Administration Of Thiopental Research Articles

The Effects of Remifentanil on Hemodynamic Changes in Endotracheal Intubation during Rapid Sequence Induction using Thiopental-succinylcholine or Propofol-succinylcholine

Background: This study evaluated the effects of remifentanil on hemodynamic changes in endotracheal intubation during rapid sequence induction using thiopental or propofol and succinylcholine. Methods: One hundred and twenty patients were divided into 4 groups (30 patients in each group). Anesthesia was induced with propofol 2 mg/kg or thiopental 5 mg/kg and succinylcholine 1 mg/kg followed by remifetanil 0.5μg/kg (group PR), remifentanil 1μg/kg (group TR) or normal saline as control (group PC, group TC). An endotracheal intubation was performed 90 s later, and vecuronium 0.08 mg/kg was given for neuromuscular block. Anesthesia was maintained using 1−3 vol% enflurane with 2 L/min N 2O and 2 L/min O2. Arterial blood pressure (ABP) and heart rate (HR) were recorded before induction, just before intubation, and at 1 min intervals for 5 min after intubation. The incidence of hypertension, hypotension, tachycardia, and bradycardia were recorded. Results: ABP in group PR was lower than in group TR, but HR was not different. The incidence of hypotension in group PR was higher than group TR or group PC. ABP in groups using remifentanil was lower than in control groups. The incidence of hypertension and tachycardia in groups using remifentanil were lower than control groups. Conclusions: During administration of propofol or thiopental and succinylcholine, remifentanil as a bolus for rapid sequence induction attenuated cardiovascular responses to endotracheal intubation effectively, but with a higher incidence of hypotension following propofol. (Korean J Anesthesiol 2008; 54: 271∼7)

Effects of changes in loading conditions and heart rate on the myocardial performance index in cats

To evaluate the effect of changes in hemodynamics on the myocardial performance index (MPI) in cats. 6 mixed-breed cats. Cats were anesthetized by administration of thiopental sodium; anesthesia was maintained by administration of isoflurane. Systolic arterial pressure and central venous pressure were measured by use of catheters, and heart rate was controlled by right atrial pacing. Afterload was increased by balloon occlusion of the descending aorta, and preload was increased by IV infusion of lactated Ringer's solution at a rate of 40 mL/kg/h. Echocardiography was performed for each condition. Atrial pacing significantly increased heart rate. The MPI did not change with heart rate. Arterial pressure and MPI increased significantly during aortic occlusion. The IV infusion increased fractional shortening but did not change the MPI. Multiple regression analysis revealed that the MPI was not affected by heart rate, systolic arterial pressure, central venous pressure, fractional shortening, or velocity of the E wave. The MPI can be used to assess cardiac function in healthy cats. The MPI is independent of heart rate and systolic arterial pressure but is sensitive to changes in afterload.

Glutamate binding is altered in hippocampus and cortex of Wistar rats after pilocarpine-induced Status Epilepticus

Several evidences have pointed to biochemical alterations in some brain structures after experimental Status Epilepticus (SE). Thus, the effects of pilocarpine-induced SE on the glutamate binding in the hippocampus and cortex of Wistar rats were evaluated. Groups of animals were submitted to a 3h SE induced by intrahippocampal microinjection of pilocarpine, which was interrupted by the administration of sodium thiopental. Two weeks later the animals were sacrificed and had their cerebral cortices and hippocampi removed in order to perform the binding experiments. The results show that the pilocarpine-induced SE provoked an increase in 2.5-fold in the B(max) values for glutamate binding in the cortex, but not in the hippocampus. Moreover, we observed a 4-fold increase for the Kd values in the hippocampus and a 2-fold increase in the cortex. These findings might indicate that the epileptogenesis involves alterations in the glutamate receptors that are not restricted to the limbic system. Moreover, changes in these receptors are not exclusively of number, but rather involve the affinity for their ligands.

