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Heatstroke causes hypotension by decreasing both mechanical efficiency and arterial elastance in rat
Author(s) -
Chang ChingPing,
Lin MaoTsun,
Cheng BorChih
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb744
Subject(s) - heatstroke , medicine , stroke volume , cardiac output , cardiology , hemodynamics , ejection fraction , anesthesia , ventricle , blood pressure , mean arterial pressure , heart rate , heart failure
We attempted to test the hypothesis that heatstroke causes arterial hypotension by modulating left ventricular performance in rats. Sprague‐Dawley male adult rats, under general anesthesia, were subjected to severe heat loss (43 °C for 70 min) to induce heatstroke. A 1.2F catheter‐tip pressure transducer was inserted into the left ventricle to record hemodynamic in the closed chest with pressure‐volume module data recording and analysis system. At the time point of heatstroke onset, compared with normothermic controls, rats with normal levels of cardiac HSP72 had significantly decreased end‐systolic pressure, decreased end‐diastolic pressure, decreased stroke volume, increased end‐systolic volume, decreased cardiac output, decreased ejection fraction, decreased stroke work, decreased arterial elastance, and increased time constant of fall in ventricular pressure by Glantz‐methods. With the overexpression of cardiac HSP72 by mild heat preconditioning (43°C for 30 min), a significant protection against heatstroke‐induced suppressed left ventricular performance was observed. Heatstroke causes hypotension by decreasing both cardiac mechanical efficiency and arterial elastance, which can be attenuated by the pre‐induction of cardiac HSP72.