Background:  Pulse pressure variation (ΔPP) and systolic pressure variation (SPV) induced by mechanical ventilation have been proposed to detect hypovolaemia and guide fluid therapy. During laparoscopic surgery, chest compliance is decreased by pneumoperitoneum. This may affect the value of SPV and ΔPP as indicators of intravascular volume status. Thereby, we investigated the effects of pneumoperitoneum and hypovolaemia on SPV and ΔPP.Methods:  We measured ΔPP, SPV and the inspiratory (Δup) and expiratory (Δdown) components of SPV, at baseline, during pneumoperitoneum, during pneumoperitoneum and hypovolaemia and after the return to baseline conditions, in 11 mechanically ventilated rabbits. Pneumoperitoneum was induced by inflating the abdomen with carbon dioxide, and hypovolaemia was induced by controlled haemorrhage.Results:  Pneumoperitoneum induced an increase in SPV from 8.5 ± 1.6 to 13.3 ± 2.6 mmHg (+56%, P < 0.05) as a result of an increase in Δup from 2.0 ± 1.0 to 6.7 ± 2.1 mmHg (+236%, P < 0.05), but no significant change in Δdown, nor in ΔPP. Haemorrhage induced a significant (P < 0.05) increase in SPV from 13.3 ± 2.6 to 19.9 ± 3.7 mmHg (+50%), in Δdown from 6.6 ± 3.3 to 14.0 ± 4.9 mmHg (+112%) and in ΔPP from 11.1 ± 4.8 to 24.9 ± 9.8% (+124%) but no change in Δup. All parameters returned to baseline values after blood re‐infusion and abdominal deflation.Conclusions:  SPV is modified by haemorrhage but it is also influenced by pneumoperitoneum. In contrast, ΔPP is modified by haemorrhage but not by pneumoperitoneum. These findings suggest that ΔPP should be used preferentially instead of SPV to detect hypovolaemia and guide fluid therapy during laparoscopic surgery.

Stress is an important condition of modern life. Nicotine addiction can modulate the physiological response to stress. Cutaneous healing is a complex process resulting in scar formation, which can be delayed by stress. Therefore, the aim of this study was to investigate the effects of nicotine administration on cutaneous wound healing in chronically stressed mice. Male mice were submitted to rotational stress, whereas control animals were not subjected to stress. These stressed and control animals were treated with a transdermal nicotine patch that was changed every day. A full-thickness excisional lesion was also generated, and 14 days later, lesions had recovered. However, the Stress + Nicotine group presented a delay in wound contraction. These wounds showed a decrease in inflammatory cell infiltration and lower expression of transforming growth factor-β (TGF-β), whereas there was an increase in angiogenesis and tumor necrosis factor-α (TNF-α) expression. In vitro fibroblast migration was also impaired by the nicotine treatment of stressed-stimulated cells. In conclusion, nicotine administration potentiates the delay in wound closure observed in mice submitted to stress.