Identification of independent predictors for intravenous thiopental-induced yawning

To explore risk factors for the yawning response induced by the intravenous administration of thiopental during the induction of general anesthesia. We analyzed data from a cohort of 1322 patients who underwent elective surgery under general anesthesia plus intravenous thiopental. The data collected were: (a) the patients' demographic findings (age, sex, height, weight, cigarette smoking, hypertension, and presence of cerebral lesion), and (b) anesthesia-related findings (the kind of preanesthetic medication, i.e., atropine, epidural lidocaine, priming dose of vecuronium, fentanyl, and the dose of intravenous thiopental). An association between an individual variable in the evaluation model and the likelihood of thiopental-induced yawning behavior was characterized by means of the odds ratio. Multiple logistic regression was used to examine the independent contribution of each candidate variable, while controlling for all variables. After the intravenous administration of thiopental, 461 patients exhibited a yawning response. The probability of this response was decreased by the prior use of intravenous fentanyl, by female sex, and by premedication with clonidine, but the probability was unaffected by premedication with hydroxyzine, by the prior use of atropine, or by the presence of hypertension or a cerebral lesion. Thiopental-induced yawning may be suppressed by female sex, prior use of intravenous fentanyl, and premedication with clonidine. These findings may allow insights into the physiologic and pharmacological aspects of yawning in humans, thereby leading to the development methods to prevent thiopental-induced yawning.

Can lethal injection for execution really be “fixed”?

After months of intensive investigation, US District Court Judge Jeremy Fogel recently concluded that California's “implementation of lethal injection is broken”,1 creating “an undue and unnecessary risk that an inmate will suffer pain so extreme that it offends the Eighth Amendment”. Fogel identified “critical deficiencies”, including unreliable screening of members of the execution team, lack of meaningful training and supervision, unreliable record-keeping, improper preparation and administration of the anaesthetic thiopental, and inadequate and poorly designed facilities.

Fentanyl reduces desflurane‐induced airway irritability following thiopental administration in children

Airway irritation is a major drawback of desflurane anesthesia. This study was designed to evaluate the effect of intravenous fentanyl given before thiopental induction on airway irritation caused by a stepwise increase in desflurane in children. Eighty children (2-8 years) were enrolled in a randomized, double-blind study. Forty received saline and 40 received 2 microg/kg of fentanyl intravenously; this was followed by thiopental sodium 5 mg/kg in both groups. Patients were assistant-ventilated with desflurane 1%, which was then increased by 1% every six breaths up to 10%. During this period, cough, secretion, excitation and apnea were graded and the desflurane concentration at which airway irritation symptoms first occurred was recorded. The results were analyzed using Pearson's chi-squared test. The incidence of typical airway irritation events was lower with fentanyl than with saline (cough, 2.5% vs. 42.5%; secretion, 27.5% vs. 82.5%; excitation, 10% vs. 82.5%; apnea, 20% vs. 65%; P < 0.05). The mean expired desflurane concentration at which the first airway irritation symptom occurred was greater with fentanyl than with saline (7.3% vs. 5.5%, P < 0.05). Intravenous fentanyl in children reduces airway complications caused by desflurane.

Deep Hypothermia and the Vascular Response to Thiopental

The vascular response to intravenous thiopental in patients on cardiopulmonary bypass during deep hypothermia was examined. This was a prospective observational study. A university teaching hospital. Twenty-one consecutive adult patients undergoing pulmonary thromboendarterectomy during which deep hypothermic circulatory arrest was instituted. Immediately before circulatory arrest, each patient was administered a 500-mg dose of thiopental intravenously. Arterial blood pressure was monitored and recorded by using a femoral artery catheter and serum electrolytes, acid-base status and arterial hematocrit were determined immediately before the administration of thiopental. Thiopental was associated with a dose-related increase in mean arterial pressure of 32 +/- 11 mmHg (p < 0.0001). Thiopental also resulted in an increase in arterial pH of 0.08 +/- 0.03. A positive correlation between the magnitude of the pH change and the magnitude of the hypertensive response was suggested but did not reach statistical significance (p = 0.066). Of the other factors investigated, only serum-ionized calcium had a statistically significant association with the vascular response in that higher ionized calcium was associated with less hypertensive response (p = 0.014). The administration of thiopental to deeply hypothermic patients during cardiopulmonary bypass is associated with a dramatic increase in mean arterial blood pressure. The mechanism responsible for this vasoconstrictive response may involve thiopental's potentiation of the effects of norepinephrine in the peripheral vasculature.

