Brain damage after general anesthesia

Suárez, Pablo Mesa; Ramos, Victoria Ramos; García, María Ángela González; Ramos, Santiago Pérez; Huertas, David Portilla; Hoyos, Antonio Muñoz

doi:10.1016/j.medcle.2016.06.052

Cited by 5 publications

(5 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…S100β, another astrocytic marker, plays a key role in neuroinflammation by activating signaling cascades that lead to the production and secretion of inflammatory cytokines. Its levels increase in hippocampal tissue, cerebrospinal fluid and serum during anoxic brain damage and pathophysiological situations, acting as a neuroapoptotic factor [ 153 , 154 ]. Serum S100β levels increased in pediatric patients following general anesthesia by a combination of fentanyl with non-opioid drugs; only the total dose of fentanyl was significantly correlated with the difference between post-exposure and baseline S100β levels [ 154 ].…”

Section: Discussionmentioning

confidence: 99%

“…Its levels increase in hippocampal tissue, cerebrospinal fluid and serum during anoxic brain damage and pathophysiological situations, acting as a neuroapoptotic factor [ 153 , 154 ]. Serum S100β levels increased in pediatric patients following general anesthesia by a combination of fentanyl with non-opioid drugs; only the total dose of fentanyl was significantly correlated with the difference between post-exposure and baseline S100β levels [ 154 ]. In turn, acute administration of remifentanil also led to increased serum S100β levels in rats, which was associated with cognitive dysfunction [ 155 ].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

et al. 2021

View full text Add to dashboard Cite

Tramadol and tapentadol, two structurally related synthetic opioid analgesics, are widely prescribed due to the enhanced therapeutic profiles resulting from the synergistic combination between μ-opioid receptor (MOR) activation and monoamine reuptake inhibition. However, the number of adverse reactions has been growing along with their increasing use and misuse. The potential toxicological mechanisms for these drugs are not completely understood, especially for tapentadol, owing to its shorter market history. Therefore, in the present study, we aimed to comparatively assess the putative lung, cardiac, and brain cortex toxicological damage elicited by the repeated exposure to therapeutic doses of both prescription opioids. To this purpose, male Wistar rats were intraperitoneally injected with single daily doses of 10, 25, and 50 mg/kg tramadol or tapentadol, corresponding to a standard analgesic dose, an intermediate dose, and the maximum recommended daily dose, respectively, for 14 consecutive days. Such treatment was found to lead mainly to lipid peroxidation and inflammation in lung and brain cortex tissues, as shown through augmented thiobarbituric acid reactive substances (TBARS), as well as to increased serum inflammation biomarkers, such as C reactive protein (CRP) and tumor necrosis factor-α (TNF-α). Cardiomyocyte integrity was also shown to be affected, since both opioids incremented serum lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) activities, while tapentadol was associated with increased serum creatine kinase muscle brain (CK-MB) isoform activity. In turn, the analysis of metabolic parameters in brain cortex tissue revealed increased lactate concentration upon exposure to both drugs, as well as augmented LDH and creatine kinase (CK) activities following tapentadol treatment. In addition, pneumo- and cardiotoxicity biomarkers were quantified at the gene level, while neurotoxicity biomarkers were quantified both at the gene and protein levels; changes in their expression correlate with the oxidative stress, inflammatory, metabolic, and histopathological changes that were detected. Hematoxylin and eosin (H & E) staining revealed several histopathological alterations, including alveolar collapse and destruction in lung sections, inflammatory infiltrates, altered cardiomyocytes and loss of striation in heart sections, degenerated neurons, and accumulation of glial and microglial cells in brain cortex sections. In turn, Masson’s trichrome staining confirmed fibrous tissue deposition in cardiac tissue. Taken as a whole, these results show that the repeated administration of both prescription opioids extends the dose range for which toxicological injury is observed to lower therapeutic doses. They also reinforce previous assumptions that tramadol and tapentadol are not devoid of toxicological risk even at clinical doses.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Anesthesia is widely used in experiments to prevent animal suffering during the induction of TBI. In general, anesthesia, especially long-term exposure can result in brain damage, specifically the induction of the mitochondrial apoptosis, which evokes neuronal death ( Mesa Suarez et al, 2016 ; Wu et al, 2019 ). Furthermore, the following studies revealed the effect of different chemicals used for anesthesia on the reaction of various glial cells.…”

