Background: The α₂-adrenoreceptor agonist dexmedetomidine is known to provide renoprotection against ischemia and reperfusion (I/R) injury. However the underlying molecular mechanisms remain unclear. The purpose of this study was to investigate whether the Janus kinase and signal transducer and activator of transcription (JAK/STAT) signaling pathway plays a role in dexmedetomidine’s renoprotection. Methods: I/R model was induced by bilateral renal pedicle clamping for 45 min followed by 48 h of reperfusion in male Wistar rat. Sham laparotomy served as controls. Animals received dexmedetomidine (50 μg/kg, i.p.) in the absence or presence of atipamezole (250 μg/kg, i.p.), or vehicle (DMSO) in the absence or presence of selective JAK2 inhibitor tyrphostin AG490 (10 mg/kg, i.p.) before ischemia. Renal function, histology, apoptosis, expression of cleaved caspase 3 protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and phosphorylations of JAK2, STAT1 and STAT3 were assessed. Results: The animals treated with either dexmedetomidine or AG490 exhibited an improved renal functional recovery, attenuated histological lesions and reduced number of apoptotic tubular epithelial cells. Either dexmedetomidine or AG490 inhibited the phosphorylations of JAK2 and its downstream molecule STAT1 and STAT3, accompanied by down-regulation the expression of cleaved caspase 3, ICAM-1 and MCP-1 proteins, and significantly ameliorated renal I/R injury. Conclusions: Dexmedetomidine protects kidney against I/R injury, at least in part, through its inhibitory effects on injury-induced activation of JAK/STAT signaling pathway. If our data can be extrapolated to clinical setting, then dexmedetomidine may therefore serve as a clinical strategy to treat/prevent perioperative renal I/R injury.

Acute kidney injury (AKI) is a common and serious complication after the repair of Type A acute aortic dissection (TA-AAD). However, previous models have failed to account for the impact of blood pressure fluctuations on predictive performance. This study aims to develop machine learning (ML) models combined with intraoperative medicine and blood pressure time-series data to improve the accuracy of early prediction for postoperative AKI risk. Indicators reflecting the duration and depth of hypotension were obtained by analyzing continuous mean arterial pressure (MAP) monitored intraoperatively with multiple thresholds (<65, 60, 55, 50) set in the study. The predictive features were selected by logistic regression and the least absolute shrinkage and selection operator (LASSO), and 4 ML models were built based on the above features. The performance of the models was evaluated by area under receiver operating characteristic curve (AUROC), calibration curve and decision curve analysis (DCA). Shapley additive interpretation (SHAP) was used to explain the prediction models. Among the indicators reflecting intraoperative hypotension, 65 mmHg showed a statistically superior difference to other thresholds in patients with or without AKI (p < .001). Among 4 models, the extreme gradient boosting (XGBoost) model demonstrated the highest AUROC: 0.800 (95% 0.683–0.917) and sensitivity: 0.717 in the testing set and was verified the best-performing model. The SHAP summary plot indicated that intraoperative urine output, cumulative time of mean arterial pressure lower than 65 mmHg outside cardiopulmonary bypass (OUT_CPB_MAP_65 time), autologous blood transfusion, and smoking were the top 4 features that contributed to the prediction model. With the introduction of intraoperative blood pressure time-series variables, we have developed an interpretable XGBoost model that successfully achieve high accuracy in predicting the risk of AKI after TA-AAD repair, which might aid in the perioperative management of high-risk patients, particularly for intraoperative hemodynamic regulation.