Influence of metoclopramide on gastroesophageal reflux in anesthetized dogs

To determine the effect of 2 doses of metoclopramide on the incidence of gastroesophageal reflux (GER) in anesthetized dogs. 52 healthy dogs undergoing elective orthopedic surgery. In this prospective clinical study, dogs were evaluated before and during orthopedic surgery. The anesthetic protocol used was standardized to include administration of acepromazine, morphine, thiopental, and isoflurane. Dogs were randomly selected to receive an infusion of saline (0.9% NaCl) solution, a low dose of metoclopramide, or a high dose of metoclopramide before and during anesthesia. Treatment groups were similar with respect to age, body weight, duration of food withholding before surgery, duration of surgery, and dose of thiopental administered. Dogs were positioned in dorsal recumbency during surgery. A sensor-tipped catheter was inserted to measure esophageal pH during anesthesia. We defined GER as a decrease in esophageal pH to < 4 or an increase to > 7.5 that lasted more than 30 seconds. The high dose of metoclopramide (bolus loading dose of 1.0 mg/kg, IV, followed by continuous infusion at a rate of 1.0 mg/kg/h) was associated with a 54% reduction in relative risk of developing GER. The low dose did not significantly affect the incidence of GER. Administration of metoclopramide by bolus and constant rate infusion at doses much higher than commonly used will reduce the incidence but not totally prevent GER in anesthetized dogs undergoing orthopedic surgery.

Comparison of two thiopental infusion rates for the induction of anaesthesia in dogs

ObjectiveTo compare the induction dose requirements of thiopental using two different infusion rates for induction of anaesthesia in dogs. Study designProspective, randomized study. AnimalsFifty, healthy (ASA I or II) client-owned dogs with a mean age of 4.1 years and a mean mass of 20.4 kg undergoing elective surgery. Materials and methodsAnimals were randomly assigned to receive an infusion of 2.5% thiopental at a rate of either 0.1 ml kg−1 minute−1 or 0.4 ml kg−1minute−1, 30–40 minutes after pre-anaesthetic medication with intramuscular acepromazine (0.025 mg kg−1) and pethidine (3.5 mg kg−1). Thiopental administration was controlled by a precision syringe driver. Statistical analyses of the results, using the outcome ‘mg kg−1 required for induction’ (log-transformed) included unpaired t-tests for all categorical data (thiopental infusion rate, breed, sex, obesity, sedation quality) and univariable linear regression for continuous variables (mass, age). All variables were then considered in a multivariable linear regression model. The quality of induction with the two different infusion rates was also assessed. ResultsAfter controlling for quality of sedation, the thiopental induction dose requirement was significantly less (p < 0.001) with the slower infusion rate (median = 7.5 mg kg−1; range 4.9–13.7) compared with the faster infusion rate (median =11.0 mg kg−1; range 6.6–18.0). The quality of sedation also affected the dose required (p = 0.03). The slower infusion rate was associated with a significantly poorer induction quality (p = 0.3). ConclusionsSlow thiopental infusion (0.1 ml kg−1 minute−1) for anaesthesia induction after acepromazine/pethidine pre-anaesthetic medication reduced the induction dose requirement, although the quality of induction was inferior. Clinical relevanceThe induction dose of thiopental was reduced with a slower administration rate and so slow administration is recommended in thiopental-sensitive animals.

Pre- or Postinsult Administration of Lidocaine or Thiopental Attenuates Cell Death in Rat Hippocampal Slice Cultures Caused by Oxygen-Glucose Deprivation

Lidocaine and thiopental improve recovery when administrated during hypoxia and ischemia; however, the effect of pre- or postinsult treatment alone is unknown. We applied either lidocaine or thiopental to hippocampal slice cultures from 20-day-old rats either before or after 10 min of oxygen-glucose deprivation (OGD). Propidium iodide (PI) fluorescence was used as an indicator of neuronal death for 7 days after OGD. OGD-induced neuronal death, in both the Cornus Ammonis 1 (CA1) and the dentate gyrus regions, peaked the first day after ischemia. Preinsult administration of either lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly reduced the damage measured on the first and second days after OGD; these drugs also significantly decreased the summed daily post-OGD PI fluorescence in both regions. Postinsult administration of lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly decreased the PI fluorescence on the first day after OGD; postinsult administration of these drugs also attenuated the summed daily post-OGD PI. These data indicate that the administration of lidocaine or thiopental either before or directly after OGD reduced neuronal damage in this in vitro model of cerebral ischemia. Postischemic administration is frequently the first opportunity for treatment. Lidocaine or thiopental applied either 10 min before or 10 min directly after oxygen-glucose deprivation reduced neuronal cell death in rat hippocampal slice cultures. Postinsult administration is often the first opportunity for treatment after stroke; lidocaine and thiopental reduced damage caused by oxygen-glucose deprivation, an in vitro model of stroke.

