Effect of Dexmedetomidine Preconditioning on Hepatic Ischemia-Reperfusion Injury in Acute Hyperglycemic Rats.

BACKGROUND: Acute hyperglycemia frequently occurs in stressful situations, including liver transplantation or hepatic surgery, which may affect the protective effects of dexmedetomidine preconditioning and increase postoperative mortality. Therefore, this study aimed to investigate the effects of dexmedetomidine on hepatic ischemia-reperfusion injury in acute hyperglycemia. METHODS: Thirty-six Sprague-Dawley rats were randomly assigned to 6 groups, including a combination between 2 glycemic (normo- and hyperglycemia) and 3 ischemia-reperfusion conditions (sham, ischemia-reperfusion only, and dexmedetomidine plus ischemia-reperfusion). Dexmedetomidine 70 µg/kg was preconditioned 30 minutes before ischemic injury. After 6 hours of reperfusion, serum aminotransferase levels were measured to confirm the hepatic tissue injury. Furthermore, inflammatory (nuclear factor-κb, tumor necrosis factor-α, and interleukin-6) and oxidative stress markers (malondialdehyde and superoxide dismutase) were detected. RESULTS: Ischemia-reperfusion injury significantly increased the serum levels of aminotransferase and inflammatory and oxidative stress markers. These ischemia-reperfusion-induced changes were further exacerbated in hyperglycemia and were significantly attenuated by dexmedetomidine preconditioning. However, the effects of dexmedetomidine in hyperglycemia were lesser than those in normoglycemia (P < .05 for aminotransferases, inflammatory markers, malondialdehyde, and superoxide dismutase). CONCLUSIONS: These findings suggest that the protective effects of dexmedetomidine preconditioning may be intact against hepatic ischemia-reperfusion injury in acute hyperglycemia. Although its effects appeared to be relatively reduced, this may be because of the increase in oxidative stress and inflammatory response caused by acute hyperglycemia. To determine whether the effects of dexmedetomidine itself would be impaired in hyperglycemia, further study is needed.

Suspected Malignant Hyperthermia in a Brain-Dead Donor During Anesthesia for Organ Procurement Surgery: A Case Report.

We report an unusual case of highly suspected malignant hyperthermia after inducing anesthesia in a brain-dead 18-year-old male patient undergoing organ procurement surgery. The patient was administered desflurane (3 vol%) and rocuronium bromide (50 mg) to induce and maintain general anesthesia. He experienced hypercapnia and tachycardia within 5 minutes of anesthesia induction; however, his body temperature rapidly rose only after 15 minutes. The volatile anesthetic was discontinued, and dantrolene was administered at a low dose (1 mg/kg) to avert possible hepatotoxic effects on the donor liver. Fortunately, the clinical course of the brain-dead donor until the organs were harvested and the liver transplantation outcome of the recipient was favorable. A comprehensive understanding of the pathophysiology of brain death, organ transplantation, and malignant hyperthermia is essential to respond promptly and appropriately. Based on our experience, low-dose dantrolene may be clinically used in brain-dead donors while accounting for its potential hepatotoxic effects.

Effects of remote ischemic postconditioning on hepatic injury in lipopolysaccharide-induced endotoxemic rats.

BACKGROUND: Remote ischemic postconditioning (RIPoC) is induced by several cycles of brief, reversible, mechanical blood flow occlusion, and reperfusion of the distal organs thereby protecting target organs. We investigated if RIPoC ameliorated liver injury in a lipopolysaccharide (LPS)-induced endotoxemic rats. METHODS: Protocol 1) Rats were administered LPS and samples collected at 0, 2, 6, 12, and 18 h. 2) After RIPoC at 2, 6, and 12 h (L+2R+18H, L+6R+18H, and L+12R+18H), samples were analyzed at 18 h. 3) RIPoC was performed at 2 h, analysis samples at 6, 12, 18 h (L+2R+6H, L+2R+12H, L+2R+18H), and RIPoC at 6 h, analysis at 12 h (L+6R+12H). 4) Rats were assigned to a control group while in the RIPoC group, RIPoC was performed at 2, 6, 10, and 14 h, with samples analyzed at 18 h. RESULTS: Protocol 1) Liver enzyme, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and nuclear factor-κB (NF-κB) levels increased while superoxide dismutase (SOD) levels decreased over time. 2) Liver enzyme and MDA levels were lower while SOD levels were higher in L+12R+18H and L+6R+18H groups when compared with L+2R+18H group. 3) Liver enzyme and MDA levels were lower while SOD levels were higher in L+2R+6H and L+6R+12H groups when compared with L+2R+12H and L+2R+18H groups. 4) Liver enzyme, MDA, TNF-α, and NF-κB levels were lower while SOD levels were higher in RIPoC group when compared with control group. CONCLUSIONS: RIPoC attenuated liver injury in the LPS-induced sepsis model by modifying inflammatory and oxidative stress response for a limited period.

