Apoptosis of the GABAergic interneuron in the dorsal horn of the chronic post-ischemic pain model / 대한마취과학회지

BACKGROUND: It is well known that the GABAergic inhibitory interneuronal system plays an important role in modulation of the noxious stimulation transmitted from the primary afferent input. Some studies have revealed the role that the GABA inhibitory interneuronal system plays in the modulation of pain transmission and the changes in the GABAergic interneurons that occur during the neuropathic pain. This study was conducted to evaluate the apoptosis of the GABAergic interneuron, which is assumed to contribute to neuropathic pain. METHODS: Male Sprague-Dawley rats weighing 290-310 g were used to create a CPIP (chronic post-ischemic pain) model, which was made by placing a tourniquet on the left hindpaw of the rats. The tourniquet was maintained for 3 hours, after which it was released to allow reperfusion. Thirty minutes prior to reperfusion, N-acetyl-L-cysteine (NAC group) or normal saline (control group) was injected. After reperfusion, mechanical allodynia and cold allodynia were measured. In addition, the release of cytochrome c into the cytosol was evaluated through western blot or immunohistochemistry of the spinal cord. RESULTS: Mechanical and cold allodynia developed and the number of GABA interneurons was reduced in the control group. Additionally, The cytochrome c from the GABA interneuron was released into the cytosol in the control group, but the amount released was reduced in response to treatment with NAC. CONCLUSIONS: The results of this study showed that the GABA interneuron in the Rexed laminae I, II released cytochrome c into the cytosol in CPIP neuropathic pain model, which is known to lead to apoptosis. However, treatment with N-acetyl-L-cysteine prevented this process.

The Effects of the Lidocaine or Fentanyl Pretreatment on Inhalational Induction with Sevoflurane / 대한마취과학회지

BACKGROUND: Sevoflurane has been widely used for inhalation induction and intubation in children and adults. There are some reports about hemodynamic instability and respiratory effects during inhalation induction. We evaluated the effects of fentanyl, lidocaine, or both on inhalation induction and intubation using sevoflurane without neuromuscular blocking agents. METHODS: Forty healthy adult female patients, 20 to 60 years old, premedicated with midazolam 3 mg were randomly received iv saline (Group A), lidocaine 1 mg/kg (Group B), fentanyl 1microgram/kg (Group C) or both lidocaine 1 mg/kg and fentanyl 1microgram/kg (Group D). Anesthesia was induced with 8% sevoflurane inhalation and intubation was done without muscle relaxant. A blind observer recorded the change of blood pressure, heart rate, BIS score, and the time needed for induction and intubation. RESULTS: The mean times for BIS score below 40 were 87 +/- 34 seconds and there were no significant difference among groups. The mean time for loss of self respiration and intubation in group A were significantly longer than those of other groups. The heart rates during induction and intubation of group A were significantly greater than those of other groups. There was no significant difference in blood pressure and side effects during intubation among groups. CONCLUSIONS: Pre-treatment with fentanyl or lidocaine makes smoother and faster induction and intubation during vital capacity rapid inhalation induction with sevoflurane.

The Effect of Sevoflurane and Propofol on Expression of Inducible Nitric Oxide Synthase in Endotoxemic Rats / 대한구급학회지

BACKGROUND: It is a well-known phenomenon that alveolar and peritoneal macrophages exposed to bacterial lipopolysaccharide (LPS) induce a large output of nitric oxide (NO) and an inducible nitric oxide synthase (iNOS) mRNA expression. The purpose of this study is actually how much NO production and iNOS mRAN expression are effected by anesthetics (sevoflurane and propofol) on endotoxemic rats. METHODS: To examine the production of NO in peritoneal macrophages, NO concentration were measured from the rats following 2 hours exposure to LPS and 2 hours administration of sevoflurane and propofol, respectively. Culture supernatants were collected 24 hours after exposure to LPS and anesthetics and assayed by ELISA (Enzyme Linked Immunosorbent Assay) for production of NO. The iNOS mRNA expression was measured using PCR (Polymerase Chain Reaction) techniques and autoradiography. RESULTS: In the control group, the NO concentration was measured at 2 hours after infusion of LPS to rats, and showed 12 4micrometer. After insufflations of anesthetics to experimental animals, NO concentration increased in the sevoflurane and propofol groups, 37 13 (p<0.05) and 29 12micrometer (p<0.05) respectively. The size and brightness of the iNOS mRAN bands were distinct in sevoflurane and propofol in order. CONCLUSIONS: There were no different in regard of NO production and hemodynamic changes but iNOS mRNA expression between sevoflurane and propofol group in endotoxemic rats. The mechanism is not clear, but it is related to the strong stimulating effects on the respiratory tract of inhalation anesthetics.