Inadequate anaesthesia in lethal injection for execution

Anaesthesia during lethal injection is essential to minimise suffering and to maintain public acceptance of the practice. Lethal injection is usually done by sequential administration of thiopental, pancuronium, and potassium chloride. Protocol information from Texas and Virginia showed that executioners had no anaesthesia training, drugs were administered remotely with no monitoring for anaesthesia, data were not recorded and no peer-review was done. Toxicology reports from Arizona, Georgia, North Carolina, and South Carolina showed that post-mortem concentrations of thiopental in the blood were lower than that required for surgery in 43 of 49 executed inmates (88%); 21 (43%) inmates had concentrations consistent with awareness. Methods of lethal injection anaesthesia are flawed and some inmates might experience awareness and suffering during execution.

The Effects of Transcranial Electrical Stimulation on Anaesthesia and Analgesia in Rats

In this study, we determined the effects of transcranial electrical stimulation (TCES) on the anaesthetic requirements of thiopental and the analgesic requirements of remifentanil, in rats. The experiments were performed on 120 albino male Wistar rats, which were randomly allocated to four groups (n=30). (Thiopental, Thiopental+TCES, Thiopental+Remifentanil, and Thiopental+Remifentanil+TCES). Animals were anaesthetized with thiopental, and 15 min later, remifentanil was injected to rats in the Remifentanil groups. TCES was started in the stimulated groups 20 min after thiopental administration. Rats were stimulated 5 times for this experiment. The times for recovery, herein called Cognition Recovery Time and Motion Recovery Time were measured. Cognition Recovery and Motion Recovery Times were not affected by the stimulation. Analgesia was assessed using the wet tail-flick latency (TFL). In the Thiopental group, the analgesia level returned to control values on the 35th min. In the Thiopental+Remifentanil group, the analgesia level returned to control values on the 50th min. In the Thiopental+ TCES group, the analgesia level reached the peak value on the 65th min. In the Thiopental+Remifentanil+TCES group, the analgesia level reached the peak value on the 35th min and analgesia remained high during the 90 min after cessation of the stimulation. The analgesic potency for the Thiopental+Remifentanil+TCES group was increased by 30-40% when compared with the prior TFL values, 160% when compared with the control group, and 50-75% when compared with Thiopental+TCES group on the 35th min (P<0.001). In conclusion, TCES markedly decreases the anaesthetic and analgesic requirements for thiopental and remifentanil in rats.

Propofol and Thiopental Do Not Interfere with Regional Cerebral Blood Flow Response at Sedative Concentrations

Anesthetics may affect the regional cerebral blood flow (rCBF) response associated with increased brain activity in humans. rCBF was measured as auditory stimulus rate was increased during propofol and thiopental administration. After informed consent, 10 right-handed male volunteer participants (aged 33.5 +/- 10.4 yr, weighing 74.5 +/- 8.4 kg) received thiopental (n = 4) or propofol (n = 6) intravenously at stepwise target concentrations of propofol 1.2 and 2.5-3, or thiopental 4 and 7-9 microg/ml, representing sedative and hypnotic drug concentrations. The latter made volunteers unresponsive to voice or mild stimulation. Quantitative positron emission tomographic brain images were obtained at 0, 20, and 40 auditory words per minute at each drug concentration. Using SPM99 analysis, 10-mm spherical regions of interest were identified by peak covariation of word rate with rCBF across all conditions and drug concentrations. Individual mean rCBF responses in these and primary auditory cortex (Heschl's gyri) were obtained. Significant increases in rCBF with auditory word rate occurred in temporal lobes bilaterally at baseline (significance, T = 4.95). There was no change in this response during sedation (T = 5.60). During unresponsiveness seven of 10 participants had a diminished response in the left temporal lobe (T = 3.18). Global CBF, corrected for changes in PCO2 (3% .mmHg PCO2), was reduced 15% by sedation and 27% during unresponsiveness. The presence of propofol or thiopental does not affect the rCBF response to increasing stimulus rate during consciousness. Thus, changes in rCBF activation patterns with sedative concentrations of these drugs represent effects on brain activity itself. The neuroanatomical targets of drug effect on memory and attention may be revealed by changes in rCBF patterns associated with these cognitive activities.