Hepatic ischemia-reperfusion injury with respect to oxidative stress and inflammatory response: a narrative review.

Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.

The Role of Dexmedetomidine in Hepatic Ischemia-Reperfusion Injury Via a Nitric Oxide-Dependent Mechanism in Rats.

BACKGROUND: Dexmedetomidine is known to protect against ischemia-reperfusion (IR) in various organs; however, the mechanisms of dexmedetomidine in the liver remain unclear. We investigated whether dexmedetomidine preconditioning leads to hepatic protection and whether nitric oxide was associated with this protective mechanism by employing N-nitro-l-arginine methyl ester (l-NAME), a nitrous oxide synthase inhibitor. METHODS: Experiment 1 included 24 rats in 4 groups: sham, IR, 30 µg/kg of dexmedetomidine, and 50 µg/kg of dexmedetomidine. Experiment 2 included 36 rats in 6 groups: IR, 50 µg/kg of dexmedetomidine, 10 mg/kg of l-NAME, 10 mg/kg of l-NAME + 50 µg/kg of dexmedetomidine, 30 of mg/kg l-NAME, and 30 mg/kg of l-NAME + 50 µg/kg of dexmedetomidine. All drugs were administered intraperitoneally. The levels of serum transaminases, malondialdehyde, superoxide dismutase, tumor necrosis factor-α, nuclear factor-κB, and c-Jun N-terminal kinase were measured 6 hours after hepatic surgery. RESULTS: Dexmedetomidine demonstrated a dose-dependent decrease in serum transaminase levels. The 50-µg/kg dexmedetomidine group showed a significant decrease in malondialdehyde levels (P = .002), increase in superoxide dismutase levels (P = .002), and a significantly lower level of phosphorylated tumor necrosis factor-α, nuclear factor-κB, and c-Jun N-terminal kinase (P = .002, respectively) compared with the IR injury group. These protective effects of dexmedetomidine were partially reversed by pretreatment with l-NAME (P < .01 for 20 and 30 mg/kg of l-NAME). CONCLUSION: In hepatic IR injury, dexmedetomidine might protect the liver via antioxidative and anti-inflammatory responses, and nitric oxide production could play a role in these protective mechanisms.

Role of Remote Ischemic Preconditioning in Hepatic Ischemic Reperfusion Injury.

The effect of remote ischemic preconditioning (RIPC) has been proposed that mediates the protective response in ischemia reperfusion injury (IRI) of various organs. In this study, we investigated the effect of RIPC in hepatic IRI, by assessing biomarker of oxidative stress and inflammatory cytokines. Moreover, we intended to demonstrate any such protective effect through nitric oxide (NO). Twenty-five rats were divided into the 5 groups: (1) Sham; (2) RIPC; (3) hepatic IRI; (4) RIPC + hepatic IRI; (5) C-PTIO, 2-(4-carboxyphenyl)-4,5dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3oxide, + RIPC + hepatic IRI. RIPC downregulated the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), histologic damage, and activity of Malondialdehyde (MDA). However, there was no significant reduction in the level of tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB). AST and ALT levels, and hepatic tissue morphology in the C-PTIO group showed a significant improvement compared to those of the RIPC + hepatic IRI group. The application of RIPC before hepatic ischemia downregulated the oxidative stress, not the inflammatory cytokines. Moreover, these protective effect of RIPC would be mediated through the activation of NO as well as anti-oxidant effect.

Asystole due to stimulation of the supraorbital nerve: abrupt and potentially fatal presentation of the trigeminocardiac reflex.

We present a case of sudden asystole that was elicited via the trigeminocardiac reflex in a patient undergoing surgery for a frontal sinus fracture. Asystole occurred after mild stimulation of the supraorbital nerve during dissection along the superior orbital rim. Anticholinergics were administered and lidocaine-soaked gauze was applied to the exposed wound. The patient was an athlete and had pre-existing sinus bradycardia. We hypothesise that the severe reflex response was associated with his underlying increased vagal tone. When performing surgery in patients with increased vagal tone, preventative measures to diminish the trigeminocardiac reflex are recommended. Further studies are needed.

