Changes in cardiac contractile function and myocardial.
Cutaneous burn trauma causes cardiac contraction and relaxation defects, but the mechanism is unclear. Previous studies suggest that burn-related changes in myocyte handling of calcium may play an important role in postburn cardiac dysfunction. With the use of a high dissociation constant (K(d)) calcium indicator 1,2-bis(2-amino-5,6-difluorophenoxy)-ethane-N,N,N',N'-tetraacetic acid (TF-BAPTA) and (19)F NMR spectroscopy, this study examined the correlation between the changes in cytosolic free calcium concentration ([Ca(2+)](i)) and cardiac function after burn trauma. Sprague-Dawley rats were given scald burn (over 40% of the total body surface area) or sham burn. 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 (LV) developed pressure (LVDP), calculated from peak systolic LV pressure and LV end-diastolic pressure, was assessed through a catheter attached to an intraventricular balloon. At the same time, (31)P and (19)F NMR spectroscopy was performed before and after TF-BAPTA loading. LVDP measured in hearts from burned rats was <40% than that measured in hearts from sham burn rats (65 +/- 6 vs. 110 +/- 12 mmHg, P < 0.01); [Ca(2+)](i) was increased fourfold in hearts from the burned group compared with that measured in the sham burn group (0.807 +/- 0.192 vs. 3.891 +/- 0.929 microM). Loading TF-BAPTA in hearts transiently decreased LVDP by 15%. Phosphocreatine-to-P(i) ratio decreased, but ATP and intracellular pH remained unchanged by either TF-BAPTA loading or burn trauma. In conclusion, burn trauma impaired cardiac contractility, and this functional defect was paralleled by a significant rise in [Ca(2+)](i) in the heart.
Xia
Z F
ZF
Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160, USA.
Zhao
P
P
Horton
J W
JW
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000378:metabolism / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology / Q000502:physiology; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D005462:Fluorine Radioisotopes; D006321:Heart / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D066298:In Vitro Techniques; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley
D002614:Chelating Agents; D005462:Fluorine Radioisotopes; C087511:1,2-bis(2-amino-5,6-difluorophenoxy)ethane-N,N,N',N'-tetraacetic acid; D004533:Egtazic Acid; D000255:Adenosine Triphosphate; D002118:Calcium