BackgroundAcute lung injury (ALI) is a serious clinical syndrome with a high rate of mortality. In this study, the effects of triptolide on lipopolysaccharide (LPS)-induced ALI in rats were investigated.MethodsSixty-five male Sprague Dawley rats(approved by ethics committee of the First Affiliated Hospital of Soochow University) were randomly divided into five groups. The control group was injected with 2.5 mL saline/kg body weight via the tail vein and intraperitoneally with 1% dimethyl sulfoxide (DMSO) (n = 5). The L group was administered with 0.2% LPS dissolved in saline (5 mg/kg) to induce ALI via the tail vein (n = 15). The TP1, TP2, and TP3 groups were treated as rats in the L group and then intraperitoneally injected with 25, 50, and 100 μg triptolide/kg body weight, respectively (15 rats per group). Blood samples from the left heart artery were taken for blood gas analysis at 1 hour before injection and at 1, 3, 6, and 12 hours after saline and DMSO administration in the control group, LPS injection in the L group, and triptolide injection in the TP1, TP2, and TP3 groups. Lung wet-to-dry weight (W/D) ratio, diffuse alveolar damage (DAD) score, TNF-α levels, and mRNA and protein expression of toll-like receptor 4 (TLR4) were analyzed.ResultsCompared with the control group, the arterial partial pressure of oxygen (PaO2) declined (P <0.05), the W/D ratio and DAD score increased (P <0.05), and TNF-α levels in serum and bronchoalveolar lavage fluid (BALF) and mRNA and protein expression of TLR4 were significantly increased in the L group (P <0.05). Compared with the L group, PaO2 significantly increased in the TP2 and TP3 groups (P <0.05), while the W/D ratio and DAD score were significantly decreased in the TP2 and TP3 groups (P <0.05). TNF-α levels and mRNA and protein expression of TLR4 were significantly decreased in the TP2 and TP3 groups compared with the L group (P <0.05).ConclusionsTriptolide can ameliorate LPS-induced ALI by reducing the release of the inflammatory mediator TNF-α and inhibiting TLR4 expression.
Background
This study was conducted to investigate the effects and safety of remimazolam versus propofol on cerebral oxygen saturation and cerebral hemodynamics during the induction of general anesthesia in patients receiving carotid endarterectomy (CEA), so as to provide theoretical basis for better clinical application of remimazolam.
Methods
Forty-three patients (60–75 years old) with carotid artery stenosis (carotid artery stenosis greater than 70%) were randomly divided into the remimazolam group (R group) and the propofol group (P group). Anesthesia was induced with remimazolam (0.3 mg/kg) or propofol (1.5-2 mg/kg) individually. At time of admission (T0), post-anesthesia induction (T1), consciousness disappears (T2), 1 min after loss of consciousness (T3), 2 min after loss of consciousness (T4) and pre-endotracheal intubation (T5), measurement in patients with regional cerebral oxygen saturation (SrO2), average blood flow velocity (Vm), resistance index (RI), mean arterial pressure (MAP), heart rate (HR) and cardiac index (CI) were recorded.
Results
SrO2 increased significantly in both groups after induction of anesthesia compared with baseline (P < 0.05) and decreased after loss of consciousness (P < 0.05). There was no difference in the mean value of the relative changes in SrO2 between the groups. Meanwhile, the Vm, RI, HR and CI of each time point between two groups showed no statistically significant difference (P > 0.05) while MAP in group P at T5 was lower than that in group R individually(P < 0.05). In each group, Vm, HR, CI and MAP at T2-T5 were all significantly reduced compared with T1, with statistically differences(P < 0.05). Specifically, there was no difference of RI at each time between or within groups(P > 0.05).
Conclusions
Our study revealed that remimazolam can be administered safely and effectively during the induction of general anesthesia for carotid endarterectomy in elder population and it demonstrated superiority in hemodynamic changes compared with propofol.
Clinical trial registration
This trial was retrospectively registered with the Chinese Clinical Trial Registry. Registration number: ChiCTR2300070370. Date of registration: April 11, 2023.
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