The Effect of Nitric Oxide on Remote Ischemic Preconditioning in Renal Ischemia Reperfusion Injury in Rats.

Although remote ischemic preconditioning (RIPC) is an organ-protective maneuver from subsequent ischemia reperfusion injury (IRI) by application of brief ischemia and reperfusion to other organs, its mechanism remains unclear. However, it is known that RIPC reduces the heart, brain, and liver IRI, and that nitric oxide (NO) is involved in the mechanism of this effect. To identify the role of NO in the protective effect of RIPC in renal IRI, this study examined renal function, oxidative status, and histopathological changes using N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. Remote ischemic preconditioning was produced by 3 cycles of 5 minutes ischemia and 5 minutes reperfusion. Blood urea nitrogen, creatinine (Cr), and renal tissue malondialdehyde levels were lower, histopathological damage was less severe, and superoxide dismutase level was higher in the RIPC + IRI group than in the IRI group. The renoprotective effect was reversed by L-NAME. Obtained results suggest that RIPC before renal IRI contributes to improvement of renal function, increases antioxidative marker levels, and decreases oxidative stress marker levels and histopathological damage. Moreover, NO is likely to play an important role in this protective effect of RIPC on renal IRI.

Sodium Nitrite Attenuates Hepatic Ischemia-Reperfusion Injury in Rats.

OBJECTIVES: Nitrite as an alternative source of nitric oxide has been proposed, as it can mediate the protective response in the presence of ischemia or hypoxic conditions and inorganic nitrite can be reduced to nitric oxide by xanthine oxidoreductase. Here, we investigated whether pretreatment with sodium nitrite can attenuate liver damage in hepatic ischemia-reperfusion injury and identified the possible mechanism of nitrite reduction using 2-(4-carboxyphenyl)-4,5dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3oxide (C-PTIO), a nitric oxide scavenger, and allopurinol, a xanthine oxidoreductase inhibitor. MATERIALS AND METHODS: In experiment 1, 30 male Sprague-Dawley rats were divided into 5 groups: (1) sham-operated; (2) hepatic ischemia-reperfusion injury; and (3-5) sodium nitrite administered intra-peritoneally 30 minutes before ischemia at 2.5, 25, and 250 µmol/kg, respectively. In experiment 2, 24 male Sprague-Dawley rats were divided into 4 groups: (1) hepatic ischemia-reperfusion injury; (2) sodium nitrite + hepatic ischemia-reperfusion injury; (3) C-PTIO + sodium nitrite + hepatic ischemia-reperfusion injury; and (4) allopurinol + sodium nitrite + hepatic ischemia-reperfusion injury. Sodium nitrite (25 µmol/kg) was then administered 30 minutes before hepatic ischemia, and C-PTIO or allopurinol was administered 5 minutes before sodium nitrite administration. Blood aspartate aminotransferase, alanine aminotransferase, hepatic tissue malondialdehyde, histologic changes, and expression of mitogen-activated protein kinase family members were evaluated. RESULTS: Sodium nitrite limited serum elevation of alanine aminotransferase and aspartate aminotransferase induced by hepatic ischemia-reperfusion with a peak effect occurring at 25 µmol/kg sodium nitrite. Pre-treatment with allopurinol abolished the protective effect of sodium nitrite, and C-PTIO treatment attenuated the hepatoprotection of sodium nitrite in rats with hepatic ischemia-reperfusion injury. Liver malondialdehyde activity after ischemia-reperfusion decreased in sodium nitrite-treated rats. Sodium nitrite also prevented hepatic ischemia-reperfusion-induced c-Jun N-terminal kinase and extracellular signal-regulated kinase phosphorylation. CONCLUSIONS: Exogenous sodium nitrite had protective effects against hepatic ischemia-reperfusion injury. Catalytic reduction to nitric oxide and attenuation of hepatic ischemia-reperfusion is dependent on xanthine oxidoreductase.

Beneficial Role of Hydrogen Sulfide in Renal Ischemia Reperfusion Injury in Rats.

