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).

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.

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.

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.

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).

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 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.

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.

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 β-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.

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.

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.

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.

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).

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.

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.

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.

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.

Effect of superoxide on the development and maintenance of mechanical allodynia in a rat model of chronic post-ischemia pain.

Background: Reactive oxygen species and inflammatory responses contribute to the development of neuropathic pain. Superoxide serves to mediate cell signaling processes and tissue injury during inflammation. We examined the effects of superoxide on the development and maintenance of mechanical allodynia, as well as its contribution to central sensitization in a superoxide-rich animal model of neuropathic pain.

N-Acetyl-l-Cysteine Attenuates Ischemia/Reperfusion Injury-Induced Allodynia and N-Methyl-d-Aspartate Receptor Activation in Rats.

Background: Although reactive oxygen species (ROS) are believed to be involved in pathogenic mechanisms that underlie complex regional pain syndrome type I (CRPS-I), the role of ROS in the central mechanism of CRPS is not fully understood.

Objective: In this study we investigated whether ROS scavenger N-acetyl-l-cysteine (NAC) was capable of attenuating mechanical allodynia and whether pain was decreased through modulating N-methyl-d-aspartate (NMDA) receptor activation in a chronic postischemia pain (CPIP) animal model that mimics the symptoms of CRPS-I.

Methods: Thirty male Sprague-Dawley rats were randomly allocated to 5 different groups: (1) sham rats and CPIP rats treated with (2) vehicle; (3) NAC 30 mg/kg; (4) NAC 100 mg/kg; and (5) NAC 300 mg/kg intraperitoneally at 15 minutes before reperfusion.

Analysis of expert consultation referrals for anesthesia-related issues (December 2008-July 2010): KSA legislation committee report.

Background: Since 2009, database construction of anesthesia-related adverse events has been initiated through the legislation committee of the Korean Society of Anesthesiologists (KSA), based on expert consultation referrals provided by police departments, civil courts, and criminal courts.

Methods: This study was a retrospective descriptive analysis of expert consultation referrals on surgical anesthesia-related cases between December 2008 and July 2010.

Results: During the given period, 46 surgical anesthesia-related cases were referred to the KSA legislation committee for expert consultation.

Superoxide and Nitric Oxide Involvement in Enhancing of N-methyl-D-aspartate Receptor-Mediated Central Sensitization in the Chronic Post-ischemia Pain Model.

Background: Recent studies indicate that reactive oxygen species (ROS) are involved in persistent pain, including neuropathic and inflammatory pain. Since the data suggest that ROS are involved in central sensitization, the present study examines the levels of activated N-methyl-D-aspartate (NMDA) receptors in the dorsal horn after an exogenous supply of three antioxidants in rats with chronic post-ischemia pain (CPIP). This serves as an animal model of complex regional pain syndrome type-I induced by hindpaw ischemia/reperfusion injury.

Contralateral allodynia and central change in the chronic post-ischemic pain model rats.

Background: Mirror-image allodynia is a mysterious phenomenon that occurs in association with many clinical pain syndromes including complex regional pain syndromes (CRPS). Underlying mechanisms for the development of such pain are still a matter of investigation. Several studies suggest that activation of the N-methyl-D-aspartate (NMDA) receptor is essential for central sensitization as a base for persistent pain.