Effects of different doses of dexmedetomidine on analgesic efficacy and inflammatory cytokines in patients undergoing laparoscopic surgery

Wan, Zhigang; Wang, Jie; Cao, Hui; Wu, Limin

doi:10.3892/etm.2018.6355

Cited by 7 publications

(11 citation statements)

References 18 publications

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“…Wan et al administered 0.25, 0.5 and 1 μg/kg doses of dexmedetomidine to patients undergoing laparoscopic surgery with general anesthesia and examined CRP, TNF-α and IL-10 levels. Compared to the 0.25 μg/kg dose, patients receiving 0.5 and 1 μg/kg had lower CRP and TNF-α levels, while the IL-10 level was observed to be highest in the 1 μg/kg group (40). Based on this result, this may be a new research topic in terms of the effect of DEX on APAP toxicity and there is a need for new studies involving different dose applications.…”

Section: Discussionmentioning

confidence: 71%

“…When the literature is examined, it is possible to see many molecules with therapeutic or preventive properties used in research about APAP toxicity (2,4,6). Dexmedetomidine is an effective agent used for sedation in intensive care and anesthesia administration with increasing use as an adjuvant (39,40,41). With antioxidant properties proven in many researches, DEX is understood not to have been used in experimental research related to APAP toxicity in the literature.…”

Section: Discussionmentioning

confidence: 99%

“…Though the histopathologic improvement in terms of the liver was clear in the DEX group, there was no similar amelioration in kidney tubular injury histologic scores which leads to the consideration that the renal injury mechanism may be different to the liver injury mechanism (34,35). It is possible to fi nd clinical and experimental studies with different doses of DEX in the literature (39,40,41). Behmenburg et al used low (0.1-1 nM) and high (3-30 nM) doses of DEX during ischemia and reperfusion of isolated rat hearts and reported high-dose DEX ensured better regression of infarct dimensions compared to low doses (41).…”

Section: Discussionmentioning

confidence: 99%

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Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

Taş¹,

Altınbaş²,

Noyan³

et al. 2019

BLL

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OBJECTIVE AND BACKGROUND: Acute acetaminophen (APAP) overdose has been shown to cause toxicity and the primary treatment medication is N-acetylcysteine (NAC). Dexmedetomidine (DEX) is a sedative drug with known antioxidant properties. We researched whether DEX has an injury-reducing effect on toxicity. METHODS: Rats were divided into: Group I (control), Group II (APAP) Group III (NAC) Group IV (DEX) and Group V (NAC+DEX). Histopathologic investigations of tissues were performed and glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), myeloperoxidase (MPO) and beta trace protein (PGD2S) levels were studied in blood samples. RESULTS: DEX administration for hepatotoxicity and nephrotoxicity induced with APAP, caused a signifi cant reduction in oxidative injury markers like MDA and MPO, a signifi cant increase in GSH-Px level and a signifi cant degree of amelioration in liver histopathologic scores. CONCLUSION: DEX administration for APAP toxicity causes a reduction in oxidative injury biomarkers, increased antioxidant biomarker levels and signifi cant reduction in liver histopathologic scores. The benefi cial effect of DEX use for detection of toxicity induced by acute APAP overdose, was shown in this study for the fi rst time (Tab. 5, Fig. 2, Ref. 41).

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

Taş¹,

Altınbaş²,

Noyan³

et al. 2019

BLL

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“…Prior work also has suggested that medium dosage of dexmedetomidine cannot only effectively relieve the pain of laparoscopic patients but also regulate the secretion of inflammatory cytokines. 31 Endothelial cells, astrocytes, pericytes, and extracellular matrix integrity. 33 GFAP is a cytoskeletal protein of astrocytes and serum GFAP concentration is of great value in the diagnosis of brain injury or stroke and prognosis.…”

Section: Discussionmentioning

confidence: 99%

“…In our study, a statistically signifcant difference in serum TNF‐α and IL‐10 was shown between the two groups, suggesting that dexmedetomidine could significantly reduce neuroinflammation of elderly patients with MCI. Prior work also has suggested that medium dosage of dexmedetomidine cannot only effectively relieve the pain of laparoscopic patients but also regulate the secretion of inflammatory cytokines 31 …”

Section: Discussionmentioning

confidence: 99%

Intraoperative dexmedetomidine for prevention of postoperative delirium in elderly patients with mild cognitive impairment

