scholarly journals The Ameliorative Effects of Ascorbic Acid on Critical Illness Polyneuropathy in Rodent Sepsis Model

2020 ◽  
Vol 09 (04) ◽  
pp. 265-270
Author(s):  
Eda Sunnetci Silistre ◽  
Oytun Erbas
Keyword(s):  
Ascorbic Acid ◽  
Critical Illness ◽  
Sciatic Nerve ◽  
Compound Muscle Action Potential ◽  
Antioxidant Properties ◽  
Cecal Ligation ◽  
Critical Illness Polyneuropathy ◽  
Hsp 70 ◽  
Sepsis Model ◽  
Tnf Α

AbstractAlthough the exact pathophysiology of critical illness polyneuropathy (CIP) is still unknown, there are several hypotheses, some of which are increased inflammation and oxidative stress. We used rodent sepsis model in which we induced sepsis through cecal ligation followed by cecal puncture. We then administered ascorbic acid (AA) and evaluated outcomes. The levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukins (IL)-6 in the plasma, and heat shock protein-70 (HSP-70) levels in the sciatic nerve were measured, and also electromyography analyses were performed. While plasma MDA, TNF-α, and IL-6 levels were decreased significantly with AA treatment, sciatic nerve levels of HSP-70 were significantly elevated in the AA group. A significant increase in compound muscle action potential (CMAP) amplitude and a significant decrease in CMAP latency were detected in the AA group. We observed healing effects of AA on a rat model of CIP and these effects seem to be related to its anti-inflammatory and antioxidant properties.

scholarly journals Validation of the peroneal nerve test to diagnose critical illness polyneuropathy and myopathy in the intensive care unit: the multicentre Italian CRIMYNE-2 diagnostic accuracy study

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 127 ◽  
Author(s):  
Nicola Latronico ◽  
Giovanni Nattino ◽  
Bruno Guarneri ◽  
Nazzareno Fagoni ◽  
Aldo Amantini ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Critical Illness ◽  
Peroneal Nerve ◽  
Compound Muscle Action Potential ◽  
False Negative ◽  
High Specificity ◽  
Critical Illness Polyneuropathy ◽  
True Positive ◽  
True Negative

Objectives: To evaluate the accuracy of the peroneal nerve test (PENT) in the diagnosis of critical illness polyneuropathy (CIP) and myopathy (CIM) in the intensive care unit (ICU). We hypothesised that abnormal reduction of peroneal compound muscle action potential (CMAP) amplitude predicts CIP/CIM diagnosed using a complete nerve conduction study and electromyography (NCS-EMG) as a reference diagnostic standard.Design: prospective observational study.Setting: Nine Italian ICUs.Patients: One-hundred and twenty-one adult (≥18 years) neurologic (106) and non-neurologic (15) critically ill patients with an ICU stay of at least 3 days.Interventions: None.Measurements and main results: Patients underwent PENT and NCS-EMG testing on the same day conducted by two independent clinicians who were blind to the results of the other test. Cases were considered as true negative if both NCS-EMG and PENT measurements were normal. Cases were considered as true positive if the PENT result was abnormal and NCS-EMG showed symmetric abnormal findings, independently from the specific diagnosis by NCS-EMG (CIP, CIM, or combined CIP and CIM). All data were centrally reviewed and diagnoses were evaluated for consistency with predefined electrophysiological diagnostic criteria for CIP/CIM.During the study period, 342 patients were evaluated, 124 (36.3%) were enrolled and 121 individuals with no protocol violation were studied. Sensitivity and specificity of PENT were 100% (95% CI 96.1-100.0) and 85.2% (95% CI 66.3-95.8). Of 23 patients with normal results, all presented normal values on both tests with no false negative results. Of 97 patients with abnormal results, 93 had abnormal values on both tests (true positive), whereas four with abnormal findings with PENT had only single peroneal nerve neuropathy at complete NCS-EMG (false positive).Conclusions: PENT has 100% sensitivity and high specificity, and can be used to diagnose CIP/CIM in the ICU.