PURPOSE: Hydrogen sulfide (H2S) is an endogenous gaseous molecule with important physiological roles. It is synthesized from cysteine by cystathionine γ-lyase (CGL) and cystathionine ß-synthase (CBS). The present study examined the benefits of exogenous H2S on renal ischemia reperfusion (IR) injury, as well as the effects of CGL or CBS inhibition. Furthermore, we elucidated the mechanism underlying the action of H2S in the kidneys. MATERIALS AND METHODS: Thirty male Sprague-Dawley rats were randomly assigned to five groups: a sham, renal IR control, sodium hydrosulfide (NaHS) treatment, H2S donor, and CGL or CBS inhibitor administration group. Levels of blood urea nitrogen (BUN), serum creatinine (Cr), renal tissue malondialdehyde (MDA), and superoxide dismutase (SOD) were estimated. Histological changes, apoptosis, and expression of mitogen-activated protein kinase (MAPK) family members (extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38) were also evaluated. RESULTS: NaHS attenuated serum BUN and Cr levels, as well as histological damage caused by renal IR injury. Administration of NaHS also reduced oxidative stress as evident from decreased MDA, preserved SOD, and reduced apoptotic cells. Additionally, NaHS prevented renal IR-induced MAPK phosphorylation. The CGL or CBS group showed increased MAPK family activity; however, there was no significant difference in the IR control group. CONCLUSION: Exogenous H2S can mitigate IR injury-led renal damage. The proposed beneficial effect of H2S is, in part, because of the anti-oxidative stress associated with modulation of the MAPK signaling pathways.

Effect of preoperative pregabalin on postoperative pain after gastrectomy.

Background: Pregabalin has been studied as a single or multimodal analgesic drug for postoperative pain management in different types of surgeries. We evaluated the analgesic effect of 150 mg of pregabalin in resolving post-gastrectomy pain. Methods: Forty-four patients were randomized into two groups: a pregabalin group that received oral pregabalin (150 mg) 2 h before anesthetic induction, and a control group that received placebo tablets at the same time. Data on postoperative pain intensity (visual analog scale [VAS], at 30 min, 2 h, 4 h, and 24 h), consumption of fentanyl in patient-controlled analgesia (PCA), and the proportion of patients requiring rescue analgesics at different time intervals (0-2 h, 2-4 h, and 4-24 h) were collected during the 24 h postoperative period. Results: The VAS scores did not show significant differences at any time point and consumption of fentanyl in PCA and the proportion of patients requiring rescue analgesics did not differ between the two groups. The groups did not differ in the occurrence of dizziness, sedation, and dry mouth. Conclusion: A preoperative 150 mg dose of pregabalin exerts no effect on acute pain after gastrectomy.

Postoperative nausea and vomiting after thyroidectomy: a comparison between dexmedetomidine and remifentanil as part of balanced anesthesia.

BACKGROUND: Postoperative nausea and vomiting (PONV) is the major complication related to general anesthesia, occurring in 60-80% of patients after thyroidectomy. The objective of this study was to compare the effects of an intraoperative dexmedetomidine infusion with remifentanil, as anesthetic adjuvants of balanced anesthesia, on PONV in patients undergoing thyroidectomy. METHODS: Eighty patients scheduled for thyroidectomy were randomized into the following two groups: 1) The dexmedetomidine group (Group D), who received an initial loading dose of dexmedetomidine (1 µg/kg over 10 min) during the induction of anesthesia, followed by a continuous infusion at a rate of 0.3-0.5 µg/kg/h; 2) the remifentanil group (group R), who received remifentanil at an initial target effect site concentration of 4 ng/ml during the induction of anesthesia, followed by a target effect site concentration of 2-3 ng/ml. PONV was assessed during the first 24 hours in 2 time periods (0-2 h and 2-24 h). The pain intensity, sedation score, extubation time, and hemodynamics were also assessed. RESULTS: During the 2 time periods, the incidence and severity of PONV in group D were significantly lower than in group R. In addition, the need for rescue antiemetics was significantly lower in group D than in group R. The effect of dexmedetomidine on postoperative pain relief (2-24 h) was superior to that of remifentanil. The hemodynamics were similar in both groups, whereas eye opening and extubation time were delayed in group D. CONCLUSIONS: Adjuvant use of intraoperative dexmedetomidine infusion may be effective for the prevention of PONV.

Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury.

