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Many studies have demonstrated that the ventrolateral medulla (VLM) plays an important role in the maintenance of systemic arterial pressure (SAP) and vascular tone. The VLM is divided into rostral (RVLM) and caudal (CVLM) portions which play opposing roles in regulating cardiovascular functions. The purposes of this study are to explore the relationship of fibers projecting between the RVLM and CVLM, and to investigate the effect of propofol (PPF, 2 mg/kg), an anesthetic agent, on modulating their neuronal firing rate (NFR). Forty-four adult cats were anaesthetized intraperitoneally with urethane (400 mg/kg) and alpha-chloralose (40 mg/kg). The femoral artery was cannulated to allow monitoring of SAP and heart rate (HR). The femoral vein was cannulated for intravenous drug administration. Microinjection of glutamate (Glu, 3.0 nmol/30 nl), kynurenic acid (Kyn, 3.0 nmol/30 nl), gamma-aminobutyric acid (GABA, 4.0 nmol/30 nl), or bicuculline (Bicu, 4.0 nmol/30 nl) into the RVLM produced SAP increases or decreases, but did not significantly change the NFR in the CVLM. This occurred even after intravenous administration of PPF. This shows that there are few fiber projections from the RVLM to the CVLM. Conversely, microinjection of Glu, Kyn, GABA or Bicu into the CVLM produced SAP changes, and the NFR in the RVLM was significantly changed. These changes were more significant after intravenous administration of PPF. These results show that there are more fibers projecting from the CVLM to the RVLM and fewer fibers projecting from the RVLM to the CVLM to affect the SAP and its NFR.

Monitoring hypnotic depth is used to prevent awareness during general anesthesia. We used the A-line ARX index (AAI) to assess the effect of shortterm inhalation of sevoflurane in the prevention of intubation-induced inadequate hypnotic depth during anesthetic induction.Thirty patients were randomly divided into the sevoflurane and non-sevoflurane groups, both of which were given 3 μg kg⁻¹ fentanyl, 4 mg kg⁻¹ thiamylal, and 0.2 mg kg⁻¹ cis-atracurium intravenously to induce general anesthesia. The sevoflurane group then inhaled 6% sevoflurane and 4 L/min O₂ for 3 minutes, whereas the non-sevoflurane group was given 4 L/min O₂ alone. Both groups were intubated 3 minutes after induction. Measurements of the AAI, non-invasive blood pressure, and heart rate were performed every minute, starting 3 minutes prior to induction until 9 minutes after intubation.Intubation induced a significant AAI elevation in the non-sevoflurane group (47.13 ± 20.88, 48.13 ± 20.05, 40.87 ± 15.86 and 31.27 ± 15.26 at 1, 2, 3 and 4 minutes after intubation, respectively, vs. 17.67 ± 6.44 at 3 minutes after induction; p0.05), whereas the AAI remained unchanged for the sevoflurane group following intubation. Moreover, the non-sevoflurane group demonstrated higher AAI values after intubation compared with the sevoflurane group. There were no significant differences in blood pressure and heart rate between the two groups throughout the study.Adding 6% sevoflurane with 4 L/min O₂ for 3 minutes during the induction period prevented inadequate hypnotic depth caused by intubation but was not sufficient to inhibit fluctuations in hemodynamics.

The effect of propofol on neuronal activity in the rostral ventrolateral medulla (RVLM) is not well established. Therefore, we performed extracellular recording on neurons of the RVLM to investigate neuronal activity before and after administration of intravenous propofol. The mean systemic arterial pressure (MSAP), heart rate and integrated neuronal firing rate (INFR) in the RVLM were continuously recorded in anesthetized cats before and after intravenous injection of 2 mg/kg propofol or supplemental injections of 1, 2 and 4 mg/kg propofol that were given respectively. Additionally, we compared the MSAP, heart rate (HR), and INFR in the RVLM following intravenous injection of 2 mg/kg propofol or 12.5 microg/kg nitroprusside. Neuronal firing was dose-dependently and reversibly inhibited after the supplemental doses of 1, 2 and 4 mg/kg propofol. The control INFR was 14.2 +/- 9.9 Hz, and this decreased to 12.1 +/- 9.4 Hz after the first dose of propofol (P = 0.085 vs. control), and further decreased to 9.3 +/- 7.7 Hz (P = 0.001 vs. control) and 7.5 +/- 7.7 Hz (P0.001 vs. control) after the second and third doses of propofol, respectively. Besides, SAP and HR were dose-dependently decreased by propofol as well. However, the effects of propofol and nitroprusside on neuronal activity in the RVLM differed. Propofol inhibited neuronal firing, whereas nitroprusside activated neuronal firing. In conclusion, propofol may dose-dependently inhibit spontaneous neuronal activity and the baroreflex in the RVLM.

