bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spinal Action of Ketorolac, S(+)- and R(-)-ibuprofen on Non-noxious Activation of the Cathechol Oxidation in the Rat Locus Coeruleus
Authors: Hall Sean R. , Milne Brian , Loomis Christopher 
Published: November 2003

Background
Blockade of spinal glycine receptors with intrathecal strychnine produces an allodynia-like state in the anesthetized rat. Innocuous hair deflection in the presence of intrathecal strychnine induces a nociceptive-like activation of catechol oxidation in the locus coeruleus and enhances cardiovascular responses. Because prostaglandins play a central role in augmenting pain, this study evaluated the effect of intrathecal nonsteroidal antiinflammatory drugs in strychnine-induced allodynia.

Methods
In urethane-anesthetized rats, changes in catechol oxidation in the locus coeruleus, measured using in vivo voltammetry, and cardiovascular parameters evoked by hair deflection of caudal dermatomes were determined after strychnine (40 microg) or saline were administered intrathecally. Subsequently, the effects of 30 microg ketorolac, 10 microg S(+)-ibuprofen, and 10 microg R(-)-ibuprofen administered intrathecally were evaluated.

Results
After strychnine was administered intrathecally, hair deflection evoked an increase in the locus coeruleus catechol oxidation (peak, 149.7+/-7.2% of baseline) and mean arterial blood pressure (peak, 127.5+/-3.8% of baseline). These responses were not observed after saline was administered intrathecally. All hair deflection-evoked, strychnine-dependent peak responses were attenuated significantly with intrathecally administered ketorolac and S(+)-ibuprofen but not with R(-)-ibuprofen.

Conclusions
Locus coeruleus catechol oxidation is a sensitive biochemical index of strychnine-induced allodynia and is correlated temporally with the cardiovascular responses evoked by hair deflection during spinal glycinergic inhibition. The ability of intrathecally administered ketorolac and S(+)-ibuprofen, but not R(-)-ibuprofen, to suppress the locus coeruleus catechol oxidation and cardiovascular peak responses evoked during strychnine-induced allodynia provide evidence that central prostaglandins play an important role in the abnormal sensory processing of strychnine-induced allodynia.
Increasing Isoflurane from 0.9 to 1.1 Minimum Alveolar Concentration Minimally Affects Dorsal Horn Cell Responses to Noxious Stimulation
Authors: Antognini Joseph F. , Carstens Earl 
Published: November 2003

Background
The spinal cord appears to be the site at which isoflurane suppresses movement that occurs in response to a noxious stimulus. In an attempt to localize its site of suppressant action, the authors determined the effect of isoflurane on dorsal horn neuronal responses to supramaximal noxious stimulation at end-tidal concentrations that just permitted and just prevented movement.

Methods
Rats (n = 14) were anesthetized with isoflurane, and after lumbar laminectomy, the minimum alveolar concentration (MAC) for each rat was determined using a supramaximal mechanical stimulus. In these same rats, after extracellular microelectrode placement in the lumbar spinal cord, dorsal horn neuronal responses to the supramaximal stimulus were determined at the concentrations of isoflurane that bracketed each rat's MAC (0.1% higher and lower than MAC). The MAC of isoflurane was then re-determined.

Results
Dorsal horn neuronal response was 1,757+/-892 impulses/min at 0.9 MAC and 1,508+/-988 impulses/min at 1.1 MAC, a 14% decrease (P < 0.05). Cell responses varied, with some cells increasing their response at the higher concentration of isoflurane. The MAC of isoflurane was 1.38+/-0.2% before and 1.34+/-0.2% after determination of dorsal horn neuronal responses.

Conclusions
Isoflurane, at concentrations that bracket MAC, has a variable and minimal depressant effect on dorsal horn cell responses to noxious mechanical stimulation. These data suggest that the major action of isoflurane to suppress movement evoked by a noxious stimulus might occur primarily at a site other than the dorsal horn.
Effect of Propofol on Arachidonate Cascade by Vasopressin in Aortic Smooth Muscle Cells
Authors: Tanabe Kumiko , Kozawa Osamu , Matsuno Hiroyuki , Niwa Masayuki , Dohi Shuji , Uematsu Toshihiko 
Published: November 2003

Background
The mechanisms underlying the vascular effects of propofol are not fully understood. Vasopressin, a potent vasoactive peptide, stimulates the arachidonate cascade and the synthesis of prostacyclin (PGI2; the main metabolite of the cascade in vascular smooth muscle cells). Arachidonic acid (AA) release by phospholipases is the rate-limiting step in the cascade. We investigated the mechanisms underlying vasopressin-induced AA release and the effect of propofol on PGI2 synthesis in a rat aortic smooth muscle cell line: A10 cells.