BACKGROUND: Superoxide, nitric oxide (NO), and peroxynitrite are important mediators in the pathogenesis of ischemia-reperfusion (I/R) injury. We tested the renoprotective effects of allopurinol (ALP), a xanthine oxidase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and 5,10,15,20-tetrakis (N-methyl-4-pyridyl) porphyrinato iron (III) (FeTMPyP) by selective inhibition of superoxide, NO, and peroxynitrite, respectively. METHODS: Male Sprague-Dawley rats were randomly assigned to 5 groups (n = 6 per group). Group 1 was a sham-operated group. Group 2 was the renal I/R group (30-minute ischemia followed by 24-hour reperfusion). Rats in groups 3, 4, and 5 received ALP, L-NAME, or FeTMPyP, respectively, at 5 minutes before the reperfusion. Serum creatinine (Cr), blood urea nitrogen (BUN), renal tissue malondialdehyde, superoxide dismutase, histological changes, apoptosis, and monocyte infiltration were evaluated. In addition, the combined treatment with ALP and L-NAME was compared with FeTMPyP in a second independent experiment. RESULTS: The administration of ALP, L-NAME, and FeTMPyP diminished the increase in Cr (P = .0066 for all) and BUN (P = .0066 for ALP; and P = .013 for L-NAME) induced by I/R injury and decreased the histological damage (P = .0066 for all). In addition, ALP, L-NAME, and FeTMPyP attenuated the oxidative stress response as determined by a decrease in malondialdehyde level (P = .0066 for all), apoptotic renal tubular cells (P = .0066 for all), and monocyte infiltration (P = .0066 for all). The combined treatment of ALP and L-NAME decreased Cr and BUN levels to a greater degree than FeTMPyP (P = .016 for Cr; P = .0079 for BUN). CONCLUSIONS: Superoxide, NO, and peroxynitrite are involved in renal I/R injury. The reduction of peroxynitrite formation, via inhibition of superoxide or NO, or the induction of peroxynitrite decomposition may be beneficial in renal I/R injury.

Reversible Induction of Pain Hypersensitivity following Optogenetic Stimulation of Spinal Astrocytes.

While glial activation is an integral part of pain pathogenesis, the existence of a causal relationship between glia and pain processing has yet to be demonstrated in vivo. Here, we have investigated whether the activation of spinal astrocytes could directly evoke pain hypersensitivity in vivo via the use of optogenetic techniques. Optogenetic stimulation of channelrhopdopsin-2 (ChR)-expressing spinal astrocytes induced pain hypersensitivity in a reversible and time-dependent manner, which was accompanied by glial activation, NR1 phosphorylation, ATP release, and the production of proalgesic mediators. Photostimulation of ChR2-expressing astrocytes in culture and spinal slices recapitulated in vivo findings, demonstrating the release of proalgesic mediators and electrophysiological disinhibition of spinal projection neurons. These findings deepen our understanding of the role of astrocytes in pain pathogenesis and provide the scientific basis for an astrocyte-oriented pain treatment.

Inhibition of reactive oxygen species downregulates the MAPK pathway in rat spinal cord after limb ischemia reperfusion injury.

INTRODUCTION: We examined the activity of mitogen-activated protein kinase (MAPK) family members, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, in rats pinal cord after hind limb ischemia reperfusion (IR) and analyzed the role of reactive oxygen species (ROS) as mediators of MAPK signaling under these conditions. METHODS: In experiment 1, hind limb IR rats were treated intraperitoneally with one of following agents at 30 min before reperfusion: allopurinol (4, 40 mg/kg), superoxide dismutase (SOD, 4000 U/kg), N-nitro-l-arginine methyl ester (l-NAME, 10 mg/kg), or SOD (4000 U/kg) + l-NAME (10 mg/kg). In experiment 2, 5,10,15,20-tetrakis (N-methyl-4'-pyridyl) porphyrinato iron (III) (FeTMPyP) was administered intraperitoneally (1, 3, or 10 mg/kg) 30 min before reperfusion. After 3 d reperfusion period, the spinal cord (L4-6) was harvested to investigate MAPK signaling activity. RESULTS: In experiment 1, p-ERK and p-JNK levels were significantly higher in the IR group than sham group. Administration of allopurinol, SOD, l-NAME, or SOD + l-NAME significantly reduced the IR-induced increase in p-ERK and p-JNK levels. There were no significant differences in p-p38 levels. In experiment 2, FeTMPyP significantly reduced the IR-induced increase in p-ERK and p-JNK levels in a dose-dependent manner. CONCLUSIONS: Activation of ERK and JNK in the spinal cord was induced by hind limb IR and was not accompanied by p38 activation. IR-induced MAPK phosphorylation was reduced by inhibition of superoxide, nitric oxide, and peroxynitrite, indicating that ROS produced by hind limb IR mediate the activation of these signaling pathways in the spinal cord, potentially affecting distant organs.

A peroxynitrite decomposition catalyst prevents mechanical allodynia and NMDA receptor activation in the hind-paw ischemia reperfusion injury rats.

