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Early myocardial contractility depression in female endotoxemic rats

Although several in vitro studies have addressed heart function in sepsis, this subject has been scarcely investigated in vivo. Using a pressure‐volume (PV) conductance catheter, we evaluated the cardiac function in situ in Wistar rats injected 6 or 24 h before with E. coli lipopolysaccharide (LPS, 10 mg/kg, i.p.). The rats were anesthetized with xylazine (2 mg/kg) and isoflurane (1–3%), plus lidocaine on surgical sites. The catheter was inserted into the left ventricle (LV) through the carotid artery. Compared to control, stroke work (SW) and LV relaxation time constant Tau were reduced by 57% and 63% in LPS 6 h, and by 36% and 57% in LPS 24 h group, respectively. LV mean pressure was decreased ~ 20 mmHg both 6 and 24 h after LPS (control: 48.9 ± 7 mmHg; p < 0.05). Interestingly, the mean arterial pressure was reduced from 88.7 ± 7.3 in control to 63.2 ± 3.2 mmHg in LPS 24 h, but it was unchanged in LPS 6 h. Heart rate did not change in LPS 24 h, but was increased from 253 ± 21 to 314 ± 13 bpm in control and LPS 6 h groups, respectively. Our study suggests that heart function is impaired in early stages of sepsis, even before the well‐described hypotension, and that this dysfunction may be hidden by compensatory mechanisms.