Section: Factors Affecting Traumatic Brain Injury Outcome In Experimentsmentioning

confidence: 99%

Reactive gliosis in traumatic brain injury: a comprehensive review

Amlerova,

Chmelova,

Anderova

et al. 2024

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is one of the most common pathological conditions impacting the central nervous system (CNS). A neurological deficit associated with TBI results from a complex of pathogenetic mechanisms including glutamate excitotoxicity, inflammation, demyelination, programmed cell death, or the development of edema. The critical components contributing to CNS response, damage control, and regeneration after TBI are glial cells–in reaction to tissue damage, their activation, hypertrophy, and proliferation occur, followed by the formation of a glial scar. The glial scar creates a barrier in damaged tissue and helps protect the CNS in the acute phase post-injury. However, this process prevents complete tissue recovery in the late/chronic phase by producing permanent scarring, which significantly impacts brain function. Various glial cell types participate in the scar formation, but this process is mostly attributed to reactive astrocytes and microglia, which play important roles in several brain pathologies. Novel technologies including whole-genome transcriptomic and epigenomic analyses, and unbiased proteomics, show that both astrocytes and microglia represent groups of heterogenic cell subpopulations with different genomic and functional characteristics, that are responsible for their role in neurodegeneration, neuroprotection and regeneration. Depending on the representation of distinct glia subpopulations, the tissue damage as well as the regenerative processes or delayed neurodegeneration after TBI may thus differ in nearby or remote areas or in different brain structures. This review summarizes TBI as a complex process, where the resultant effect is severity-, region- and time-dependent and determined by the model of the CNS injury and the distance of the explored area from the lesion site. Here, we also discuss findings concerning intercellular signaling, long-term impacts of TBI and the possibilities of novel therapeutical approaches. We believe that a comprehensive study with an emphasis on glial cells, involved in tissue post-injury processes, may be helpful for further research of TBI and be the decisive factor when choosing a TBI model.

show abstract

“…Because of the case studies that have shown early onset or deterioration in neurological symptoms with exposure to excessive alcohol or general anesthesia or environmental toxins mentioned above we recommend that carriers avoid environmental toxins and avoid excessive alcohol intake. 82 , 83 For many patients this means a significant change in their lifestyle particularly in those who have had daily drinking. Lifestyle modifications in premutation carriers involve alteration of long-term habits.…”

Section: Lifestyle Modificationsmentioning

confidence: 99%

Fragile X Premutation: Medications, Therapy and Lifestyle Advice

Sodhi¹,

Hagerman²

2021

PGPM

View full text Add to dashboard Cite

The fragile X premutation is characterized by 55–200 CGG repeats in the 5ʹ untranslated region of FMR1, whereas full fragile X mutation has greater than 200 repeats and full methylation, which manifests as fragile X syndrome (FXS). The premutation spectrum of clinical involvement includes fragile X-associated tremor/ataxia syndrome (FXTAS), fragile X-associated primary ovarian insufficiency (FXPOI), and fragile X-associated neuropsychiatric disorders (FXAND). In addition, premutation carriers also suffer from various other health problems such as endocrine abnormalities and autoimmune problems. In this paper, we have discussed different health issues faced by the carriers and interventions including medications, therapy and lifestyle changes that could improve their health.

show abstract

Brain damage after general anesthesia

Cited by 5 publications

References 22 publications

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

Reactive gliosis in traumatic brain injury: a comprehensive review

Fragile X Premutation: Medications, Therapy and Lifestyle Advice

Contact Info

Product

Resources

About