Xin

Chen

Hua

et al. 2020

Int J Geriat Psychiatry

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Objectives: Delirium is the most common postoperative neurological complication and some evidence suggests that dexmedetomidine is associated with a decreased incidence of delirium. This study is designed to assess the effect of dexmedetomidine on postoperative delirium (POD) in elderly patients with mild cognitive impairment (MCI). Methods: Sixty geriatric patients with MCI were enrolled and ramdomly divided into two groups by a computer-generated randomisation sequence: dexmedetomidine group (D group) and normal saline group (C group). Patients in D group received a loading dose of 0.5 μg/kg dexmedetomidine over 10 minutes before anesthesia induction, followed by a continuous infusion of 0.4 μgÁkg −1 Áh −1 until 30 minutes before the end of surgery; equal volume of normal saline was given in C group. Blood samples were extracted to detect the concentration of cytokines, including tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), heme oxygenase-1 (HO-1), matrix metalloproteinase-9 (MMP-9), and glial fibrillary acidic protein (GFAP) before anesthesia induction (T 1), before suture (T 2), and 30 minutes after surgery (T 3). Postoperative recovery times were recorded. Delirium was assessed with the 3-Minute Diagnostic Interview for confusion assessment method during the first 7 days postoperatively. Results: POD occurred in 10 (33.3%) of 30 patients in C group, and in 3 (10%) of 30 patients given dexmedetomidine (odds ratio [OR] 0.222, 95% CI 0.054-0.914; P = 0.028). The serum concentrations of TNF-α, MMP-9, and GFAP were significantly increased and IL-10 was decreased in the C group than in the D group at T 2 and T 3. No differences were observed between groups in the level of HO-1. Analysis using random-effect multivariable logistic regression indicated that POD was associated with GFAP (odds ratio [OR] 16.691, 95% CI 2.288-121.746; P = 0.005). The positive predictive ability of the multivariate logistic regression model tested by ROC analysis showed an area under the curve of 0.713 (95% CI, 0.584-0.842). Conclusions: Dexmedetomidine can alleviate POD in elderly patients with MCI and may be related to reduce the neuroinflammation by lowering the permeability of blood-brain barrier. Xi Xin and Jing Chen should be considered joint first author.

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Dexmedetomidine activates the PKA/CREB pathway and inhibits proinflammatory factor expression through β2 adrenergic receptors

Zhang,

Shen

2024

Immunity Inflam & Disease

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IntroductionDexmedetomidine (DEX) is primarily utilized for sedation in the context of general anesthesia or intensive care. However, the exact regulatory mechanism by which DEX affects cytokines remains unclear. This study aims to investigate the underlying mechanism by which DEX inhibits proinflammatory factors through activation of the β2 adrenergic receptor (β2 AR).MethodsThe inflammatory cell model of human mononuclear macrophage (THP‐1) cells induced by lipopolysaccharide (LPS) was established to study the effect of DEX on the expression of cell‐related inflammatory factors. ADRA2A gene knockout THP‐1 cells (THP‐1KO) were constructed by CRISPR technology, and the effect of DEX on the expression of inflammatory factors of THP‐1KO cells was detected. The target sites of DEX on β2 AR were screened by molecular docking. Reversion experiments were performed using ADRB2‐siRNA. Western blot was used to detect the activation of β2 AR/PKA/CREB pathway and NF‐κB, and ELISA was used to detect the release level of inflammatory factors.ResultsThe results demonstrated a significant reduction in the expression levels of MCP‐1, interleukin‐06, and IL‐8 in both THP‐1 and THP‐1KO cells when induced by LPS following treatment with DEX. Additionally, DEX treatment led to an increase in IL‐10 expression. Immunofluorescence analysis revealed an upregulation of β2 AR expression after DEX treatment. Western blot results indicated that DEX notably enhanced the activation of the β2 AR and PKA/CREB pathways, while concurrently suppressing the activation of NF‐κB. Notably, the use of ADRB2 siRNA reversed the effects of DEX treatment and promoted the release of inflammatory cytokines.ConclusionDEX initiates the activation of the PKA/CREB pathway through the activation of β2 AR. Simultaneously, it exerts an inhibitory effect on the activation of NF‐κB, consequently reducing the transcription of proinflammatory factors while increasing the transcription of anti‐inflammatory factors.

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Effects of different doses of dexmedetomidine on analgesic efficacy and inflammatory cytokines in patients undergoing laparoscopic surgery

Cited by 7 publications

References 18 publications

Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

Intraoperative dexmedetomidine for prevention of postoperative delirium in elderly patients with mild cognitive impairment

Dexmedetomidine activates the PKA/CREB pathway and inhibits proinflammatory factor expression through β2 adrenergic receptors

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