This study compared the effects of sevoflurane and propofol on the inflammatory response and pulmonary function of patients with lung cancer during the perioperative period. Forty patients who underwent a selective resection of the inferior lobe of the left lung were randomly divided into two groups, with one group anesthetized with sevoflurane and the other with propofol (groups S and P, respectively). Radial arterial and mixed venous blood were extracted for blood gas analysis, in order to calculate the alveolar-arterial oxygen partial pressure difference (PA-aDO2), respiratory index (RI) and pulmonary shunt ratio (Qs/Qt) prior to the induction of anesthesia (T0), prior to one-lung ventilation (OLV) (T1), 1 h subsequent to the commencement of OLV (T2), 1 h following restoration of two-lung ventilation (T3), 2 h following restoration of two-lung ventilation (T4) and 24 h post-surgery (T5). In addition, blood was extracted from the radial artery at T0, T1, T2, T3, T4 and T5 in order to detect the presence of tumor necrosis factor-α (TNF-α), IL-6 and IL-10 in the blood serum. Between T1 and T4, the tidal volume, airway plateau pressure and end-expiratory positive airway pressure were recorded, in order to calculate the lung dynamic compliance (Cdyn). Heart rate, mean arterial pressure, central venous pressure, cardiac output and the duration of OLV (OLV-T) were recorded at T0–5. Compared with T0, the levels of TNF-α, IL-6 and IL-10 significantly increased during T2 to T4 in both groups (P<0.05). PA-aDO2 and RI increased during T1 to T4, and Qs/Qt increased at T2 (P<0.05). Compared with T1, Cdyn decreased during T2 to T4 in the S group, whereas Cdyn was reduced at T2 in the P group (P<0.05). Compared with the P group, TNF-α level increased and IL-10 decreased at T3 and T4 in the S group. PA-aDO2 and RI increased, but Cdyn decreased at T2 and T3 in the S group. Qs/Qt increased at T2 in the S group. The results of the present study demonstrated that, in comparison with propofol, sevoflurane exhibited an enhanced capacity to aggravate injury to pulmonary function during the perioperative stages. This occurred via the release of inflammatory factors, the aggravation of lung edema and the inhibition of hypoxic pulmonary vasoconstriction.
Background. Renal dysfunction after kidney transplantation may be influenced by many reasons. This study was designed to evaluate whether the administration of dexmedetomidine (Dex) could ameliorate renal function and prognosis after kidney transplantation. Methods. A total of 65 patients were divided into Dex group ( n = 33 ) and Con group (Con, n = 32 ). Dex group intravenously received an initial loading dose of 0.6 μg/kg Dex for 15 min before anaesthesia induction, followed by a rate of 0.4 μg/kg/h until 30 min after kidney reperfusion. By contrast, Con group received saline. The concentration of urinary kidney injury molecule-1 (KIM-1), serum creatinine (Cr), blood urea, urine output, β2 microglobulin (β2-MG), Cystatin C (CysC), and estimated glomerular filtration rate (eGFR) was recorded and compared between two groups during the course of the hospitalization or follow-up. Mean arterial pressure (MAP) and heart rate (HR), vasoactive drugs, and anaesthetics were recorded during the operation. Pain degree was evaluated using a visual analogue scale (VAS) after operation. Delayed graft function (DGF), graft loss, length of hospital stay, and mortality were compared between groups. Results. The concentration of KIM-1 in Dex group was lower than Con group at 2 h ( P = 0.018 ), 24 h ( P = 0.013 ), 48 h ( P < 0.01 ), and 72 h ( P < 0.01 ) after reperfusion. MAP of Dex group after tracheal intubation ( P = 0.012 ) and incision ( P = 0.018 ) and HR after intubation ( P = 0.021 ) were lower than that of Con group. The dosage of sufentanil during operation in Dex group was less than Con group ( P = 0.039 ). Patients that used atropine in Dex group were more than Con group ( P = 0.027 ). Patients who received Dex presented with lower VAS scores at 6 h ( P = 0.01 ) and 12 h ( P = 0.002 ) after operation. Concentration of serum Cr and blood urea had no significant differences between groups before operation and on postoperative day 1 to 6. Urine output was recorded for 6 days after operation and had no differences between groups. Also, no differences were identified between two groups in urea, Cr, β2-MG, CysC, and eGFR in the first 3 months after operation. Incidence of DGF after operation was detected no difference between groups, while length of hospital stay in Dex group was less than Con group ( P = 0.012 ). Conclusion. Dex can decrease kidney injury marker level, attenuate perioperative stress, relieve the dosage of sufentanil and postoperative pain, and reduce length of hospital stay. However, Dex is not associated with changes in prognosis in the first 3 months after transplantation.
