bluuebunny/crossref_metadata_2025_split huggingface dataset:
Equianalgesic Doses of Subcutaneous but Not Intrathecal Morphine Alter Phenotypic Expression of Cell Surface Markers and Mitogen-induced Proliferation in Rat Lymphocytes
Authors: Hamra Jena G. , Yaksh Tony L. 
Published: November 2003

Background
Surgical trauma and opioids are linked with suppression of immune function. Evidence suggests a probable supraspinal action of morphine in altering immune function, although the role of spinal systems have not been evaluated. Therefore, this study compared the effect of equianalgesic doses of subcutaneous and intrathecal morphine on lymphocyte proliferative responses and phenotypic expression of lymphocyte cell surface markers in rats.

Methods
Equianalgesic doses of subcutaneous (10 mg/kg) or intrathecal (30 micrograms, by a chronic intrathecal catheter) morphine were given twice for 5 h (time 0 and 2.5 h). Immediately after the 5-h period or 24 h after the initial injection, spleens were harvested and lymphocytes isolated. Mitogen-induced (phytohemagglutinin, concanavalin A, pokeweed, lipopolysaccharide) lymphocyte proliferation and monoclonal antibody labeling of cell surface markers (T cell, B cell, CD4+, CD8+) were then performed.

Results
Subcutaneous morphine acutely suppressed lymphocyte proliferation to the mitogens phytohemagglutinin, pokeweed, and concanavalin A by 37%, 21%, and 20% respectively; however, proliferative responses returned to baseline within 24 h. Morphine treatment did not alter the response to lipopolysaccharide. The number of splenic lymphocytes also decreased, whereas the percentage of lymphocytes expressing the CD4+ marker (T helper/inducer cells) modestly increased. Intrathecal morphine did not alter lymphocyte proliferative responses, nor did it change phenotypic expression of cell surface markers.

Conclusions
Subcutaneous morphine inhibited lymphocyte proliferation, decreased splenic lymphocyte number, and altered phenotypic expression of cell surface markers, whereas equianalgesic doses of intrathecal morphine did not. Although these results suggest that spinal opioids may have theoretical benefits for the analgesic management of immunocompromised patients, further studies are clearly indicated.
Effect of Cranial Surgery and Brain Tumor Size on Emergence from Anesthesia
Authors: Schubert Armin , Mascha Edward J. , Bloomfield Eric L. , DeBoer Glenn E. , Gupta Manjula K. , Ebrahim Zeyd Y. 
Published: November 2003

Background
Knowing which neurosurgical patients are at risk for delayed awakening may lead to better utilization of intensive care resources and avoid the risk and cost of pharmacologic reversal and diagnostic tests.

Methods
The authors compared anesthetic emergence from complex spinal surgery (spine; n = 47) with that from craniotomy for supratentorial nonfrontal (n = 22), frontal (n = 34), or posterior fossa tumor (n = 28). A further comparison involved patients with small versus large (diameter > 30 mm, mass effect) tumors. The standardized anesthetic regimen consisted of induction with 2-4 mg/kg-1 thiopental and 1-2 micrograms/kg-1 sufentanil, followed by maintenance with nitrous oxide, 0.2-0.5 micrograms.kg-1.h-1 sufentanil and < or = 0.5% isoflurane. Sufentanil administration was terminated on dural or spinal muscle closure, isoflurane during skin closure, and nitrous oxide during dressing application. After discontinuing nitrous oxide, a minineurologic examination was performed every 15 min for 1 h, then hourly for 4 h and at 24 h.

Results
Craniotomy patients performed less well than spinal surgery patients on the minineurologic examination 15 and 30 min after discontinuing nitrous oxide. At 15 min, fewer patients with large (vs. small) tumors were oriented to time (58% vs. 87%; P < 0.01) or place (67% vs. 90%; P < 0.01). Forty-two percent of patients with large tumors still had an abnormal minineurologic examination score versus 15% of patients with small tumors. At 30 min, these values were 28% and 8%, respectively (P < 0.05). Seventy-one percent of patients with large tumors were oriented to time compared to 97% for small lesions (P < 0.01). Emergence from anesthesia was similar for spinal surgery patients and patients with small brain tumors.

