Coordinated activation of sympathetic and respiratory nervous systems is crucial in responses to noxious stimuli such as intermittent hypoxia. Acute intermittent hypoxia (AIH) is a valuable model for studying obstructive sleep apnea (OSA) pathophysiology, and stimulation of breathing during AIH is known to elicit long-term changes in respiratory and sympathetic functions. The aim of this study was to record the renal sympathetic nerve activity (RSNA) and phrenic nerve activity (PNA) during the AIH protocol in rats exposed to monoanesthesia with sevoflurane or isoflurane. Adult male Sprague-Dawley rats (n = 24; weight: 280–360 g) were selected and randomly divided into three groups: two experimental groups (sevoflurane group, n = 6; isoflurane group, n = 6) and a control group (urethane group, n = 12). The AIH protocol was identical in all studied groups and consisted in delivering five 3 min-long hypoxic episodes (fraction of inspired oxygen, FiO₂ = 0.09), separated by 3 min recovery intervals at FiO₂ = 0.5. Volatile anesthetics, isoflurane and sevoflurane, blunted the RSNA response to AIH in comparison to urethane anesthesia. Additionally, the PNA response to acute intermittent hypoxia was preserved, indicating that the respiratory system might be more robust than the sympathetic system response during exposure to acute intermittent hypoxia.

Cardiac surgery-related acute kidney injury (CS-AKI) is a decrease in kidney function after open-heart surgery, affecting up to 50% of patients. The pathophysiology of CS-AKI involves ischemia–reperfusion injury, inflammation, and oxidative stress. Ubiquinone is a potent antioxidant, and we hypothesized that it could decrease both the incidence and severity of CS-AKI. The intervention group received ubiquinone (8 mg/kg/day) divided into three daily doses, while the control group received a placebo. The primary outcome was the incidence of CS-AKI, which was manifested as an increase in creatinine ≥26.5 µmol/L or a urine output below 0.5 mL/kg/h for 6 h. Out of 73 patients, 39.7% (N = 29) developed CS-AKI, including 35.3% of the ubiquinone group and 43.6% of the placebo group (X²(1,N = 73) = 0.4931, p = 0.4825). The secondary outcomes revealed that the ubiquinone group experienced reduced postoperative bleeding, with a median (IQR) drainage of 320 mL (230–415) compared to the drainage of 420 mL (242.5–747.5) in the placebo group (t(35.84) = 2.055, p = 0.047). The median hs-TnI level in the ubiquinone group was 239.5 ng/mL (113.25–382.75) after surgery compared to a level of 366 (234.5–672.5) ng/mL in the placebo group (p = 0.024). In conclusion, there was no significant difference in the incidence of CS-AKI between groups. Postoperative hs-TnI and bleeding were significantly reduced among patients receiving ubiquinone.