Advances in Anesthesia Techniques for Postoperative Pain Management in Minimally Invasive Cardiac Surgery: An Expert Opinion.

Minimally invasive cardiac surgery (MICS) often leads to severe postoperative pain. At present, multimodal analgesia schemes for MICS have attracted much attention, and the application of various chest wall analgesia techniques is becoming increasingly widespread. However, research on anesthesia techniques for postoperative pain management in MICS remains relatively limited at present.

The Protective Effect of Melatonin on LPS-Induced Myocardial Injury via the Caspase-11/GSDMD Pathway.

Background: Melatonin (MT) has been demonstrated to have cardioprotective effects. Nevertheless, the precise mechanism through which MT provides protection against the etiology of LPS-induced myocardial injury remains uncertain. In this investigation, our objective was to explore the impact of MT on LPS-induced myocardial injury in an in vitro setting.

ZBP1-mediated PANoptosis: A possible novel mechanism underlying the therapeutic effects of penehyclidine hydrochloride on myocardial ischemia-reperfusion injury.

Although penehyclidine hydrochloride (PHC) has been identified to alleviate myocardial injury induced by ischemia/reperfusion (I/R), the regulatory molecules and related mechanisms are unknown. In this study, bioinformatics, molecular biology, and biochemistry methods were used to explore the molecular mechanisms and targets of PHC. In the myocardial ischemia-reperfusion injury (MIRI)-induced rat model, PHC pretreatment significantly improved cardiac function (p < 0.

Melatonin protects against myocardial ischemia-reperfusion injury by inhibiting excessive mitophagy through the Apelin/SIRT3 signaling axis.

Excessive or uncontrolled mitophagy may result in a drastic shortage of healthy mitochondrial for ATP supply after reperfusion, leading to irreversible myocardial damage. Melatonin, a hormone produced by the pineal gland, has been proven to ameliorate myocardial ischemia-reperfusion (I/R) injury via regulating mitophagy. However, its underlying mechanism has not been fully elucidated.

A New Aspect of Penehyclidine Hydrochloride in Alleviating Myocardial Ischemia-Reperfusion Injury: Ferroptosis.

Penehyclidine hydrochloride (PHC) is an anticholinergic drug with cardioprotective effects. Ferroptosis is closely related to myocardial ischaemia-reperfusion injury (MIRI). In the present study, MIRI was induced in rats by left anterior descending coronary artery ligation.

Isoflurane Preconditioning May Attenuate Cardiomyocyte Injury Induced by Hypoxia/Reoxygenation Possibly by Regulating miR-363-3p.

This study attempted to explore whether miR-363-3p play a role in the isoflurane (ISO)-mediated protective effect of cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). A myocardial cell injury model was established, and the different preconditioning ISO concentrations were screened and determined. The miR-363-3p level was detected by RT-qPCR.

Penehyclidine Hydrochloride Protects Rat Cardiomyocytes from Ischemia- Reperfusion Injury by Platelet-derived Growth Factor-B.

Aims And Objective: The lack of effective treatments for myocardial ischemiareperfusion (MI-R) injury severely restricts the effectiveness of the treatment of ischemic heart disease. In the present research, we aimed to investigate the protective effect and molecular mechanism of penehyclidine hydrochloride (PHC) on MI-R cells.

Methods: Cell viability was quantified using CCK8.

Temporal effect of melatonin posttreatment on anoxia/reoxygenation injury in H9c2 cells.

Melatonin has been proven to reduce myocardial ischemia-reperfusion (MI/R) injury. However, in most studies, melatonin was administered before MI/R, thus, the results lack clinical significance in patients with acute myocardial infarction. We hypothesize that melatonin posttreatment at different times has different curative effects.

Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation.

Introduction: Isoflurane (ISO) may cause neuronal apoptosis and synaptic disorder during development, and damage long-term learning and memory function. This observation aimed to study the function of H19 in vitro and in vivo tests and the further mechanism was identified.

Methods: ISO cell models and rat models were established and reactive oxygen species (ROS) identified.

Renal tissue desaturation and acute kidney injury in infant cardiac surgery: a prospective propensity score-matched cohort study.

Background: Previous studies on the association between renal tissue desaturation and acute kidney injury (AKI) in infant cardiac surgery are limited by small sample sizes and inconsistent results. This prospective study aimed to determine the association between renal desaturation and AKI in infants undergoing surgical repair of an isolated ventricular septal defect (VSD).

Methods: Infants undergoing VSD repair involving cardiopulmonary bypass participated in this prospective cohort study.

Effects of different ventilation on cerebral oxygen saturation and cerebral blood flow before and after modified ultrafiltration in infants during ventricular septal defect repair.

Objective: To analyse the changes of different ventilation on regional cerebral oxygen saturation and cerebral blood flow in infants during ventricular septal defect repair.

Methods: Ninety-two infants younger than 1 year were enrolled in the study. End-expiratory tidal pressure of carbon dioxide was maintained at 40-45 and 35-39 mmHg in relative low and high ventilation groups.

Age-related cerebrovascular carbon dioxide reactivity in children with ventricular septal defect younger than 3 years.

Background: Impaired cerebrovascular reactivity to carbon dioxide was proposed to contribute to neurological morbidity in children undergoing cardiac surgery. The objective of this study was to assess carbon dioxide reactivity and regional cerebral oxygen saturation in children younger than 3 years.

Methods: This study enrolled children younger than 3 years undergoing ventricular septal defect repair.

MiR-183-5p protects rat hearts against myocardial ischemia/reperfusion injury through targeting VDAC1.

MicroRNAs have been reported to be implicated in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to investigate the effect of miR-183-5p on I/R injury. Overexpression of miR-183-5p by agomiR transfection alleviated cardiac dysfunction and significantly reduced the infarct size in rats with myocardial I/R.

Regulation of VDAC1 contributes to the cardioprotective effects of penehyclidine hydrochloride during myocardial ischemia/reperfusion.

Penehyclidine hydrochloride (PHC) preconditioning can alleviate myocardial ischemia/reperfusion (I/R) injury and inhibits the upregulation of voltage-dependent anion channel 1 (VDAC1) during I/R. To validate that VDAC1 is a bona fide target of PHC for the protection against myocardial I/R injury, VDAC1 expression construct was delivered by lentiviruses into rat left ventricular myocardium before PHC preconditioning and myocardial I/R. Overexpression of VDAC1 exacerbated cardiac dysfunction and myocardial injury following I/R, and abolished the cardioprotective effect of PHC during I/R injury.