The Hemodynamic Effects of Ephedrine on the Onset Time of Rocuronium in Pigs

Several studies have found a correlation between the onset time of muscle relaxants, cardiac index, and muscle blood flow. Ephedrine increases these hemodynamic variables and shortens onset time of rocuronium in humans. Our aim in this animal study was to determine the effect of ephedrine on the onset time of rocuronium, cardiac index, and muscle blood flow after administration of thiopental. At predefined measuring points, mean arterial blood pressure and cardiac index were measured invasively and onset time was determined mechanomyographically. Twenty-four pigs were randomly assigned to three groups. Group I received etomidate and subsequently rocuronium (2 x 95% effective dose). Instead of etomidate, Group II received thiopental. In Group III, ephedrine 100 mug/kg was given before thiopental; additionally, muscle blood flow was measured (fluorescent microspheres). Although there were differences in hemodynamics between Groups I and II, this was not reflected in different onset times of rocuronium. In Group III, ephedrine compensated the thiopental-induced decrease of mean arterial blood pressure, cardiac index, and muscle blood flow, but no significant shortening of onset time (Group I: 74 +/- 21 s; Group II: 71 +/- 24; Group III: 69 +/- 22 s) was found. Our results demonstrated that ephedrine-related increases in cardiac index and blood flow did not shorten onset time of rocuronium in healthy pigs.

Thiopental and Nuclear Factor κB: Some Questions

In Reply:—We appreciate the points raised by Drs. Haeberle and Kiefer and offer the following responses.First, Drs. Haeberle and Kiefer state that the concentration of thiopental used in our study would be “much higher than plasma concentrations noted during clinical practice or in other models presenting inhibitory effects of thiopental on IFN-γ production.” However, in addition to the study cited by them, much higher plasma concentrations of thiopental have been reported to occur in patients during long-term administration of thiopental for the treatment of intracranial hypertension—concentrations that are comparable to those used in the present study. 1Moreover, as already pointed out in detail within the article, tissue concentrations of thiopental in organs that play a central role in the development of nosocomial infections may be even 3 to 10 times higher than the plasma concentrations. 2Second, Drs. Haeberle and Kiefer note, “inhibition of NF-κB activation may not reflect general immune suppression.” However, we neither conclude nor state this. In our article, we wrote that our results “may provide a molecular mechanism for some of the immunosuppressing effects associated with thiopental treatment.” Nuclear factor κB (NF-κB) plays a crucial role in the control of the activation, proliferation, and differentiation of neutrophils, macrophages, and T and B lymphocytes. 3Therefore, the reduced function of immune cells “would be consistent with an inhibition of NF-κB by thiopental.”Third, the authors suggest, “it would be helpful to give some more information beyond that provided by the authors in their statement that ‘other transcription factors may be involved.’” In view of the large amount of data included within our article, communicating additional results about the effect of barbiturates on other transcription factors was far beyond the scope of the paper. However, we do have evidence that thiopental may also inhibit the nuclear factor of activated T cells in human T lymphocytes. These findings were presented at the 10th Meeting of the European Society of Anesthesiologists (2002) in Nice, France. 4Fourth, Drs. Haeberle and Kiefer state, “cytokine expression is regulated in a cell-type and stimuli-specific manner.” We fully agree with this statement. To briefly recapitulate, we examined the effects of anesthetics in T lymphocytes on the tumor necrosis factor–dependent activation of NF-κB, as well as the cytokine expression induced by phorbol-12-myristate-13-acetate (125 ng/ml) in mononuclear cells. Therefore, the cited study 5is not comparable because cytokine expression in mononuclear cells was induced by lipopolysaccharide. Likewise, in this study, the effects of thiopental were investigated at concentrations of less than 200 μg/ml, whereas we used 400-μg/ml thiopental. At this lower concentration, Takaono et al. 5did not note a significant effect; however, a trend toward inhibition could be observed.Later in their letter, Haeberle and Kiefer state that “ketamine decreases cytokine production…and suppresses endotoxin-induced NF-κB activation.” These studies used whole blood, 6a human glioma cell line, or extracts of mice brain. 7Kawasaki et al. 6observed the inhibition of tumor necrosis factor–induced interleukin 6 and interleukin 8 production by ketamine at concentrations higher than 100 μg/ml. In contrast, we used 60 μg/ml or less ketamine in our study. Sakai et al. , 7while observing an inhibition of lipopolysaccharide-induced NF-κB activation at 30 μg/ml, used a glioma cell line and brain extracts in these experiments. Therefore, we believe that the comparability of these studies with ours is impaired because of the different experimental settings and the fact that cytokine expression is, indeed, “regulated in a cell-type and stimuli-specific manner.”