Methods
In cultured A10 cells pretreated with propofol, the stimulation by vasopressin of AA release and PGI2 synthesis was evaluated by measuring [3H]AA and 6-keto PGF1alpha, respectively, in the culture medium. The effects of propofol on vasopressin-induced activation of phosphoinositide-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D were evaluated by measuring inositol phosphate formation and choline formation, respectively.

Results
A phospholipase C inhibitor and a phosphatidic acid phosphohydrolase inhibitor both attenuated vasopressin-induced AA release and PGI2 synthesis, as did a phospholipase A2 inhibitor. Propofol inhibited vasopressin-induced activation of phosphoinositide-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D, but this effect of propofol was significant only at supraclinical concentration (0.1 mM). Propofol reduced vasopressin-induced PGI2 synthesis. The inhibitory effect was observed at concentrations (10 microM-0.1 mM) higher than those used clinically.

Conclusions
Propofol suppresses the arachidonate cascade caused by vasopressin at least partly by inhibiting phosphoinositide-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D, resulting in the inhibition of PGI2 synthesis. Propofol-mediated inhibition of vasopressin-stimulated synthesis of PGI2 may reduce the vasorelaxation by propofol.
A Cost-construction Model to Assess the Total Cost of an Anesthesiology Residency Program
Authors: Franzini Luisa , Berry James M. 
Published: November 2003

Background
Although the total costs of graduate medical education are difficult to quantify, this information may be of great importance for health policy and planning over the next decade. This study describes the total costs associated with the residency program at the University of Texas--Houston Department of Anesthesiology during the 1996-1997 academic year.

Methods
The authors used cost-construction methodology, which computes the cost of teaching from information on program description, resident enrollment, faculty and resident salaries and benefits, and overhead. Surveys of faculty and residents were conducted to determine the time spent in teaching activities; access to institutional and departmental financial records was obtained to quantify associated costs. The model was then developed and examined for a range of assumptions concerning resident productivity, replacement costs, and the cost allocation of activities jointly producing clinical care and education.

Results
The cost of resident training (cost of didactic teaching, direct clinical supervision, teaching-related preparation and administration, plus the support of the teaching program) was estimated at $75,070 per resident per year. This cost was less than the estimated replacement value of the teaching and clinical services provided by residents, $103,436 per resident per year. Sensitivity analysis, with different assumptions regarding resident replacement cost and reimbursement rates, varied the cost estimates but generally identified the anesthesiology residency program as a financial asset.

Conclusions
In most scenarios, the value of the teaching and clinical services provided by residents exceeded the cost of the resources used in the educational program.
Antiemetic Prophylaxis Does Not Improve Outcomes after Outpatient Surgery When Compared to Symptomatic Treatment
Authors: Scuderi Phillip E. , James Robert L. , Harris Lynne , Mims Grover R. 
Published: November 2003

Background
Although prophylactic administration of antiemetics reduces the incidence of postoperative nausea, vomiting, or both (PONV), there is little evidence to suggest this improves patient outcomes. The authors hypothesized that early symptomatic treatment of PONV will result in outcomes, including time to discharge, unanticipated admission, patient satisfaction, and time to return to normal daily activities, that are similar to those achieved with routine prophylaxis.

Methods
Men and women (n = 575) scheduled for outpatient surgery during general anesthesia were randomized to receive either 4 mg intravenous ondansetron or placebo before operation and either 1 mg intravenous ondansetron or placebo if postoperative symptomatic treatment of PONV was necessary. Patients were stratified into subgroups by risk factors for PONV.

Results
No differences occurred in the time to discharge, rate of unanticipated admission, or time to return to normal activity between the prophylaxis and treatment groups. The reported level of satisfaction with control of PONV was 93% in the treatment arm and 97% in the prophylaxis arm, which fall within the limits defined a priori as clinically equivalent. Female patients with a history of motion sickness or PONV who were undergoing highly emetogenic procedures had a higher reported level of satisfaction with prophylaxis than with treatment (100% vs. 90%, P = 0.043); however, the level of satisfaction with the overall outpatient surgical experience was not different.

