• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.27 no.4
• /
• pp.344-348
• /
• 2001

Isoflurane and enflurane are currently used on orthognathic surgery in Korea. Since starting to use enflurane and isoflurane in orthognathic surgery, we have questioned their effect on liver function. Many studies have reported liver function after enflurane and isoflurane anesthesia. Although both enflurane and isoflurane are less hepatotoxic than halothane, some cases of liver dysfunction have been reported after enflurane and isoflurane anesthesia. And, we know that isoflurane is less hepatotoxic than its predecessors, enflurane. But, fulminant liver failure and necrosis were also reported after isoflurane anesthesia. The purpose of this study was to compare immediate liver function in healthy orthognathic surgical patients receiving enflurane or isoflurane anesthesia. To assess the effect of enflurane and isoflurane on liver function, we measured pre-and post-operative serum concentrations of aspartate aminotransferase(AST), and alanine aminotransferase(ALT), alkaline phosphatase(ALP), total bilirubin(Tbil).

• Journal of Veterinary Clinics
• /
• v.29 no.6
• /
• pp.460-463
• /
• 2012

The present study was aimed to evaluate and compare the oxidative stress status of isoflurane and propofol in pigs undergoing surgery with measuring the activities of antioxidant enzymes. The pigs were divided into 2 groups according to the type of anesthesia used for the surgical procedure. In the isoflurane group (group 1), anesthesia was induced and maintained with 2-2.5% isoflurane under 100% oxygen. The propofol group (group 2) received 8 mg/kg/h of IV propofol with 0.5-1% isoflurane under 100% oxygen. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities of isoflurane group were significantly lower at the end of surgery than at induction of anesthesia, while that of the propofol group maintained their baseline values. There were significant differences in all enzymes activities between groups at the end of surgery. These results indicate that propofol is capable of preserving the antioxidant capacity in pigs anesthetized with the combination of isoflurane and propofol infusion.

• Journal of Korean Neurosurgical Society
• /
• v.53 no.3
• /
• pp.139-144
• /
• 2013

Objective : Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. Methods : Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. Results : Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. Conclusion : In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.

• Journal of Veterinary Clinics
• /
• v.32 no.2
• /
• pp.148-153
• /
• 2015

This study was performed to compare two opioid drugs with isoflurane and to determine the difference between isoflurane/remifentanil anesthesia and isoflurane/fentanyl anesthesia in terms of the anesthetic effects in beagle dogs. Isoflurane was maintained at 0.5 MAC, and the opioid drug was administered as a constant rate infusion. The anesthesia was maintained for 2 hours, and isoflurane and opioid drugs were discontinued 2 hours later. After discontinuing the anesthetics, the extremity movement time, eye global positioning time, gag reflex time, head up time, sternal recumbency time, standing time, walking time and complete recovery times were recorded for each dog. Both of the studied anesthetic protocols were suitable in beagle dogs because the anesthetic status was well maintained until the end of the procedure, and rapid recovery times were demonstrated in this experiment. And this study shows that the isoflurane/remifentanil group was more reliable than the isoflurane/fentanyl group because the recovery time CV was lower. Therefore, isoflurane/remifentanil combination anesthesia could be a better choice than isoflurane/fentanyl anesthesia if the patient is severely ill and stable recovery time is needed.