Conclusion
Patients undergoing craniotomy for large intracranial mass lesions awaken more slowly than patients after spinal surgery or craniotomy for small brain tumor.
Reduction of Isoflurane Minimal Alveolar Concentration by Remifentanil
Authors: Lang E. , Kapila A. , Shlugman D. , Hoke J. F. , Sebel P. S. , Glass P. S. A. 
Published: November 2003

Background
Remifentanil is a new micro-specific opioid receptor agonist currently under investigation. The interaction between opioids and volatile anesthetics is complex. Defining this interaction provides a basis for more rational dosing schemes when such combinations are used for anesthesia and allows the anesthetic potency of remifentanil relative to other opioids to be determined.

Methods
Two centers enrolled a total of 220 patients. Patients were randomized to receive a target concentration of remifentanil via a computer-assisted continuous infusion device of either 0.0, 0.5, 1.0, 1.5, 2.0, 4.0, 8.0, 16.0, and 32.0 ng/ml initiated before the administration of isoflurane. Patients were also stratified by groups 18-30, 31-55, and 56-65 yr. After induction of anesthesia with isoflurane the initial patient in each dose group was assigned an age-adjusted isoflurane concentration. The isoflurane concentration for each subsequent patient was adjusted according to the up/down technique until a minimum of 12 patients were enrolled in each group. Arterial blood samples for remifentanil whole blood concentrations were obtained. The patient was observed for purposeful movement for up to 1 min after skin incision. The minimum alveolar concentration (MAC) of isoflurane (0 ng/ml remifentanil group) and MAC reduction of isoflurane by remifentanil were determined.

Results
The MAC of isoflurane alone was 1.3%. Remifentanil caused an exponential reduction in the MAC of isoflurane with 1.37 ng/ml remifentanil a 77% reduction and 32 ng/ml a 91% reduction of isoflurane MAC.

Conclusion
The MAC reduction of isoflurane by remifentanil is similar to that produced by other opioids. Although remifentanil was given at extremely high concentrations in the absence of isoflurane, it did not provide adequate anesthesia. A 50% isoflurane MAC reduction is produced by 1.37 ng/ml remifentanil whole blood concentration compared to previously published plasma concentrations of fentanyl of 1.67 ng/ml or sufentanil of 0.14 ng/ml.
Dose-Response Characteristics of Spinal Bupivacaine in Volunteers
Authors: Liu Spencer S. , Ware Paul D. , Allen Hugh W. , Neal Joseph M. , Pollock Julia E. 
Published: November 2003

Background
Small doses of bupivacaine may be a reasonable choice for spinal anesthesia for patients having ambulatory surgery. However, few dose-response data are available to guide the selection of reasonable doses of bupivacaine for different ambulatory procedures.

Methods
Eight volunteers per group were randomized to receive 3.75, 7.5, or 11.25 mg of 0.75% bupivacaine with 8.25% dextrose in a double-blind manner. Sensory block was assessed with pinprick, transcutaneous electrical stimulation equivalent to surgical incision at the ankle, knee, pubis, and umbilicus, and with duration of tolerance to pneumatic thigh tourniquet. Motor block at the quadriceps and gastrocnemius muscles was assessed with isometric force dynamometry. Times until recovery from spinal anesthesia were recorded. Dose-response relationships were determined by linear regressions. Mean (95% confidence intervals) for durations of sensory and motor block per milligram of bupivacaine administered were calculated from linear regressions.

Results
Significant dose-response relationships (P < 0.006) were determined for sensory block, motor block, and time until recovery (R from 0.6 to 0.9). Within the range of doses studied, each additional milligram of bupivacaine was associated with an increase in duration of tolerance to transcutaneous electrical stimulation of 10 (7 to 13) min, an increase in tolerance to tourniquet of 7 (2 to 11) min, an increase in duration of motor block of 8 (5 to 12) min, and an increase in time until recovery of 21 (17 to 25) min.