The contributions of superoxide and nitric oxide to ischemia/reperfusion (I/R)-induced neuropathic pain have previously been demonstrated in an animal model that mimics the symptoms of complex regional pain syndrome type I (CRPS I). Targeting peroxynitrite, which is the product of their interaction, may provide effective treatments for I/R-induced neuropathic pain. In this study, the effect of the peroxynitrite decomposition catalyst FeTMPyP [5,10,15,20-tetrakis (N-methyl-4'-pyridyl)porphyrinato iron (III)], administered at doses of 1, 3 and 10 mg/kg via intraperitoneal injection 30 min prior to reperfusion, was evaluated in rats with chronic post-ischemic pain. The pain behavior of the rats was tested with a von Frey filament. Phosphorylation of N-methyl-D-aspartate (NMDA) receptors in the L4/6 section of the spinal cord was measured on the third day following reperfusion by western blotting. The rats treated with 3 or 10 mg/kg FeTMPyP demonstrated significant increases in their paw withdrawal thresholds and decreased levels of phosphorylated NMDA receptor subunit 1 compared with those of the vehicle group (all P<0.001). These findings suggest that nitrosative stress, specifically that associated with peroxynitrite, may be involved in the mechanical allodynia and central sensitization that are associated with CRPS I and may provide a rationale for CRPS I treatment strategies using peroxynitrite decomposition catalysts.

Fabrication of metal-coated carbon nanowalls synthesized by microwave plasma enhanced chemical vapor deposition.

In this study, the coating of synthesized carbon nanowalls (CNWs) with various metal layers (Ni, Cu, and W) was investigated. CNWs were synthesized by microwave plasma enhanced chemical vapor deposition (PECVD) with a methane (CH4) and hydrogen (H2) gas mixture on a p-type Si wafer, and then coated with metal films (Ni, Cu, and W) using an RF magnetron sputtering system with four-inch targets. Different sputtering times (5, 10, 20, and 30 min) were established to obtain different thicknesses of the metal layers with which the CNWs were coated. Field emission scanning electron microscopy (FE-SEM) was used to examine the cross-sectional and planar conditions of the CNWs, and energy dispersive spectroscopy (EDS) was used to analyze the CNW elements. The FE-SEM analysis of the cross-sectional and planar images confirmed that the metal layers were synthesized to a depth of 0.5 µm from the surfaces of the CNWs, and to a greater depth at the ends of the CNWs, irrespective of the deposition time and the metal species. The resistivity of the as-deposited CNWs appeared as 4.18 x 10(-3) Ω cm; that of the metal-coated CNWs was slightly lower; and that of the Ni-coated CNWs was the lowest (1.74 x 10(-3) Ω cm). The mobility of the metal-coated CNWs was almost unchanged, and that of the as-deposited CNWs was 1.23 x 10(3) cm2 V(-1) s(-1).

Antiallodynic effects of vitamin C and vitamin E in chronic post-ischemia pain rat model.

BACKGROUND: Recent research has shown that reactive oxygen species (ROS) play a significant role in the development and persistence of neuropathic pain through central sensitization via N-methyl-D-aspartate (NMDA) receptor activation. In the present study, we examined whether the intraperitoneal administration of vitamins C and E alone or together could alleviate mechanical allodynia in a chronic post-ischemia pain (CPIP) rat model. METHODS: Vitamins C and E were administered intraperitoneally to 48 male Sprague Dawley rats once per day for 3 days before hindpaw ischemia-reperfusion (I/R) injury was induced. On the third day, the CPIP rat model was produced by inducing ischemia in the left hindpaw by applying an O-ring for 3 h, followed by reperfusion. Three days after reperfusion, hindpaw mechanical allodynia was assessed by measuring the withdrawal response to von Frey filament stimulation. The rats were sacrificed immediately after behavioral testing to determine the phosphorylated NMDA receptor subunit 1 (pNR1) and extracellular-signal-regulated kinases (pERK) levels in the spinal cord. RESULTS: When the antioxidant vitamins C and E were administered intraperitoneally to CPIP rats, I/R injury-induced mechanical allodynia was attenuated, and pNR1 and pERK levels were decreased in the rat spinal cord. Additionally, the co-administration of both vitamins had an increased antiallodynic effect. CONCLUSIONS: The reduced phosphorylated NR1 and ERK levels indicate that vitamins C and E inhibit the modulation of spinal cord neuropathic pain processing. Co-administration of vitamins C and E had a greater antiallodynic effect.