BACKGROUND: Recent reports have identified a role for cyclic adenosine monophosphate (cAMP) transduction in nociceptive processing. Spinal activation of the cAMP induced gene transcription through the activation of protein kinase A and cAMP response element-binding protein (CREB). Intrathecal injection of protein kinase A inhibitor reversed the mechanical hyperalgesia, whereas injection of CREB antisense attenuated tactile allodynia caused by partial sciatic nerve ligation (PSNL) in rats. In the present study, we aimed to assess the effects of spinal cAMP transduction on the nociceptive processing in a chronic neuropathic pain model. METHODS: PSNL was performed in male Sprague-Dawley rats 1 wk after intrathecal catheterization. Nociception to mechanical and thermal stimuli was assessed at the hindpaw 2 h, 3, 7, and 14 days after PSNL. The effects of adenylate cyclase inhibitor, SQ22536 (0.7 mol, intrathecal) on these nociceptions were evaluated. Changes in the expression and immunoreactivity of CREB and its phosphorylated proteins (CREB-IR and pCREB-IR) in the dorsal horn of the spinal cord were also measured. RESULTS: The expression of CREB-IR and pCREB-IR proteins was shown to increase for 2 wk after PSNL. The increase in pCREB was partially reversed by the blockade of the cAMP pathway in the early 3 days, with a parallel increase in mechanical and thermal withdrawal thresholds. CONCLUSION: These results revealed the possible contribution of an increase in pCREB to the PSNL-induced tactile allodynia and thermal hyperalgesia. Modulation of the cAMP pathway may be clinically relevant if early intervention can be achieved in patients with chronic neuropathic pain.

We examined the effects of serotonin (5-HT) on cardiovascular responses and blood flows in the right common carotid artery (RCCA), superior mesenteric artery (SMA) and right femoral artery (RFA), stimulated by glutamate (Glu) in the dorsomedial medulla (DM), rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM). Microinjection of Glu into the DM produced increases in systemic arterial pressure (SAP) and flows in the RCCA and RFA, and decrease in flow in the SMA. Microinjection of Glu into the RVLM produced increases in SAP and decreases in flows in the RCCA, SMA and RFA. Prior microinjections of 5-HT into the same sites attenuated all the Glu-induced responses. Microinjection of Glu into the CVLM produced decreases in SAP and flows in the RCCA, SMA and RFA. These decreases were potentiated by prior injection of 5-HT. These findings suggest that 5-HT modulates the cardiovascular and blood flow responses induced by Glu in the medulla.

The aim of this study was to compare students' satisfaction between problem-based learning (PBL) and lecture-based traditional teaching of anesthesia.One hundred and thirty-seven fifth-year medical students were enrolled in a course which used a hybrid curriculum for teaching about anesthesia. The hybrid curriculum included 9 essential lectures and 3 related PBL case discussions. A Linkert 5-point scale was used for to assess students' satisfaction levels between PBL and lecture-based traditional teaching. Data were collected through a year-end questionnaire over 2 academic years from 2002 to 2003. Scores regarding the satisfaction levels between these 2 teaching methods were analyzed using a 2-sided paired t-test.Most students preferred PBL over the lecture-based traditional teaching in the following 6 aspects: learning about anesthesia, understanding other medical knowledge, being interested in and motivated to learn, training for future work, training of personal abilities, and being confident and satisfied with the teaching method (p0.05). However, traditional teaching was superior to PBL in enhancing the speed of learning with greater understanding of a basic knowledge of anesthesia, as well as in providing more solid content with understanding of a greater number of anesthetic techniques (p0.05). Satisfaction levels with this curriculum did not generally differ between students enrolled in different classes in 2002 and 2003.Although the assessment tools and content of PBL need to be modified, implementation of PBL for teaching anesthesia showed satisfactory results.

