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

Abstract

Objective: We attempted to test the hypothesis that preinduction of heat shock protein (HSP) 72 in the heart would improve left ventricular performance in rat heatstroke.

Methods: Cardiac expression of HSP 72 was quantitatively evaluated by western blot analysis in rats 0h, 12h, or 72h after mild heat preconditioning (MHP; 43°C for 30min). They were subjected to severe heat stress (SHS; 43°C for 70min) to induce heatstroke. A 1.2F 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.

Results: At the time point of heatstroke onset, compared with normothermic controls, group rats with 12h 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 72h in post-MHP group rats, an insignificant protection against left ventricular performance was observed.

Conclusion: Preinduction of cardiac HSP 72 may improve hypotension in heatstroke rats by increasing both cardiac mechanical efficiency and arterial elastance.

Keywords: Arterial elastance; Cardiac contractility; Heat shock protein 72; Hypotension.