Cortical activity assessed by Narcotrend® in relation to haemodynamic responses to tracheal intubation at different stages of cortical suppression and reflex control

Background and objective: Many anaesthesiologists still interpret haemodynamic responses as signs of insufficient cortical suppression. The aim was to illustrate how haemodynamics may only poorly reflect the level of cortical suppression and that electroencephalographic monitoring could indicate different relationships between cortical effects and haemodynamics. Methods: Anaesthesia was induced with thiopental (7 mg kg−1), and fentanyl (2 μg kg−1) with succinylcholine (1.5 mg kg−1) for neuromuscular blockade in the 11 patients of Group 1. In Group 2 (n = 15), thiopental (7 mg kg−1) and succinylcholine (1.5 mg kg−1) were given. In Group 3, the patients (n = 13) received thiopental (7 mg kg−1), fentanyl (2 μg kg−1) and cisatracurium (0.1 mg kg−1), and they were intubated 3 min later than the patients in Groups 1 and 2. We determined conventional electroencephalographic (EEG) variables and classified 14 EEG stages in real-time ranging from A (= 1), indicating full wakefulness, to F1 (= 14), at profound cortical suppression. Results: All groups had profound cortical suppression 45 s after thiopental administration, which rapidly decreased (EEG stage, 11 (6-13) versus 7 (2-13) at 4 min, P < 0.0001). Decreasing EEG stages were associated with increasing SEF 95, relative α and β power and decreasing relative δ power. During tracheal intubation, profound cortical suppression remained unchanged in Groups 1 and 2. In Group 3, cortical suppression had decreased before laryngoscopy (P < 0.005). In Group 2, 11 patients had heart rate responses to tracheal intubation, whereas only two responded in Group 1 (P = 0.015) and three in Group 3 (P = 0.02). Thirteen patients in Group 2 had arterial pressure responses, and five in Group 1 (P = 0.038). Circulatory responses did not differ between Groups 1 and 3. Conclusions: Electroencephalographic monitoring was suitable to indicate in real-time that haemodynamics only poorly reflect rapidly changing levels of cortical suppression, and how haemodynamics and cortical activity depend on the applied combination of hypnotic and analgesic drugs during anaesthesia induction with thiopental.

Comparison of Sevoflurane with Enflurane Anesthesia for Cesarean Section

Background: Sevoflurane has a low blood-gas partition coefficient resulting in rapid induction and recovery. We compared the effects of sevoflurane with those of enflurane anesthesia on parturients and neonates during and after elective cesarean section. M ethods: Ninety-six parturients were divided into two groups: E (enflur ane n = 47 and S (sevoflurane n = 49. After endotracheal intubation with intravenous administration of thiopental 4 mg/kg and succinylcholine 1.5 mg/kg anesthesia was maintained with 50% nitrous oxide in oxygen and enflurane 1 vol% or sevoflurane 1 vol%. Maternal hemodynamic parameters blood loss and recovery were monitored. Neonatal outcome was evaluated by Apgar scores umblical artery blood gas analysis and acid-base status. Results: Recovery times were faster with sevoflurane anesthesia (P ＜ 0.05. All patients in two groups developed transient hypertension and tachycardia after intubation which returned to baseline in approximately 5 minutes. Maternal blood loss did not differ significantly between the two groups and one patient in S group developed postoperative recall. Neonatal outcome was equally good in the two groups. Conclusions: Parturients anesthetized with sevoflurane for cesarean section recovered more rapidly compared with enflurane without any differences in hemodynamic parameters and neonatal outcome. (Korean J Anesthesiol 2003; 44: 770～776

Transmission through the dorsal spinocerebellar and spinoreticular tracts: wakefulness versus thiopental anesthesia.