Conclusion
Although PONV is unpleasant, the data indicate little difference in outcomes when routine prophylactic medications are administered versus simply treating PONV should symptoms occur.
Airway Obstruction and Perioperative Complications in Smokers Undergoing Abdominal Surgery
Authors: Warner David O. , Warner Mark A. , Offord Kenneth P. , Schroeder Darrell R. , Maxson Pamela , Scanlon Paul D. 
Published: November 2003

Background
The goal of this study was to determine whether airway obstruction determined by preoperative spirometry predicts perioperative complications in smokers undergoing abdominal surgery whose treatment is managed according to current clinical practice.

Methods
A pulmonary function database identified patients undergoing abdominal surgery who met the following criteria for airway obstruction (n = 135): a forced expiratory volume less than 40% of predicted normal value, a forced expiratory volume:forced vital capacity ratio less than the lower limit of predicted normal, a smoking history of more than 20 pack-years, and an age older than 35 yr. A group of patients without airway obstruction (n = 135) was matched for gender, surgical site (upper vs. lower abdominal), smoking history, and age. Medical records were reviewed by an abstractor to identify perioperative complications that occurred within 30 days after surgery.

Results
The forced expiratory volume values were 0.9+/-0.21 (mean +/- SD) and 2.9+/-0.61 in patients with and without airway obstruction, respectively. When analyzed by conditional logistic regression using the 1:1 matched-pairs feature, including age, pack-year smoking history, site of incision, and current smoking status as covariates, in patients with airway obstruction bronchospasm was more likely to develop (odds ratio, 6.9 [95% confidence interval, 1.2 to 38.4]) but the patients were not more likely to need prolonged endotracheal intubation (odds ratio, 1.1 [95% confidence interval, 0.4 to 3.2]). They were also no more likely to need prolonged intensive care admission or readmission. The frequency of other complications was less than 5%.

Conclusion
When other factors were considered, preoperative airway obstruction predicted the occurrence of bronchospasm, but not prolonged endotracheal intubation, in smokers undergoing abdominal surgery who are treated according to current clinical practices.
Effect of Oxygen Treatment on Heart Rate after Abdominal Surgery
Authors: Rosenberg-Adamsen Susan , Lie Claus , Bernhard Anne , Kehlet Henrik , Rosenberg Jacob 
Published: November 2003

Background
Cardiac complications are common during the postoperative period and may be associated with hypoxemia and tachycardia. Preliminary studies in high-risk patients after operation have shown a possible beneficial effect of oxygen therapy on arterial oxygen saturation and heart rate.

Methods
The authors studied the effect of oxygen therapy on arterial oxygen saturation and heart rate in 100 consecutive unselected patients randomly and double blindly allocated to receive air or oxygen therapy between the first and fourth day after major abdominal surgery.

Results
The median arterial oxygen saturation rate increased significantly from 96% to 99% (P < 0.0001) and the heart rate decreased significantly from 85 beats/min to 81 beats/min (P < 0.0001) during oxygen supplementation compared with air administered by a binasal catheter. The greatest decrease in heart rate occurred in patients with the lowest oxygen saturation or the highest heart rate values before oxygen supplementation. Overall, 73% of this unselected group of patients responded with decreased heart rate during supplemental oxygen therapy. No significant differences in changes in heart rate after oxygen supplementation were found between patients with or without an epidural catheter or between the postoperative day studied.

Conclusion
Postoperative oxygen therapy increased arterial oxygen saturation and decreased heart rate after uncomplicated abdominal surgery in a consecutive unselected group of patients who received routine postoperative care.
Endotracheal Intubation, but Not Laryngeal Mask Airway Insertion, Produces Reversible Bronchoconstriction
Authors: Kim Eun S. , Bishop Michael J. 
Published: November 2003

Background
Tracheal intubation frequently results in an increase in respiratory system resistance that can be reversed by inhaled bronchodilators. The authors hypothesized that insertion of a laryngeal mask airway would be less likely to result in reversible bronchoconstriction than would insertion of an endotracheal tube.

