Protective role of heat stress in burn trauma.
OBJECTIVE
This study was designed to determine whether cutaneous burn injury up-regulated expression of myocardial heat shock protein (HSP)70 and to determine a potential cardioprotective role of inducible HSP70 (iHSP70) in postburn myocardial contractile function.


METHODS
Experimental study.


METHODS
Research laboratory.


METHODS
Adult Hartley guinea pigs.


METHODS
The first set of studies determined whether heat stress (increasing body temperature to 42 degrees C for 20 mins) in adult Hartley guinea pigs would increase expression of myocardial iHSP70.


RESULTS
Our model of heat stress increased expression of inducible HSP in the myocardium (Western blot), and this response persisted 1, 2, 4, and 24 hrs after the initial heat stress. We then determined whether burn trauma over 40% total body surface area (TBSA) increased myocardial expression of iHSP70. Time-matched sham and burned guinea pigs were killed 1, 2, 4, 12, 18, or 24 hrs postburn, and hearts were used either to examine myocardial iHSP70 expression by Western blot or to determine myocardial contractile function (Langendorff). Burn trauma produced a two-fold increase in myocardial iHSP70 that was evident as early as 1 hr postburn and persisted 24 hrs postburn; increased iHSP70 expression occurred despite only a modest and transient increase in body temperature after burn trauma. We then determined whether heat shock stress before burn trauma provided a protective or detrimental effect on cardiac function. Body temperature was increased to 42 degrees C for 20 mins, animals were allowed to recover, and body temperature returned to baseline; burn trauma was then produced (40% TBSA) either 1, 2, 4, or 24 hrs after the initial heat stress. Myocardial contraction and relaxation deficits were evident after burn trauma alone; however, heat stress 1 hr before burn trauma improved left ventricular developed pressure and positive or negative maximum change in pressure in time and shifted left ventricular function curves upward and leftward from those calculated for burn in the absence of heat stress, indicating improved ventricular performance. Increasing the time between the initial heat stress and burn injury decreased the cardioprotective effects of heat stress. Thus, organ protection was evident only when the time period between the initial heat stress and the second insult was brief (1 hr).


CONCLUSIONS
Our finding that the amount of myocardial iHSP70 remained constantly elevated after heat stress while the cardio-protective effect afforded by a prior heat stress declined with time suggested that the initial heat stress evoked several compensatory/adaptive mechanisms that may include modulation of autonomic nervous system responses, changes in metabolic function, modulation of pro/anti-inflammatory cytokine responses, and heat stress-related alterations in antioxidant capacity.
White
D Jean
DJ
Departments of Surgery (DJW, JWH), Pediatrics (DC), and Physiology (GAO), UT Southwestern Medical Center at Dallas, TX.
Carlson
Deborah
D
Ordway
George A
GA
Horton
Jureta W
JW
D000818:Animals; D015153:Blotting, Western; D001831:Body Temperature; D002056:Burns / Q000378:metabolism / Q000503:physiopathology*; D006168:Guinea Pigs; D018840:HSP70 Heat-Shock Proteins / Q000032:analysis; D018882:Heat Stress Disorders / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000737:chemistry; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology
D018840:HSP70 Heat-Shock Proteins