Most of what is known regarding the actions of injectable barbiturate anesthetics on the activity of lumbar sensory neurons arises from experiments performed in acute animal preparations that are exposed to invasive surgery and neural depression caused by coadministered inhalational anesthetics. Other parameters such as cortical synchronization and motor ouflow are typically not monitored, and, therefore, anesthetic actions on multiple cellular systems have not been quantitatively compared. The activities of antidromically identified dorsal spinocerebellar and spinoreticular tract neurons, neck motoneurons, and cortical neurons were monitored extracellularly before, during, and following recovery from the anesthetic state induced by thiopental in intact, chronically instrumented animal preparations. Intravenous administration of 15 mg/kg, but not 5 mg/kg, of thiopental to awake cats induced general anesthesia that was characterized by 5-10 min of cortical synchronization, reflected as large-amplitude slow-wave events and neck muscle atonia. However, even though the animal behaviorally began to reemerge from the anesthetic state after this 5-10-min period, neck muscle (neck motoneuron) activity recovered more slowly and remained significantly suppressed for up to 23 min after thiopental administration. The spontaneous activity of both dorsal spinocerebellar and spinoreticular tract neurons was maximally suppressed 5 min after administration but remained significantly attenuated for up to 17 min after injection. Peripheral nerve and glutamate-evoked responses of dorsal spinocerebellar and spinoreticular tract neurons were particularly sensitive to thiopental administration and remained suppressed for up to 20 min after injection. These results demonstrate that thiopental administration is associated with a prolonged blockade of motoneuron output and sensory transmission through the dorsal spinocerebellar and spinoreticular tracts that exceeds the duration of general anesthesia. Further, the blockade of glutamate-evoked neuronal responses indicates that these effects are due, in part, to a local action of the drug in the spinal cord. The authors suggest that this combination of lumbar sensory and motoneuron inhibition underlies the prolonged impairment of reflex coordination observed when thiopental is used clinically.

Comparison of Cerebral Blood Flow Velocities by Transcranial Doppler during Anesthetic Induction: Rocuronium and Succinylcholine

Background: In intravenous administration of a depolarizing neuromuscular blocker, succinylcholine is reported to produce activation of the electroencephalogram and increase cerebral blood flow and intracranial pressure. In this point, rocuronium was recently introduced as a non-depolarizing relaxant, and recommended as a safe alternative to succinylcholine. The purpose of this study was to evaluate the effects of rocuronium and succinylcholine on cerebral blood flow velocities during anesthetic induction. Methods: Forty patients were randomly assigned into two groups. Group 1 was administrated rocuronium 0.6 mg/kg and group 2 was administrated succinylcholine 1 mg/kg for tracheal intubation after each group had intravenous administration of thiopental 5 mg/kg. The author observed changes of mean arterial pressure, arterial carbon dioxide tension, and middle cerebral arterial blood flow velocities at 5 times: before induction (control), 30 sec after thiopental administration, 30 sec, 60 sec and 90 sec after muscle relaxant administration. Results: Mean arterial pressure decreased more at 30 sec after thiopental administration compared with the control (P

Respiratory reflexes in spontaneously breathing anesthetized dogs in response to nasal administration of sevoflurane, isoflurane, or halothane.

To characterize respiratory reflexes elicited by nasal administration of sevoflurane (Sevo), isoflurane (Iso), or halothane (Hal) in anesthetized dogs. 8 healthy Beagles. A permanent tracheostomy was created in each dog. Two to 3 weeks later, dogs were anesthetized by IV administration of thiopental and alpha-chloralose. Nasal passages were isolated such that inhalant anesthetics could be administered to the nasal passages while the dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of each anesthetic at 1.2 and 2.4 times the minimum alveolar concentration (MAC) and the full vaporizer setting (5%) were recorded. Reflexes in response to administration of 5% of each anesthetic also were recorded following administration of lidocaine to the nasal passages. Nasal administration of Sevo, Iso, and Hal induced an immediate ventilatory response characterized by a dose-dependent increase in expiratory time and a resulting decrease in expired volume per unit of time. All anesthetics had a significant effect, but for Sevo, the changes were smaller in magnitude. Responses to administration of each anesthetic were attenuated by administration of lidocaine to the nasal passages. Nasal administration of Sevo at concentrations generally used for mask induction of anesthesia induced milder reflex inhibition of breathing, presumably via afferent neurons in the nasal passages, than that of Iso or Hal. Respiratory reflexes attributable to stimulation of the nasal passages may contribute to speed of onset and could promote a smoother induction with Sevo, compared with Iso or Hal.