Background Spine surgery causes severe pain and can be associated with significant opioid utilization; however, the evidence for opioid-sparing analgesic techniques such as erector spinae plane (ESP) block from controlled studies is limited. We aimed to investigate the analgesic effects of ESP block in lumbar laminoplasty. Methods In this prospective, double-blind, controlled single-center trial, 62 consecutive elective lumbar laminoplasty patients were randomized into either a control group (Group G, N=32) or a treatment group (Group E, N=30). Group G received general anesthesia and multimodal analgesia, similar to group E, while Group E received additional bilateral ESP block after induction of general anesthesia. The primary outcome was postoperative pain scores for the first 48 h after surgery, and the secondary outcomes analyzed included intraoperative anesthetic usage, perioperative analgesic consumption, return of bowel function and satisfaction for acute pain management indicated by overall benefit of analgesia score (OBAS). Results Significant differences in pain scores over time were found between the two groups ( P =0.010), with Group E patients having significantly lower pain scores than Group G during the first six hours ( P =0.000). The opioid consumption in Group G was significantly higher than in Group E both intraoperatively ( P =0.000) and postoperatively ( P =0.0005). Group E patients had lower intraoperative sevoflurane requirement, improved satisfaction with pain management, and earlier return of bowel function than Group G patients. Conclusion ESP block is effective in reducing postoperative pain scores and lowering opioid utilization (both intraoperatively and postoperatively), resulting in improved patient satisfaction for pain management in lumbar laminoplasty.
Abstract. Silymarin is a traditional therapeutic used to protect the liver, acting to oppose lipid peroxidation, to enhance liver regeneration and functioning as an antioxidant. However, the effects of silymarin on pulmonary vascular dysfunction have not been investigated. In the present study, the modulatory effects of silymarin on pulmonary vascular dysfunction and the underlying mechanisms behind this were investigated in a lung ischemia-reperfusion (I/R) injury rat model. Male Sprague Dawley rats were randomly divided into 3 groups, including: i) A control group (n=10); ii) an I/R group (n=10); and iii) a silymarin-treated group (n=10). All experimental rats received 250 mg/kg/day of silymarin for 8 days. Silymarin was demonstrated to markedly improve lung I/R-induced pulmonary vascular dysfunction and lung moisture. Following silymarin treatment, inflammation and oxidative stress in the lung I/R-injury rats were demonstrably suppressed. Treatment with silymarin also inhibited the activation of caspase-3 and -9, and hypoxia inducible factor-1α (HIF-1α) and inducible nitric oxide synthase (iNOS) protein expression in the lung I/R-injury rats. Silymarin was concluded to impact upon pulmonary vascular dysfunction through the HIF-1α-iNOS pathway in the lung I/R injury rat model.
Methyltransferase-like 3 (METTL3)-modulated N6-methyladenosine (m6A) was recently identified as an important epigenetic regulation type during RNA processing and contributes to multiple pathological processes. Neuropathic pain (NP) is induced by a lesion of the somatosensory nervous system, and the detailed pathways by which METTL3/m6A regulated to modulate gene dysregulation and enable NP have remained unclear. Therefore, this study investigated the function of METTL3-mediated m6A methylation on miRNA maturation, and investigated how this regulation contributes to NP progression. A rat model characterized with typical NP was established by a spared nerve-injury (SNI) method. By analyzing the expression levels of METTL3 and m6A methylation, we found that METTL3, along with m6A methylation, was dramatically downregulated in NP rats in contrast to the sham ones. Functionally, enhanced METTL3 promoted the m6A methylation in total RNAs and inhibited NP progression, whereas silencing METTL3 suppressed m6A methylation and increased NP severity. Mechanistically, METTL3 accelerated miR-150 maturation via mediating m6A methylation of primiR-150 at locus 498, cooperating with the “m6A reader” YTHDF2. Meanwhile, miR-150 could directly target brain-derived neurotrophic factor (BDNF) mRNA, and the METTL3/miR-150/BDNF regulatory pathway was finally established. Clinically, we proved that serum METTL3 mRNA was also downregulated in Shingles patients with NP, suggesting its diagnostic potential. In conclusion, we demonstrated an essential function of METTL3-regulated N6-methyladenosine during NP progression via modulating primiR-150 maturation. Serum METTL3 could effectively differentiate NP patients from healthy people, and is useful for dynamic monitoring of diseases after treatment. Therefore, the METTL3/miR-150/BDNF pathway may be a promising therapeutic target for NP patients.
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