hearts from sham burn or burned rats (43% TBSA, 3 degrees scald burn, resuscitated for 24 hr with lactated Ringer's solution, Parkland formula). Intracellular calcium was also measured in myocytes harvested from parallel groups of sham burn and burn resuscitated rats. Burn trauma caused a 46% decrease in left ventricular developed pressure, a 69% decrease in +dP/dtmax, and a 72% decrease in -dP/dtmax. Intracellular to external standard sodium ratio increased (+58%) from 0.318 +/- 0.027 to 0.500 +/- 0.048 (P < 0.05), and intracellular calcium increased (+67%) from 206 +/- 13 to 445 +/- 37 nM (P < 0.01). Burn hearts exhibited decreased functional response to isoproterenol challenge compared to sham burn controls, but energy metabolism was similar in all hearts, regardless of burn injury. Our data suggest that burn trauma alters intracellular cardiomyocyte calcium and sodium homeostasis, and ionic derangements are not related to either altered intracellular pH or high energy phosphate deficits.
authors.affiliation: Department of Surgery, Mary Nell & Ralph B. Rogers Magnetic Resonance Center, University of Texas Southwestern Medical Center at Dallas, USA.
authors.forename: Z F
authors.initials: ZF
authors.lastname: Xia
authors.forename: J W
authors.initials: JW
authors.lastname: Horton
authors.forename: P
authors.initials: P
authors.lastname: Zhao
authors.forename: C
authors.initials: C
authors.lastname: Lin
authors.forename: A D
authors.initials: AD
authors.lastname: Sherry
authors.forename: C R
authors.initials: CR
authors.lastname: Malloy
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006335:Heart Injuries / Q000378:metabolism* / Q000503:physiopathology* / Q000628:therapy; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism; D007545:Isoproterenol / Q000494:pharmacology; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010758:Phosphorus; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation; D012964:Sodium / Q000378:metabolism
chemical_list: D000318:Adrenergic beta-Agonists; D010758:Phosphorus; D012964:Sodium; D007545:Isoproterenol; D002118:Calcium