Using in vivo voltammetry to directly measure extracellular nitric oxide (NO) levels, our previous studies suggested that the neuronal NO synthase (nNOS) and cyclic guanosine monophosphate (cGMP) signal transducing systems are involved in the cardiovascular responses elicited by activation of N-methyl-D-aspartate (NMDA) receptors in the rostral ventrolateral medulla. In this study, we examined if the depressor responses elicited by activation of NMDA receptors in the caudal ventrolateral medulla (CVLM) also depend on the actions of nNOS and soluble guanylyl cyclase. In anesthetized cats, microinjection of NMDA into the CVLM produced hypotension and bradycardia associated with NO formation. These NMDA-induced responses were attenuated by prior injections of 2-amino-5-phosphonopentanoate (a NMDA receptor competitive antagonist), 7-nitroindazole (a nNOS inhibitor) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (an inhibitor of soluble guanylyl cyclase). These findings suggest that NO is also involved in the NMDA-induced depressor responses of the CVLM.

Propofol is a potent intravenous anesthetic. The action of propofol on the medullary depressor area, the caudal ventrolateral medulla (CVLM), has not been well established. We therefore performed extracellular recordings to study the neuronal activity of the CVLM in cats before and after intravenous propofol administration, to investigate its influence on neuronal firings.Experiments were performed on 31 cats anaesthetized with a mixture of alpha-chloralose and urethane administered intraperitoneally. Mean systemic arterial pressure, heart rate, and the neuronal firing (NF) rate were continuously recorded before and after intravenous injection of a single dose of 2 mg x kg(-1) propofol or separate supplemental doses of 1, 2, and 4 mg x kg(-1) propofol until those parameters had returned to the premedication level.Propofol dose-dependently and reversibly inhibited the NF rate after the supplemental doses of 1, 2, and 4 mg x kg(-1) propofol. The control NF rate of 17.9 +/- 8.6 Hz was depressed to 15.8 +/- 8.5 Hz after the first dose of propofol (p0.05 vs. the control), and was further depressed to 12.8 +/- 8.3 Hz (p0.05 vs. the control) and 10.0 +/- 7.9 Hz (p0.05 vs. the control) after the second and the third doses of propofol, respectively.The dose-dependent inhibition of the spontaneous neuronal firing rate is the main pharmacological action of propofol in the caudal ventrolateral medulla of cats.

Burns associated with chemical disinfectants for skin preparation are rare. Skin irritation and maceration associated with pressure factors may contribute to its occurrence. We report a 24-year-old female with thyroid tumor who was admitted for subtotal thyroidectomy. After anesthetic induction, the patient was placed in the supine position with the trunk elevated to 20 degree. The skin over the anterior neck was sterilized with 10% Povidone-iodine (PI) alcohol solution. After a 3-hour surgery, the patient complained of burning pain over the back at the recovery room. Physical examination revealed a 9 x 11 cm area of skin lesion partially thickened amid on the middle of the back suggestive of chemical burn. After conservative treatment, she was discharged uneventfully 4 days later. Upon follow-up, the wound was seen to heal with minimal scarring within 3 weeks.

Rapid-sequence induction with cricoid pressure is a standard procedure for inducing anesthesia in patients with a potentially full stomach. During the induction period, if the patient develops generalized movements of the body, the pressure level of the cricoid may change unexpectedly. As a result, the increase in intragastric pressure may cause gastric regurgitation and consequent pulmonary aspiration. Rocuronium has been widely used as an alternative to succinylcholine during the induction of anesthesia. However, most patients who received rocuronium complained of severe burning pain in their arm during intravenous injection. Even after the administration of the induction agents, rocuronium injection can also cause withdrawal of the hand or other generalized movements of the body. We describe a case of gastric regurgitation with pulmonary aspiration following generalized spontaneous movements associated with rocuronium injection in a girl who received pediatric emergent surgery.