• Journal of Veterinary Clinics
• /
• v.21 no.3
• /
• pp.270-275
• /
• 2004

Anesthetic machines may be equipped with either a precision or nonprecision vaporizer. A precision vaporizer is designed to deliver an exact concentration of anesthetic agent. Goldman vaporizer is a low-flow, closed-circle circuit with a low resistance vaporizer, in circuit. Vaporizers used within circle system(VIC) are not usually temperature compensated and this is generally thought to be a disadvantage. As the volatile agent is vaporized, heat is extracted from the liquid and temperature decreases. This cooling of the liquid leads to a decrease in concentration of the anaesthetic agent delivered by the vaporizer. The purpose of this study is to examine the mechanical consistency of the delivery of isoflurane from Goldman vaporizer and precision vaporizer at various gas flow rates and temperatures. And we first studied isoflurane concentration according to room temperature changes delivered by a Goldman vaporizer and precision vaporizer using different gas flow. The room temperature of $15^{\circ}C,$ $20^{\circ}C,$ $28^{\circ}C$ and fresh gas flow rates of 0.5, 1.0, 1.5, 2.0, 3.0 l/min were used. The inspired agent concentration was measured using a Datex-Ohmeda multigas analyzer. As rose in room temperature, the isoflurane concentration of precision vaporizer approximated the dial setting. On the other hand, at a dial setting concentration of 5.0 percent the delivered isoflurane concentration of precision vaporizer was more than the dial setting in high temperature. The isoflurane concentration of precision vaporizer remained constant despite the increase in temperature. The isoflurane concentration of Goldman vaporizer was increased with rise in room temperature and decreased with rise in gas flow.

• Biomolecules & Therapeutics
• /
• v.24 no.5
• /
• pp.495-500
• /
• 2016

This study aimed to explore the neuroprotection and mechanism of isoflurane on rats with spinal cord ischemic injury. Total 40 adult male Sprague-Dawley rats were divided into the four groups (n=10). Group A was sham-operation group; group B was ischemia group; group C was isoflurane preconditioning group; group D was isoflurane preconditioning followed by ischemia treatment group. Then the expressions of TWIK-related $K^+$ channel 1 (TREK1) in the four groups were detected by immunofluorescent assay, real time-polymerase chain reactions (RT-PCR) and western blot. The primary neurons of rats were isolated and cultured under normal and hypoxic conditions. Besides, the neurons under two conditions were transfected with green fluorescent protein (GFP)-TREK1 and lentivirual to overexpress and silence TREK1. Additionally, the neurons were treated with isoflurane or not. Then caspase-3 activity and cell cycle of neurons under normal and hypoxic conditions were detected. Furthermore, nicotinamide adenine dinucleotide hydrate (NADH) was detected using NAD+/NADH quantification colorimetric kit. Results showed that the mRNA and protein expressions of TREK1 increased significantly in group C and D. In neurons, when TREK1 silenced, isoflurane treatment improved the caspase-3 activity. In hypoxic condition, the caspase-3 activity and sub-G1 cell percentage significantly increased, however, when TREK1 overexpressed the caspase-3 activity and sub-G1 cell percentage decreased significantly. Furthermore, both isoflurane treatment and overexpression of TREK1 significantly decreased NADH. In conclusion, isoflurane-induced neuroprotection in spinal cord ischemic injury may be associated with the up-regulation of TREK1.

• Journal of Veterinary Clinics
• /
• v.27 no.6
• /
• pp.668-673
• /
• 2010

This study was to evaluate the effects of tramadol and medetomidine administration on minimum alveolar concentration (MAC) of isoflurane in dogs. MAC of isoflurane was determined in four occasions; 1 ml saline (Control), $2{\mu}g$/kg medetomidine (M2), 4 mg/kg tramadol (T4), $2{\mu}g$/kg medetomidine-4 mg/kg tramadol combination (M2T4). Heart rate, blood pressure, respiratory rate, end-tidal carbon dioxide concentration, saturation of hemoglobin with oxygen and body temperature were recorded. After administration of M2 ($0.81{\times}0.18%$), T4 ($0.81{\times}0.14%$) and M2T4 ($0.62{\times}0.12%$), less isoflurane was required than the control value ($1.13{\times}0.19%$). Significantly lower heart rate than the control value was detected after treatment of M2, T4, and M2T4. When only M2T4 was administered, blood pressure was significantly higher than the control value. In conclusion, administrations of tramadol, medetomidine and medetomidine-tramadol combination decreased the MAC of isoflurane in dogs. Especially, medetomidine-tramadol combinations could be useful as a premedication because of the anesthetic sparing effect and moderate changes in cardiovascular system.