scholarly journals Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

2020 ◽  
Author(s):  
Petra Huehnchen ◽  
Klaus Viktor Toyka ◽  
Karen Gertz ◽  
Matthias Endres ◽  
Wolfgang Boehmerle
Keyword(s):  
Critical Illness ◽  
Sciatic Nerve ◽  
Brain Ischemia ◽  
Nerve Conduction ◽  
Quadriceps Muscle ◽  
Critical Illness Polyneuropathy ◽  
Positive Control ◽  
Electromyographic Activity ◽  
Conduction Function ◽  
Focal Brain Ischemia

Abstract Objective Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration. Results Focal brain ischemia was induced in adult mice by 60-minute middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham+). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham + mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity.

scholarly journals Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

2020 ◽  
Author(s):  
Petra Huehnchen ◽  
Klaus Viktor Toyka ◽  
Karen Gertz ◽  
Matthias Endres ◽  
Wolfgang Boehmerle
Keyword(s):  
Critical Illness ◽  
Sciatic Nerve ◽  
Brain Ischemia ◽  
Nerve Conduction ◽  
Quadriceps Muscle ◽  
Critical Illness Polyneuropathy ◽  
Positive Control ◽  
Electromyographic Activity ◽  
Conduction Function ◽  
Focal Brain Ischemia

Abstract Objective: Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration.Results: Focal brain ischemia was induced in adult mice by 60-minute middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham+). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham+ mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity. In conclusion, we found no peripheral nerve dysfunction/ degeneration as signs of a CIP-like phenotype after MCAo.

scholarly journals The Anti-Inflammatory Role of Bilirubin on “Two-Hit” Sepsis Animal Model

2020 ◽  
Vol 21 (22) ◽  
pp. 8650
Author(s):  
Duc Tin Tran ◽  
Yong Yeon Jeong ◽  
Jeong Min Kim ◽  
Hong Bum Bae ◽  
Sung Kuk Son ◽  
...  
Keyword(s):  
Animal Model ◽  
Inflammatory Cytokines ◽  
Tissue Injury ◽  
Antioxidant Properties ◽  
Cecal Ligation ◽  
Suppressor Cells ◽  
Inflammatory Cells ◽  
The Body ◽  
Sepsis Model ◽  
Anti Inflammatory

Introduction: Bilirubin is a product of the heme catabolism pathway, and it is excreted in bile and removed from the body through the urine. Bilirubin has potent antioxidant properties but also plays a role in anti-inflammation by protecting the body against endotoxin-induced lung inflammation, down-regulating the expression of adhesion molecules, and inhibiting the infiltration of inflammatory cells. Thus, bilirubin is a promising agent that could use in inflammation disease treatment. The application of bilirubin on the “two-hit” sepsis animal model has been, to date, unknown. Methods: we used lipopolysaccharide to induce initial insults in C57BL/6 mice. After 24 h, mice underwent cecal ligation and puncture to induce the “two-hit” sepsis model. Next, mice were administered 30 mg/kg bilirubin and we observed an improvement. Results: We observed that bilirubin inhibited the expression of pro-inflammatory cytokines, while the levels of anti-inflammatory cytokines were significantly augmented in the lung. Bilirubin improved the survival rate in the sepsis model. Furthermore, we suggest that bilirubin can modulate the accumulation of T-regulatory cells and myeloid-derived suppressor cells. Notably, bilirubin suppressed the activation and functions of T-cells. Conclusions: These results clarified that bilirubin might improve tissue injury in sepsis through anti-inflammatory mechanisms.

scholarly journals Regulation of dendritic cell function improves survival in experimental sepsis through immune chaperone

