Murine in vivo myocardial contractile dysfunction after burn injury is exacerbated by pneumonia sepsis.
We evaluated hemodynamic and cardiac contractile dysfunction in a murine model of 40% contact burn complicated by Streptococcus pneumoniae (1 x 10(5) CFU) sepsis. Male, 9- to 10-week-old C57/BL6 mice were divided into the following groups: sham burn, sham sepsis; 24 h after burn alone; 24 h after sepsis alone; 7 days after burn alone; and 7 days after burn followed by pneumonia sepsis. Hemodynamic and cardiac contractile function was assessed with carotid artery cannulation and left ventricular pressure-volume analysis. At 24 h after burn, there were significant decreases in all load-insensitive contractility variables including the end-systolic pressure volume relationship, preload-recruitable stroke work, and maximum elastance, but there were no changes in global hemodynamics. Twenty-four hours after sepsis, there was similar cardiac contractile dysfunction, along with a decrease in cardiac output, but mean arterial pressure was maintained with an increase in systemic vascular resistance. Late burn (7 days) was associated with a recovery of all contractility variables except the end-systolic pressure volume relationship. However, sepsis induced during the late burn period was associated with a significant decrease in heart rate and cardiac output, but mean arterial pressure was still maintained with increased systemic vascular resistance. With burn complicated by sepsis, all cardiac contractility variables showed profound contractile dysfunction. Our data indicate that burn complicated by sepsis is associated with more pronounced cardiac contractile dysfunction than burn alone or sepsis alone.
Tao
Weike
W
Department of Anesthesiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9068, USA. weike.tao@utsouthwestern.edu
Maass
David L
DL
Johnston
William E
WE
Horton
Jureta W
JW
D000818:Animals; D001794:Blood Pressure; D002056:Burns / Q000150:complications / Q000382:microbiology* / Q000473:pathology*; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009200:Myocardial Contraction; D011014:Pneumonia / Q000382:microbiology*; D018805:Sepsis / Q000382:microbiology* / Q000473:pathology*; D013296:Streptococcus pneumoniae; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000382:microbiology*