Background: Cardiac valve replacement (CVR) is currently the main surgical treatment for patients with valvular heart diseases (VHD). Postoperative cognitive dysfunction (POCD) is one of the most serious complications of cardiac surgery. Permissive hypercapnia (PHC), an important lung-protective ventilation strategy, has protective effects on vital organs, including the heart, lungs, and central nervous system (CNS). The main objective of this study is to assess the effect of the PHC ventilation strategy on rSO₂ and postoperative cognitive function in patients undergoing CVR. Methods: A total of 66 patients undergoing CVR were included and randomly divided into the PHC ventilation group (Group H, n=33) and conventional ventilation group (Group C, n=33). Patients of both groups were subjected to conventional ventilation before cardiopulmonary bypass (CPB). patients in Group H were subjected to the PHC ventilation strategy to keep the partial pressure of carbon dioxide (PaCO₂) at 46–60 mmHg. Results: (I) Group H had a lower HR at T0 and T1 (P<0.05) and higher CO at T3 and T4 (P<0.05) than Group C. (II) Group H had higher rSO₂ at T4 (P<0.05), lower pH and lactate (Lac) at T4 (P<0.05), higher PaCO₂ at T3 and T4 (P<0.05), and lower PaO₂ at T3 and T4 (P<0.05). (III) Compared to 1 d before surgery, the MMSE scores of both groups were lower 24 h after surgery (P<0.05). Conclusions: PHC can increase the rSO₂ of patients undergoing CVR, increase cerebral blood flow, improve the cerebral oxygen supply/consumption balance, and play a protective role in the brain. It has no significant impact on the incidence of POCD.

Background: Despite evidence that high-flow nasal cannula oxygen therapy (HFNC) promotes oxygenation, its application in sedated gastroscopy in elderly patients has received little attention. This study investigated the effect of different inhaled oxygen concentrations (FiO₂) of HFNC during sedated gastroscopy in elderly patients. Methods: In a prospective randomized single-blinded study, 369 outpatients undergoing regular gastroscopy with propofol sedation delivered by an anesthesiologist were randomly divided into three groups (n = 123): nasal cannula oxygen group (Group C), 100% FiO₂ of HFNC group (Group H100), and 50% FiO₂ of HFNC (Group H50). The primary endpoint in this study was the incidence of hypoxia events with pulse oxygen saturation (SpO₂) ≤ 92%. The secondary endpoints included the incidence of other varying degrees of hypoxia and adverse events associated with ventilation and hypoxia. Results: The incidence of hypoxia, paradoxical response, choking, jaw lift, and mask ventilation was lower in both Group H100 and Group H50 than in Group C (P < 0.05). Compared with Group H100, Group H50 showed no significant differences in the incidence of hypoxia, jaw lift and mask ventilation, paradoxical response, or choking (P > 0.05). No patients were mechanically ventilated with endotracheal intubation or found to have complications from HFNC. Conclusion: HFNC prevented hypoxia during gastroscopy with propofol in elderly patients, and there was no significant difference in the incidence of hypoxia when FiO₂ was 50% or 100%. Trial registration: This single-blind, prospective, randomized controlled trial was approved by the Ethics Committee of Nanjing First Hospital (KY20201102-04) and registered in the China Clinical Trial Center (20/10/2021, ChiCTR2100052144) before patients enrollment. All patients signed an informed consent form.

Background: In general, cerebral blood flow accounts for 10–15% of cardiac output (CO), of which about 75% is delivered through the carotid arteries. Hence, if carotid blood flow (CBF) is constantly proportional to CO with high reproducibility and reliability, it would be of great value to measure CBF as an alternative to CO. The aim of this study was to investigate the direct correlation between CBF and CO. We hypothesized that measurement of CBF could be a good substitute for CO, even under more extreme hemodynamic conditions, for a wider range of critically ill patients. Methods: Patients aged 65–80 years, undergoing elective cardiac surgery were included in this study. CBF in different cardiac cycles were measured by ultrasound: systolic carotid blood flow (SCF), diastolic carotid blood flow (DCF), and total (systolic and diastolic) carotid blood flow (TCF). CO simultaneously was measured by transesophageal echocardiography. Results: For all patients, the correlation coefficients between SCF and CO, TCF and CO were 0.45 and 0.30, respectively, which were statistically significant, but not between DCF and CO. There was no significant correlation between either SCF, TCF or DCF and CO, when CO was <3.5 L/min. Conclusions: Systolic carotid blood flow may be used as a better index to replace CO. However, the method of direct measurement of CO is essential when the patient's heart function is poor.