2019 ◽  
Vol 25 (4) ◽  
pp. 235-243 ◽  
Author(s):  
Pengfei Li ◽  
Ran Zhao ◽  
Kevin Fan ◽  
Stephen Iwanowycz ◽  
Hongkuan Fan ◽  
...  
Keyword(s):  
Cell Function ◽  
Critical Role ◽  
Cecal Ligation ◽  
Experimental Sepsis ◽  
Adaptive Immune ◽  
Sepsis Model ◽  
Novel Approach ◽  
Tnf Α ◽  
Heat Shock Protein Gp96 ◽  
Dc Maturation

Dendritic cells (DCs) are professional Ag-presenting cells that play a critical role in both innate and adaptive immune responses. DCs recognize and respond to bacteria through multiple PRRs, including TLRs. Heat shock protein gp96/grp94 is a master essential chaperone for TLRs in the endoplasmic reticulum. We generated DC-specific gp96-knockout (KO) mice and showed that gp96 KO DCs were unable to respond to multiple TLR ligands. TLR-mediated hyperinflammatory response can lead to sepsis. However, the roles of neither DCs nor the DC-intrinsic gp96 in the process are completely understood. In a LPS-induced sepsis model, we hereby found that deletion of gp96 in DCs significantly reduced serum TNF-α levels and improved survival. Furthermore, using the well-defined polymicrobial sepsis model of cecal ligation and puncture, we found that DC-specific ablation of gp96 improved survival with significantly attenuated liver and renal injuries, decreased circulating inflammatory cytokines, altered DC maturation and activation, and increased serum Ig. Collectively, we demonstrate that deletion of gp96 in DCs is beneficial in protecting mice against sepsis induced by both endotoxemia and polymicrobial infections. We conclude that targeting gp96 in DCs may provide a potential novel approach for reducing the morbidity and mortality of sepsis.

scholarly journals A New Approach to Monitoring and Evaluation of Cecal Ligation and Puncture Sepsis Model

2021 ◽  
Vol 3 (2) ◽  
pp. 97-106
Author(s):  
Arezou Khosrojerdi ◽  
◽  
Sara Soudi ◽  
Ahmad Zavaran Hosseini ◽  
Seyed Mahmoud Hashemi ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Clinical Chemistry ◽  
Cecal Ligation ◽  
Serum Levels ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Status ◽  
Sepsis Model ◽  
Tnf Α ◽  
Systemic Inflammatory Disease ◽  
Tgf Β1

Background: Sepsis is a systemic inflammatory disease in response to the pathogens that leads to vital organ failures the failure of vital organs. Appropriate animal models should be developed to measure the effectiveness of therapeutic methods. Cecal Ligation and Puncture (CLP) is the most widely used methods of creating the sepsis model. Some variables interfere in the creation of the CLP model which terminated to result in an unrepeatable dynamic of the inflammatory responses. The current research, suggests presents the simultaneous study of inflammatory responses in serum and liver as a criterion for determining the inflammatory status of the CLP model. Materials and Methods: CLP model was induced in 15 female C57bl/6 mice. IL-6, TNF-α, IL-10, and TGF-β1 cytokines levels were measured at 24, 48, and 72 hours after CLP induction in both serum and liver tissue by ELISA method. Serum levels of liver enzymes were analyzed by the clinical chemistry analyzer. All studies were performed in healthy mice as well. The results were reported as Mean±SD. Results: The levels of IL-10 and TGF- β1 in the liver is were significantly (P≤0.05) higher than serum. The production of IL-10 and TGF- β1 in the serum and liver reaches its maximum at peaked 24 and 72 hours after CLP induction. The level of TNF-α in the liver is was significantly (P≤0.05) higher than serum with a maximum production 24 hours after CLP induction. Conclusion: Serum is not a good representative of the inflammatory condition in sepsis. Therefore, it is suggested that local inflammatory responses be considered in evaluating the model, and the determination of drug efficacy.

