Heat shock protein 72 may improve hypotension by increasing cardiac mechanical efficiency and arterial elastance in heatstroke rats

ObjectiveWe attempted to test the hypothesis that preinduction of heat shock protein (HSP) 72 in the heart would improve left ventricular performance in rat heatstroke.MethodsCardiac expression of HSP 72 was quantitatively evaluated by western blot analysis in rats 0 h, 12 h, or 72 h after mild heat preconditioning (MHP; 43 °C for 30 min). They were subjected to severe heat stress (SHS; 43 °C for 70 min) to induce heatstroke. A 1.2 F catheter-tip pressure transducer was inserted into the left ventricle of these group rats under general anesthesia to record hemodynamic in the closed chest with a pressure-volume loop module data recording and analysis system.ResultsAt the time point of heatstroke onset, compared with normothermic controls, group rats with 12 h post-MHP had significantly increased cardiac HSP 72, decreased hyperthermia, decreased hypotension, decreased bradycardia, increased end-systolic pressure, increased end-diastolic pressure, increased stroke volume, decreased end-systolic volume, decreased end-diastolic pressure, increased cardiac output, increased ejection fraction, increased stroke work, increased arterial elastance, and decreased time constant of fall in ventricular pressure by Glantz-methods. With the loss of cardiac HSP 72 expression observed at 72 h in post-MHP group rats, an insignificant protection against left ventricular performance was observed.ConclusionPreinduction of cardiac HSP 72 may improve hypotension in heatstroke rats by increasing both cardiac mechanical efficiency and arterial elastance.