• Korean Journal of Veterinary Research
• /
• v.52 no.3
• /
• pp.153-155
• /
• 2012

This study investigated the effects of vitamin C on oxidative stress induced by volatile anesthetics in pigs. One group of pigs was used as an anesthesia control group (group 1), and they were anesthetized with isoflurane in oxygen and saline (0.9% NaCl) was injected intravenously. The other group (group 2) was anesthetized with isoflurane and injected intravenously with vitamin C. Total oxidant status, total antioxidant status, and the oxidative stress index in group 2 were significantly different compared with those in group 1. The results showed that intravenous administration of vitamin C decreased oxidative stress during isoflurane anesthesia in pigs.

• The Korean Journal of Physiology and Pharmacology
• /
• v.5 no.2
• /
• pp.165-175
• /
• 2001

Background: Recent in vivo experimental evidence suggests that isoflurane-induced cardioprotection may involve $K_{ATP}$ channel activation. However, it was demonstrated that isoflurane inhibited $K_{ATP}$ channel activities in the inside-out patch mode. To explain this discrepancy, the present investigation tested the hypothesis that a metabolite of isoflurane, trifluoroacetic acid (TFA), contributes to isoflurnae-induced cardioprotection via $K_{ATP}$ channel activation during myocardial ischemia and reperfusion. Methods: Single ventricular myocytes were isolated from rabbit hearts by an enzymatic dissociation procedure. Patch-clamp techniques were used to record single-channel currents. $K_{ATP}$ channel activities were assessed before and after the application of TFA with the inside-out patch mode. Results: TFA enhanced channel activity in a concentration-dependent fashion. The concentration of TFA for half-maximal activation and the Hill coefficient were 0.03 mM and 1.2, respectively. TFA did not affect the single channel conductance of $K_{ATP}$ channels. Analysis of open and closed time distributions showed that TFA increased burst duration and decreased the interburst interval without changes in open and closed time distributions shorter than 5 ms. TFA diminished ATP sensitivity of $K_{ATP}$ channels in a concentration-response relationship for ATP. Conclusions: TFA, a metabolite of isoflurane, enhanced $K_{ATP}$ channel activity in a concentration-dependent fashion. These results imply that TFA could mediate isoflurane-induced cardioprotection via $K_{ATP}$ channel activation during myocardial ischemia and reperfusion.

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.6
• /
• pp.579-589
• /
• 2017

Anesthetics are used extensively in surgeries and related procedures to prevent pain. However, there is some concern regarding neuronal degeneration and cognitive deficits arising from regular anesthetic exposure. Recent studies have indicated that brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are involved in learning and memory processes. Genistein, a plant-derived isoflavone, has been shown to exhibit neuroprotective effects. The present study was performed to examine the protective effect of genistein against isoflurane-induced neurotoxicity in rats. Neonatal rats were exposed to isoflurane (0.75%, 6 hours) on postnatal day 7 (P7). Separate groups of rat pups were orally administered genistein at doses of 20, 40, or 80 mg/kg body weight from P3 to P15 and then exposed to isoflurane anesthesia on P7. Neuronal apoptosis was detected by TUNEL assay and FluoroJade B staining following isoflurane exposure. Genistein significantly reduced apoptosis in the hippocampus, reduced the expression of proapoptotic factors (Bad, Bax, and cleaved caspase-3), and increased the expression of Bcl-2 and Bcl-xL. RT-PCR analysis revealed enhanced BDNF and TrkB mRNA levels. Genistein effectively upregulated cAMP levels and phosphorylation of CREB and TrkB, leading to activation of cAMP/CREB-BDNF-TrkB signaling. PI3K/Akt signaling was also significantly activated. Genistein administration improved general behavior and enhanced learning and memory in the rats. These observations suggest that genistein exerts neuroprotective effects by suppressing isoflurane-induced neuronal apoptosis and by activating cAMP/CREB-BDNF-TrkB-PI3/Akt signaling.