scholarly journals Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

2020 ◽  
Author(s):  
Petra Huehnchen ◽  
Klaus Viktor Toyka ◽  
Karen Gertz ◽  
Matthias Endres ◽  
Wolfgang Boehmerle
Keyword(s):  
Critical Illness ◽  
Sciatic Nerve ◽  
Brain Ischemia ◽  
Nerve Conduction ◽  
Quadriceps Muscle ◽  
Critical Illness Polyneuropathy ◽  
Positive Control ◽  
Electromyographic Activity ◽  
Conduction Function ◽  
Focal Brain Ischemia

Abstract Objective: Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration. Results: Focal brain ischemia was induced in adult mice by 60-minute middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham+). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham+ mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity. In conclusion, we found no peripheral nerve dysfunction/ degeneration as signs of a CIP-like phenotype after MCAo.

scholarly journals Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

2020 ◽  
Author(s):  
Petra Huehnchen ◽  
Klaus Viktor Toyka ◽  
Karen Gertz ◽  
Matthias Endres ◽  
Wolfgang Boehmerle
Keyword(s):  
Critical Illness ◽  
Sciatic Nerve ◽  
Brain Ischemia ◽  
Nerve Conduction ◽  
Quadriceps Muscle ◽  
Critical Illness Polyneuropathy ◽  
Positive Control ◽  
Electromyographic Activity ◽  
Conduction Function ◽  
Focal Brain Ischemia

Abstract Objective: Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration. Results: Focal brain ischemia was induced in adult mice by 60-minute middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham+). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham+ mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity. In conclusion, we found no peripheral nerve dysfunction/ degeneration as signs of a CIP-like phenotype after MCAo.

scholarly journals Impact of Intermittent Hypoxia on Sepsis Outcomes in a Murine Model

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kun-Ta Chou ◽  
Shih-Chin Cheng ◽  
Shiang-Fen Huang ◽  
Diahn-Warng Perng ◽  
Shi-Chuan Chang ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Intermittent Hypoxia ◽  
Leukocyte Count ◽  
Bacterial Load ◽  
Cecal Ligation ◽  
Sepsis Model ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Changes ◽  
Necrosis Factor

Abstract Sleep apnea has been associated with a variety of diseases, but its impact on sepsis outcome remains unclear. This study investigated the effect of intermittent hypoxia [IH]–the principal feature of sleep apnea–on murine sepsis. 5-week-old male C57BL6 mice were assigned to groups receiving severe IH (O2 fluctuating from room air to an O2 nadir of 5.7% with a cycle length of 90 seconds), mild IH (room air to 12%, 4 minutes/cycle), or room air for 3 weeks. Sepsis was induced by cecal ligation and puncture and survival was monitored. Sepsis severity was evaluated by murine sepsis scores, blood bacterial load, plasma tumor necrosis factor-α [TNF-α]/interleukin-6 [IL-6] levels and histopathology of vital organs. Compared with normoxic controls, mice subjected to severe IH had earlier mortality, a lower leukocyte count, higher blood bacterial load, higher plasma TNF-α and IL-6 levels, more severe inflammatory changes in the lung, spleen and small intestine. Mice subjected to mild IH did not differ from normoxic controls, except a higher IL-6 level after sepsis induced. The adverse impact of severe IH was reversed following a 10-day normoxic recovery. In conclusion, severe IH, not mild IH, contributed to poorer outcomes in a murine sepsis model.

scholarly journals Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Petra Huehnchen ◽  
Klaus Viktor Toyka ◽  
Karen Gertz ◽  
Matthias Endres ◽  
Wolfgang Boehmerle
Keyword(s):  
Critical Illness ◽  
Sciatic Nerve ◽  
Brain Ischemia ◽  
Nerve Conduction ◽  
Quadriceps Muscle ◽  
Critical Illness Polyneuropathy ◽  
Positive Control ◽  
Electromyographic Activity ◽  
Conduction Function ◽  
Focal Brain Ischemia

Abstract Objective Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration. Results Focal brain ischemia was induced in adult mice by 60-min middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham +). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham + mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity. In conclusion, we found no peripheral nerve dysfunction/degeneration as signs of a CIP-like phenotype after MCAo.

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