Conclusions
These dose-response data may guide the selection of reasonable doses of bupivacaine for various outpatient procedures, although individual responses vary.
Effect of Acute Respiratory Acidosis on the Limits of Oxygen Extraction during Hemorrhage
Authors: Ward Michael E. 
Published: November 2003

Background
Hypercapnia can impair cells' capacity to maintain energy status anerobically and enhances the risk of hypoxic injury when oxygen availability is reduced. The ability to maintain tissue oxygenation is determined by both bulk blood flow and the efficiency of oxygen extraction. Bulk blood flow is maintained during hypercapnia through increased sympathetic activity. The effect of hypercapnia on oxygen extraction, however, is unknown. This study evaluates the effect of hypercapnia on cells' capacity to adapt to reductions in oxygen availability by increasing oxygen extraction.

Methods
In three groups of paralyzed, mechanically ventilated dogs that were anesthetized with alpha-chloralose, the concentration of carbon dioxide in the inhaled gas mixture was adjusted to achieve normocapnia, moderate hypercapnia (Paco2 = 72 +/- 3 [SE] mmHg) or severe hypercapnia (Paco2 = 118 +/- 4 [SE] mmHg). Stepwise hemorrhage was induced until each dog's blood pressure was destabilized. At each stage in the hemorrhage protocol, the oxygen delivery, oxygen consumption, and oxygen extraction ratios (ratio of arteriovenous oxygen content difference to arterial oxygen content) were determined.

Results
At the point of onset of delivery dependence of oxygen consumption, the oxygen delivery rate (critical oxygen delivery) was 7.8 +/- 1.5 (SE) ml.kg-1.min-1 and the oxygen extraction ratio (critical oxygen extraction ratio) was 0.72 +/- 0.04 (SE) in the normocapnic dogs. Moderate hypercapnia had no effect on these parameters. In the severely hypercapnic dogs, the critical values for oxygen delivery and extraction ratios were 12.5 +/- 1.8 (SE) ml.kg-1.min-1 and 0.54 +/- 0.035 (SE), respectively (P < 0.05 for differences from the normocapnic dogs).

Conclusions
The results identify a previously unrecognized threat to tissue oxygenation and emphasize the importance of ensuring adequate oxygen delivery when adopting mechanical ventilatory strategies that permit respiratory acidosis to develop.
Ipratropium Decreases Airway Size in Dogs by Preferential M2Muscarinic Receptor Blockade In Vivo
Authors: Groeben Harald , Brown Robert H. 
Published: November 2003

Background
Two major groups of drugs are available to prevent bronchoconstriction: beta-agonists and muscarinic blocking agents. Ipratropium is the most commonly used anticholinergic agent to treat chronic obstructive pulmonary disease. The authors studied anti-muscarinic agents to determine if they are as effective bronchodilators as beta-adrenergic agents and if not to identify the mechanism of their reduced effectiveness.

Methods
Six anesthetized dogs were studied using high-resolution computed tomography to measure changes in the cross-sectional area of conducting airways induced by cumulative doses of ipratropium with and without gallamine, a selective M2 muscarinic receptor blocker, and after metaproterenol.

Results
Metaproterenol dilated the airways and ipratropium constricted the airways. Ipratropium in concentrations of 0.01 and 0.1 mg/ml constricted the airways to 22 +/- 2% and 20 +/- 3% of control, respectively (P < 0.01), whereas larger concentrations caused bronchodilation. After complete blockade of the M2 receptors by pretreatment with intravenous gallamine, the bronchoconstrictor effect of ipratropium was abolished, and ipratropium dilated the airways by 16 +/- 8% and 27 +/- 10% of pre-gallamine baseline after doses of 0.01 and 0.1 mg/ml, respectively (P < 0.01).

Conclusion
Low-dose ipratropium can decrease airway size by the initial, preferential blockade of neuronal M2 muscarinic receptors, whereas a larger dose of ipratropium blocks M3 muscarinic receptors on airway smooth muscle, resulting in bronchodilation.
Epidural Catheter Reconnection
Authors: Langevin Paul B. , Gravenstein Nikolaus , Langevin Sharon O. , Gulig Paul A. 
Published: November 2003

Background
An in vitro model of epidural catheter contamination was used to determine if disconnected catheters can be safely reconnected.

