title: Metabolic disorder in myocardiac intracellular free calcium after thermal injury.
abstract: Cutaneous burn trauma causes functional inhibition of the heart, but the mechanism is unclear. Using a high dissociation constant (K(D)) calcium indicator TF-BAPTA and 19F MR spectroscopy, the relationship between the changes of cytosolic free calcium and cardiac function after burn trauma was examined. Sprague-Dawley rats received scald (43% TBSA) or sham burns. Twenty-four hours later, the hearts were excised and perfused by the Langendorff method with a modified phosphate-free Krebs-Henseleit bicarbonate buffer. Left ventricular developed pressure (LVDP) was recorded through a catheter attached to an intraventricular balloon. At the same time, 31P and 19F nuclear magnetic resonance (NMR) spectroscopy was perforined before and after TF-BAPTA loading. LVDP of the heart from burned rats was 40% less than in sham burn rats (65+/-6 vs 110+/-12 mmHg, P<0.01). Cytosolic free calcium increased about four-fold in those hearts from the burn group compared to the sham burn group (0.807+/-0.192 vs 3.891+/-0.929 microM). Loading TF-BAPTA in those hearts only caused about a 15-20% decrease in LVDP. PCr/Pi ratio also decreased significantly with this loading, but ATP signals were not affected. In conclusion, the inhibition of cardiac contractility caused by burn trauma correlated with the overload of cytosolic free calcium in the heart.
authors.affiliation: Department of Burn Surgery, Burns Center, Changhai Hospital, 200433, Shanghai, People's Republic of China. xiazf@smmu.edu.cn
authors.forename: Z
authors.initials: Z
authors.lastname: Xia
authors.forename: J W
authors.initials: JW
authors.lastname: Horton
authors.forename: H
authors.initials: H
authors.lastname: Tang
authors.forename: Y
authors.initials: Y
authors.lastname: Yang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000150:complications*; D002118:Calcium / Q000378:metabolism*; D002128:Calcium Metabolism Disorders / Q000175:diagnosis* / Q000209:etiology*; D009202:Cardiomyopathies / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004533:Egtazic Acid / Q000031:analogs & derivatives; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D010477:Perfusion; D011336:Probability; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012680:Sensitivity and Specificity; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology
chemical_list: D002614:Chelating Agents; C087511:1,2-bis(2-amino-5,6-difluorophenoxy)ethane-N,N,N',N'-tetraacetic acid; D004533:Egtazic Acid; D000255:Adenosine Triphosphate; D002118:Calcium