BACKGROUND: The aim of this study was to explore whether ice slush (IS) causing local hypothermia can effectively inhibit the oculocardiac reflex (OCR) during strabismus surgery. METHODS: This prospective, randomized, double-blind study included 58 patients with concomitant strabismus scheduled for lateral rectus (LR) recession under general anesthesia. Patients were randomly allocated to receive IS (IS group) or standard treatment (control group) with sterile saline at room temperature before surgery. OCR was defined as a sudden decrease in heart rate (HR) of >15% from baseline. If one incidence of the OCR was found in 1 patient in any stage (0/I/II/III), the patient was defined as an OCR responder, and the incidence of overall OCR was the incidence of OCR responders. The primary outcome was the incidence of overall OCR during all stages of the surgery, which was analyzed by the Z test and computed based on the absolute risk difference with 2-sided 95% confidence intervals (CIs) using the Newcombe method. RESULTS: The overall OCR occurred in 19 of 29 patients (62.5% [95% CI, 45.7–82.1]) in the IS group and 28 of 29 patients (96.6% [95% CI, 82.2–99.9]) in the control group (absolute risk difference, −31.0% [95% CI, −49.4 to −11.0]; Z test, P < .001), which demonstrated that the incidence of overall OCR in IS group was significantly lower than that in the control group. CONCLUSIONS: IS on the ocular surface causing local hypothermia is a promising and easily accessible method to reduce the overall OCR, which can improve the safety of strabismus surgery.

The underlying mechanism of endothelial dysfunction during the aortic dissection (AD) remains unclear. The present study is aimed to uncover the intrinsic mechanism regulating the endocytosis of circulating exosomes by endothelial cells after AD takes place. Circulating exosomes extracted from both AD-patients and healthy donors (HD) were characterized and applied to human umbilical vein endothelial cells (HUVECs) in vitro with or without the co-exposure of lipopolysaccharide (LPS). The endocytosis of exosomes and inflammatory severity were evaluated. Besides, the JMJD6 expression pattern was explored, and si-RNA to knock down the JMJD6 expression was performed to test its role in exosome endocytosis. Here, it was firstly shown that circulating exosomes of the AD patients were statistically higher than the HD. In vitro, the endocytosis of both AD- and HD-exosomes was both enhanced under the co-existence of the LPS, and the uptake of AD-exosomes instead of the control exosomes further worsened the LPS-induced cell injury and gene transcriptions of serial pro-inflammatory cytokines through the p65 signaling. Notably, LPS challenged ECs exhibited increased JMJD6 expression, and silencing JMJD6 effectively decreased the LPS enhanced exosome endocytosis, and attenuated the LPS + AD-exosomes induced cell pro-inflammatory injury. The findings above indicate that LPS co-exposure enhances the AD-exosomes endocytosis by the ECs and further aggravates the inflammatory injury; Targeting on the cellular JMJD6 shall mitigate AD-exosomes endocytosis, which might serve as a potential therapeutic approach for the endothelial dysfunction.

Background: Continuous thoracic paravertebral block (TPVB) connected with patient-controlled analgesia (PCA) pump is an effective modality to reduce postoperative pain following thoracic surgery. For the PCA settings, the programmed intermittent bolus infusion (PIBI) and continuous infusion (CI) are commonly practiced. However, the comparative effectiveness between the 2 approaches has been inconsistent. Thus, the aim of this study was to explore the optimal PCA settings to treat postthoracotomy pain by combing PIBI and CI together. Methods: All enrolled patients undergoing thoracoscopic surgery accepted ultrasound-guided TPVB catheterization before the surgery and then were randomly allocated in to 3 groups depending on different settings of the PCA pump connecting to the TPVB catheter: the PIBI+CI, PIBI, and CI groups. Numerical Rating Scales were evaluated for each patient at T1 (1 h after extubation), T2 (12 h after the surgery), T3 (24 h after the surgery), T4 (36 h after the surgery), and T5 (48 h after the surgery). Besides, the consumptions of PCA ropivacaine, the number of blocked dermatomes at T3, and the requirement for extra dezocine for pain relief among the 3 groups were also compared. Results: First, the Numerical Rating Scale scores in the PIBI+CI group were lower than the CI group at T2 and T3 (P<0.05) when patients were at rest and were also lower than the CI group at T2, T3, and T4 (P<0.01) and the PIBI group at T3 when patients were coughing (P<0.01). Second, the 2-day cumulative dosage of PCA in the PIBI+CI group was lower than both the CI and PIBI groups (P<0.01). Third, the number of blocked dermatomes in the PIBI and PIBI+CI groups were comparable and were both wider than the CI group at T3 (P<0.01). Finally, a smaller proportion (not statistically significant) of patients in the PIBI+CI group (5.26%, 2/38) had required dezocine for pain relief when compared with the PIBI group (19.44%, 7/36) and the CI group (15.79%, 6/38). Conclusions: The combination of PIBI and CI provides superior analgesic modality to either PIBI or CI alone in patients undergoing thoracoscopic surgery. Therefore, it should be advocated to improve the management of postoperative pain, clinical outcomes, and ultimately patient satisfaction.

Septic cardiomyopathy (SCM) is a prevalent and severe complication associated with sepsis. This study explores the effects of sevoflurane and pentobarbital on lipopolysaccharide (LPS) -induced SCM and elucidates underlying mechanisms. The SCM model was established using an intraperitoneal injection of 10 mg/kg LPS. Pentobarbital and sevoflurane were administered thirty minutes post-model establishment. Following the echocardiographic assessment, mice were euthanized 24 h after the modeling, and cardiac samples were collected. Gene sequencing and western blot were utilized to identify potential hub genes and signaling pathways. Sevoflurane markedly reduced LPS-induced myocardial injury and cardiac dysfunction compared to the pentobarbital intervention. Transcriptome sequencing revealed that numerous genes exhibited differential expression following intervention with sevoflurane and pentobarbital, with predominant enrichment in the signaling pathways, such as the extracellular region and matrix, tumor necrosis factor (TNF), and p53 signaling. Sevoflurane significantly induced TATA-box binding protein-associated factor, RNA polymerase I subunit D (TAF1D) expression and attenuated cardiomyocyte death, oxidative stress, and the secretion of IL-6 and TNF-α compared to the pentobarbital group (p < 0.05). Furthermore, oe-TAF1D significantly exacerbated cardiomyocyte death, oxidative stress, and inflammatory responses, which were alleviated with si-TAF1D (p < 0.05). Sevoflurane mitigates sepsis-induced cell death, oxidative stress, and inflammatory responses by up-regulating TAF1D, consequently diminishing cardiac injury and preserving cardiac function.