Methods
Epidural catheters were filled with brain-heart infusion (BHI) broth or preservative-free saline containing 5 micrograms/ml fentanyl. Escherichia coli, Pseudomonas aeruginosa, or Staphylococcus aureus (1.10(5) colony-forming units) was injected into the initial 1.1 +/- 0.24 inch (2.75 +/- 0.60 cm) of the catheters. To study the effect of bacteria settling in a vertically oriented catheter on the advancement of bacteria along the catheter, bacteria were incubated with catheters in the vertical and the horizontal positions. To determine if bacteria are swept further into a catheter when fluid in it is displaced, catheters were inclined 30 degrees and the fluid in them was allowed to drain from the distal end to various extents. Bacteria were incubated with the catheter held horizontally. After incubation, the catheters were serially sectioned, and the resulting segments were eluted with buffered saline-containing gelatin (BSG), which was collected on BHI agar plates for colony counts. This determined if a segment of the catheter remained internally sterile distal to the point of disconnection. Effectiveness of decontaminating the exterior of the catheter was also tested as follows: Catheters (n = 10) were first immersed in BSG containing 1.10(5) S, aureus, immediately immersed in betadine for 2 min, exposed to air for 3 min, cut with a sterile instrument, and reconnected to a sterile screw cap catheter connector. Reconnected catheters were perfused with 10 ml BSG for 1 hr. Collected perfusate (100 microliters) was removed for direct colony count; the remaining perfusate was mixed with an equal volume of BHI and incubated overnight. A 100 microliters aliquot of BHI-BSG mixture was sampled the next day. No bacteria were cultured from either the perfusate or BHI-BSG mixture.

Results
Eight hours after contamination, as long as the fluid in the catheter was static, no bacteria were detected more than 13 inches (32.5 cm) from the contaminated end of catheters filled with BHI and no more than 8 inches (20 cm) from the end of those filled with fentanyl solution. This finding was not affected by incubation of the catheter in the vertical position. Fluid displacement less than 8 inches (20 cm) had no effect on dissemination, but when fluid was displaced 13 inches (32.5 cm), bacteria were found at the end of the catheter, 35 inches (87.5 cm) away. No bacteria were recovered from the perfusate of reconnected catheters after the catheters were cleaned with betadine and cut with a sterile instrument.

Conclusions
There may be an area distal to the disconnected end of an epidural catheter where its interior remains sterile for at least 8 hr. Such an area exists only when the fluid in the catheter remains static. Furthermore, the exterior of the catheter can be adequately cleaned to prevent bacteria from entering the catheter when reconnected at that point.
Behavioral Effects of Volatile Anesthetics in Caenorhabditis elegans
Authors: Crowder Michael C. , Shebester Laynie D. , Schedl Tim 
Published: November 2003

Background
The nematode Caenorhabditis elegans offers many advantages as a model organism for studying volatile anesthetic actions. It has a simple, well-understood nervous system; it allows the researcher to do forward genetics; and its genome will soon be completely sequenced. C. elegans is immobilized by volatile anesthetics only at high concentrations and with an unusually slow time course. Here other behavioral dysfunctions are considered as anesthetic endpoints in C. elegans.

Methods
The potency of halothane for disrupting eight different behaviors was determined by logistic regression of concentration and response data. Other volatile anesthetics were also tested for some behaviors. Established protocols were used for behavioral endpoints that, except for pharyngeal pumping, were set as complete disruption of the behavior. Time courses were measured for rapid behaviors. Recovery from exposure to 1 or 4 vol% halothane was determined for mating, chemotaxis, and gross movement. All experiments were performed at 20 to 22 degrees C.

Results
The median effective concentration values for halothane inhibition of mating (0.30 vol%-0.21 mM), chemotaxis (0.34 vol%-0.24 mM), and coordinated movement (0.32 vol% - 0.23 mM) were similar to the human minimum alveolar concentration (MAC; 0.21 mM). In contrast, halothane produced immobility with a median effective concentration of 3.65 vol% (2.6 mM). Other behaviors had intermediate sensitivities. Halothane's effects reached steady-state in 10 min for all behaviors tested except immobility, which required 2 h. Recovery was complete after exposure to 1 vol% halothane but was significantly reduced after exposure to immobilizing concentrations.