Methods
Fifty-two (45 men, 7 women) patients were randomized to receive a 7.5-mm (women) or 8-mm (men) endotracheal tube or a No. 4 (women) or No. 5 (men) laryngeal mask airway. Anesthesia was induced with 2 microg/kg fentanyl and 5 mg/kg thiopental, and airway placement was facilitated with 1 mg/kg succinylcholine. When a seal to more than 20 cm water was verified, respiratory system resistance was measured immediately after airway placement. Inhalation anesthesia was begun with isoflurane to achieve an end-tidal concentration of 1% for 10 min. Respiratory system resistance was measured again during identical conditions.

Results
Among patients receiving laryngeal mask airways, the initial respiratory system resistance was significantly less than among patients with endotracheal tubes (9.2+/-3.3 cm water x 1(-1) x s(-1) [mean +/- SD] compared with 13.4+/-9.6 cm water x 1(-1) x s(-1); P < 0.05). After 10 min of isoflurane, the resistance decreased to 8.6+/-3.6 cm water x 1(-1) x s(-1) in the endotracheal tube group but remained unchanged at 9.1+/-3.3 cm water x 1(-1) x s(-1) in the laryngeal mask airway group. The decrease in respiratory system resistance in the endotracheal tube group of 4.7+/-7 cm water x 1(-1) x s(-1) was highly significant compared with the lack of change in the laryngeal mask airway group (P < 0.01).

Conclusions
Resistance decreased rapidly only in patients with endotracheal tubes after they received isoflurane, a potent bronchodilator, suggesting that reversible bronchoconstriction was present in patients with endotracheal tubes but not in those with laryngeal mask airways. A laryngeal mask airway is a better choice of airway to minimize airway reaction.
The Effect of Fentanyl on Sevoflurane Requirements for Somatic and Sympathetic Responses to Surgical Incision
Authors: Katoh Takasumi , Kobayashi Syunji , Suzuki Akira , Iwamoto Tatsuaki , Bito Hiromichi , Ikeda Kazuyuki 
Published: November 2003

Background
Fentanyl produces a reduction in the minimum alveolar concentration (MAC) of isoflurane and desflurane needed to blockade adrenergic response (BAR) to surgical incision in 50% of patients (MAC-BAR). MAC-BAR of sevoflurane and the reduction in MAC-BAR of sevoflurane by fentanyl have not been described previously. The purpose of this study was to determine the MAC and MAC-BAR reduction of sevoflurane by fentanyl with and without nitrous oxide (N2O).

Methods
Two hundred twenty-six patients were randomly assigned to one of two groups: a sevoflurane group and a sevoflurane/N2O group. Patients in each group were randomly assigned to one of five different fentanyl concentration subgroups. Patients were anesthetized with sevoflurane and fentanyl in the sevoflurane group and with sevoflurane, fentanyl, and N2O (66 vol%) in the sevoflurane/N2O group. Somatic and sympathetic responses to surgical incision were observed for MAC and MAC-BAR assessment at predetermined concentrations of sevoflurane.

Results
Fentanyl produced an initial steep reduction in the MAC and MAC-BAR of sevoflurane, with 3 ng/ml resulting in a 61% reduction in MAC and an 83% reduction in MAC-BAR. A ceiling effect was observed for MAC and MAC-BAR, with 6 ng/ml fentanyl providing only an additional 13% and 9% reduction in MAC and MAC-BAR, respectively. In the presence of 66 vol% N2O, MAC and MAC-BAR of sevoflurane were reduced with increasing concentrations of fentanyL A ceiling effect was not observed for reduction in MAC and MAC-BAR in the presence of N2O.

Conclusions
MAC and MAC-BAR decreased similarly with increasing concentrations of fentanyl in plasma, showing an initial steep reduction followed by a ceiling effect. In the presence of N2O, MAC and MAC-BAR decreased similarly but did not exhibit a ceiling effect.
Dexmedetomidine Failed to Block the Acute Hyperdynamic Response to Electroconvulsive Therapy
Authors: Fu Wen , White Paul F. 
Published: November 2003

Background
Orally administered clonidine (0.2-0.3 mg) has been reported to decrease the acute hypertensive response to electroconvulsive therapy (ECT) without prolonging early recovery. This preliminary study was designed to evaluate the acute hemodynamic effects of the investigational alpha2-adrenergic agonist, dexmedetomidine, in patients undergoing a series of ECT treatments.

Methods
Six patients undergoing a series of three to six consecutive ECT treatments were studied according to a randomized, double-blind, placebo-controlled protocol All patients received either saline or dexmedetomidine, 0.5 or 1.0 microg/kg intravenously, 10-30 min before induction of anesthesia for ECT using a standardized anesthesia protocol. In addition to assessing the cardiovascular variables, the duration of seizure activity, degree of sedation, and time to discharge from the Phase I recovery unit were assessed.

