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Journal Article
Research Support, Non-U.S. Gov't
Gender-specific differences in the in situ cardiac function of endotoxemic rats detected by pressure-volume catheter.
Shock 2014 November
The aim of the present study was to investigate the existence of gender-related differences in the profile of changes that occur in cardiac functionality during endotoxic shock. For this, both male and female Wistar rats received a single injection of lipopolysaccharide (LPS; 10 mg/kg, i.p.) at 6 h (LPS 6-h group) or 24 h (LPS 24-h group) before the induction of anesthesia and insertion of a pressure-volume catheter using the closed-chest method. Control animals received sterile saline. Hemodynamic parameters were recorded under basal conditions and during the peak of the pressor effect of phenylephrine (30 nmol/kg i.v.). Body temperature, hematologic parameters, blood glucose, and diuresis were also evaluated. There were unremarkable differences between male and female rats in the general aspects of sepsis evaluated in our study. Both male and female rats from the LPS 6-h group presented hypotension, depressed left ventricular ejection fraction, decreased stroke work, reduced dP/dtmax (maximal rate of left ventricle pressure change), P@dP/dtmax (pressure value at the maximum dP/dtmax), dP/dtmin (minimal rate of left ventricle pressure change), and preload-recruitable stroke work indices, as well as increased end-systolic volume. Nevertheless, only male rats from the LPS 24-h group still presented decreased stroke work and reduced dP/dtmax, P@dP/dtmax, and preload-recruitable stroke work indices. The end-systolic volume presented slight changes during the pressor effects of phenylephrine in all groups of male rats, as well as in females from the control and LPS 6-h groups, but it was significantly increased in females from the LPS 24-h group. These findings suggest that after induction of endotoxic shock female rats may recover the inotropic cardiac function earlier than males, as well as present improved adaptation of their left ventricle to the pressure-loading effects of phenylephrine.
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