Conclusions
Volatile anesthetics selectively disrupt C. elegans behavior. The potency, time course, and recovery characteristics of halothane's effects on three behaviors are similar to its anesthetic properties in vertebrates. The affected nervous system molecules may express structural motifs similar to those on vertebrate anesthetic targets.
Eye Injuries after Nonocular Surgery
Authors: Roth Steven , Thisted Ronald A. , Erickson John P. , Black Susan , Schreider Bruce D. 
Published: November 2003

Background
Eye injuries after anesthesia, although infrequent, may result in visual impairment. Previous studies have not defined the risk factors associated with these injuries. To study the cause of these injuries and to determine incidence data, the authors reviewed the records from a 4.5-y period of patients who sustained eye injuries after anesthesia and nonocular surgery.

Methods
The records were surveyed of 60,965 patients who underwent anesthesia for nonocular surgery at our institution from January 1988 to July 1992. Eye injuries were identified by examining several sources of information, including quality improvement data, postoperative visits or telephone calls, and examination of medical records of postoperative patients who required an ophthalmology consultation. Records were reviewed to determine the types and causes of eye injuries. Logistic regression, with univariate and multivariate analysis, was used to identify the importance of possible risk factors.

Results
Of 34 patients who sustained eye injuries (0.056%), the most common was corneal abrasion (n = 21). Other injuries were conjunctivitis, blurred vision, red eye, chemical injury, direct trauma, and blindness. Independent factors associated with a higher relative risk of eye injury were long surgical procedures (odds ratio, 1.16 per hour of anesthetic care; CI, 1.1 to 1.3), lateral positioning during surgery (odds ratio, 4.7; CI, 2 to 11), operation on the head or neck (odds ratio, 4.4; CI, 2.2 to 9.0), general anesthesia (odds ratio, 3.0; CI, 2.2 to 38), and surgery on a Monday (odds ratio, 2.7; CI, 1.4 to 5.3). In only 21% of cases was a specific cause of injury identified.

Conclusions
For reasons not understood, eye injuries are more common in patients who are older or who undergo lengthier procedures. The cause of injury was usually not determined by the authors' methods. Until the mechanisms producing perioperative eye injuries are better understood, it is difficult to identify strategies to prevent this type of injury.
Differential Effects of Etomidate, Propofol, and Midazolam on Calcium and Potassium Channel Currents in Canine Myocardial Cells
Authors: Buljubasic Nediljka , Marijic Jure , Berczi Viktor , Supan Darko F. , Kampine John P. , Bosnjak Zeljko J. 
Published: November 2003

Background
Intravenous anesthetics etomidate, propofol, and midazolam produce negative inotropic effects of various degrees. The mechanism underlying these differences is largely unknown.

Methods
The effects of intravenous anesthetics on L-type Ca2+, transient outward and inward-rectifier K+ channel currents (ICa, IKto, and IK1) were compared in canine ventricular cells using the whole-cell voltage-clamp technique. ICa and IK were elicited by progressively depolarizing cells from -40 to +40 mV, and from -90 to +60 mV, respectively. The peak amplitude and time-dependent inactivation rate of ICa and IK were measured before, during, and after the administration of equimolar concentrations (5, 30, or 60 microM) of etomidate, propofol, or midazolam.

Results
Exposure to etomidate, propofol, and midazolam produced a concentration-dependent inhibition of ICa. Midazolam was the most potent intravenous anesthetic; at 60 microM, etomidate, propofol, and midazolam decreased peak ICa by 16 +/- 4% (mean +/- SEM), 33 +/- 5%, and 47 +/- 5%, respectively. Etomidate, propofol, and midazolam given in a 60-microM concentration decreased IKto by 8 +/- 3%, 9 +/- 2%, and 23 +/- 3%, respectively. IK1 was decreased by 60 microM etomidate and midazolam by 20 +/- 6% and 14% +/- 5%, respectively. Propofol had no effect on IK1.

Conclusions
At equimolar concentrations, intravenous anesthetics decreased the peak ICa, IKto, and IK1 with various degrees of potency. Effects of anesthetics on ICa were significantly greater compared with their effects on K+ currents. These findings suggest that the negative inotropic actions of etomidate, propofol, and midazolam are related, at least in part, to decreased ICa. Some effects, such as IK inhibition, may partially antagonize effects of decreased ICa. Indeed, the final effect of these intravenous anesthetics on myocardium will be the sum of these and other sarcolemmal and intracellular effects.