Results
Although dexmedetomidine produced dose-related increases in the level of sedation before the ECT procedure, it failed to decrease the peak blood pressure and heart rate responses after the ECT treatment. The 0.5 and 1.0 microg/kg doses of dexmedetomidine prolonged the times to orientation and to discharge from the Phase I unit.

Conclusions
The results of this pilot study suggest that dexmedetomidine (0.5-1.0 microg/kg given intravenously) is not beneficial in controlling the acute hyperdynamic response after ECT.
Ondansetron Is Effective to Treat Spinal or Epidural Morphine-induced Pruritus
Authors: Borgeat Alain , Stirnemann Hans-Ruedi 
Published: November 2003

Background
Spinally and epidurally administered morphine is frequently associated with pruritus. Isolated case reports indicate that ondansetron may be effective in this context. This study aims to investigate the effectiveness of ondansetron to treat this side effect.

Methods
In a prospective, randomized, double-blind, placebo-controlled study, 100 patients with pruritus (> 4 on a visual analog scale, on which 0 represents no pruritus and 10 represents worst pruritus imaginable) after spinal or epidural administration of morphine, received either 8 mg ondansetron intravenously (ondansetron group) in 100 ml NaCl 0.9% or vehicle (placebo group). A decrease of more than 4 points on the visual analog scale 60 min after treatment was considered a success. Changes in levels of pain and sedation, hemodynamic values, and other side effects were checked regularly. The presence or absence of pruritus was assessed for the last time 24 h later.

Results
The two groups were similar for demographic characteristics, the route of administration of morphine, and severity of pruritus at the beginning of the study. The ondansetron group showed a success rate of 70% versus 30% for the placebo group (P > 0.05). Among the successfully treated patients, three (9%) in the ondansetron group and six (40%) in the placebo group reported the recurrence of pruritus (P < 0.05). Among the successfully treated patients, none complained of residual pruritus 24 h later. No changes in pain or sedation levels were noted. Hemodynamic values remained stable, hemoglobin oxygen saturation did not decrease, and no other side effects were observed.

Conclusion
The administration of 8 mg ondansetron intravenously is an effective treatment for spinally or epidurally administered morphine-induced pruritus. In this clinical condition the treatment is safe and well tolerated.
Dose-Response Relationship of Intrathecal Morphine for Postcesarean Analgesia
Authors: Palmer Craig M. , Emerson Scott , Volgoropolous Dimitri , Alves Diane 
Published: November 2003

Background
This series investigated the quality of analgesia and the incidence and severity of side effects of intrathecal morphine for post-cesarean analgesia administered over a dose range of 0.0-0.5 mg.

Methods
ONE hundred eight term parturients undergoing cesarean delivery at term and given spinal anesthesia were randomized to receive a single dose of intrathecal morphine (0.0, 0.025, 0.05, 0.075, 0.1, 0.2, 0.3, 0.4, or 0.5 mg). A patient-controlled analgesia (PCA) device provided free access to additional analgesics. PCA morphine use, incidence and severity of side effects, and need for treatment interventions were recorded for 24 h. Data were analyzed with analysis of variance and linear regression analysis for trends among groups.

Results
Patient-controlled analgesia use differed significantly between groups; PCA use was higher in the control group than in groups receiving 0.075, 0.1, 0.3, 0.4, or 0.5 mg. Twenty-four-hour PCA morphine use was 45.7 mg lower (95% CI, 4.8-86.6 mg lower) in the 0.075-mg group than the control group. There was no difference in PCA morphine use between the 0.075- and 0.5-mg groups (95% CI, 36.8 mg lower to 45.0 mg higher); despite a fivefold increase in intrathecal morphine dose, PCA morphine use remained constant. There was no difference between control and treatment groups or among treatment groups with respect to nausea and vomiting. Pruritus and the need for treatment interventions increased in direct proportion to the dose of intrathecal morphine (linear regression, P = 0.001 and P = 0.0002, respectively).

Conclusions
These data indicate there is little justification for use of more than 0.1 mg for post-cesarean analgesia. For optimal analgesia, augmentation [corrected] of intrathecal morphine with systemic opioids may be necessary.