Propofol may cause hypotension and the mechanism is complex. The present study was designed to determine the direct actions of propofol in medulla of cats. Mean systemic arterial pressure (MSAP), heart rate (HR) and cardiac contractility (dp/dt) were compared before and after administration of propofol through the femoral vein (2, 3 or 4 mg · kg−1), vertebral artery (1 mg · kg−1) or the lateral cerebral ventnricle (0.5 mg · kg−1) in eight anaesthetized cats. To study the direct effect of propofol in medulla, pressor areas of the dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM), or the depressor area of the caudal ventrolateral medulla (CVLM) were first identified with electrical stimuli and then confirmed by pressure microinjection of glutamate (Glu, 0.25M, 30 nl) via a multibarrel-micropipette in 28 cats. One hour later, propofol (0.001%, 50 nl) was microinjected at the same site. Electrical stimulation and Glu were applied again to compare changes of SAR HR and dp/dt with that of the control. Propofol dose-dependently decreased SAR HR and cardiac contractility. The percent increase of MSAP induced by Glu were reduced by propofol in DM (59 ± 3 % vs 13 ± 2 %, n = 11.P 0.05). Our results show that propofol principally inhibits the vasomotor mechanism in the dorsomedial and ventrolateral medulla to effect its hypotensive actions. Nos resultats montrent que l’action hypotensive du propofol est causee par l’inhibition du mecanisme vasomoteur au niveau des zones bulbaires dorsomediane et ventrolaterale.

Ketamine has been administered epidurally and intrathecally for operative and post-operative pain control. Animal studies showed potentiation of analgesia induced by ketamine and morphine. We hypothesized that intrathecal ketamine would potentiate the effects of intrathecal morphine in the treatment of cancer pain.A double blind, cross over study was designed to evaluate the effect of ketamine on spinal morphine analgesia in terminal cancer pain patients. A two-phase protocol was used; phase M, intrathecal morphine alone twice daily; phase M + K, co-administration of ketamine (1.0 mg) with morphine intrathecally twice daily. The dose of morphine was titrated upwards until acceptable pain relief was achieved, defined by numeric rating scales (0-10)or = 3, and the rescue dose of morphine was less than 5 mg after each intrathecal administration for two days. The dose of intrathecal morphine was defined as the effective dose.The effective dose of intrathecal morphine in phase M of 0.38 +/- 0.04 mg.day-1 was higher than that in phase M + K (0.17 +/- 0.02 mg.day-1) (P0.05). The average pain scales were 7.95 +/- 0.25 before intrathecal drug administration. Pain scales were decreased to 2.2 +/- 0.17 (P0.05) in phase M and 1.95 +/- 0.20 (P0.05) in phase M + K after the effective dose of morphine had been reached. No serious side effects were observed in this study.The present study demonstrates that ketamine enhances the analgesic effect of morphine, thus reducing the dose of intrathecal morphine.

Nicotine (6 mg/kg/day) was administered subcutaneously via Alzet osmotic pumps to rats for 28 days. Nociception was measured by the hot-plate and tail-flick methods. A significant antinociceptive effect was demonstrated during the first week of the treatment; after that tolerance developed, lasting for the remaining period of nicotine treatment. This effect was more pronounced in the habituated, rather than in the naive, rats. Rats subjected to nicotine withdrawal tended to exhibit the nociceptive effect for 10 days with an overall P value on the border of significance. This chronic nicotine-induced antinociception and nicotine withdrawal-induced nociception was detectable only by hot-plate but not the tail-flick technique.

Propofol, a widely-used intravenous anesthetic, causes bradycardia, depression in contractility and hypotension. The cellular mechanisms responsible for these cardiac toxicity remain unclear. In this study, we examined the cellular electropharmacological actions of propofol on calcium current in guinea-pig heart. Single ventricular myocytes were freshly isolated from guinea-pig using modified enzymatic method. Whole-cell voltage-clamp technique was applied with one suction pipette. Transmembrane L-type calcium current (ICa (L) ) was separated from other ionic currents by voltage-control, ionic channel blockers and ion substitution methods. Our results show that propofol decreased ICa (L) in a concentration-dependent manner (K D = 54.2 M). Slope conductance of current-voltage relation was decreased by 56 M propofol. Propofol did not affect the steady-state activation curve, but shifted the inactivation curve to hyperpolarizing direction. Recovery from inactivation was slowed down by propofol. Marked resting block and use-dependent block were noted. In conclusion, our results indicate that propofol inhibits cardiac L-type calcium current mainly by shifting inactivation curve and retarding the recovery from inactivation.