bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characteristics of Programs Involving Canine Visitation of Hospitalized People in Ontario
Authors: Lefebvre Sandra L. , Waltner-Toews David , Peregrine Andrew , Reid-Smith Richard , Hodge Leslie , Weese J. Scott 
Published: June 2006

Objective.To determine the distribution of canine-visitation programs in Ontario and to characterize the nature of the programs the dogs are affiliated with.Design.A cross-sectional survey of hospitals in Ontario was used to determine whether they permitted dogs to visit patients and, if so, where the dogs originated. On the basis of this information, dog owners were then contacted through their respective associations and interviewed using a standardized questionnaire.Setting.A cross-section of hospitals in Ontario.Participants.A total of 223 (97%) of the 231 hospitals surveyed responded. Ninety owners of 102 visitation dogs were interviewed.Results.A total of 201 (90%) of the 223 hospitals indicated that dogs were permitted in their facilities. Origins ranged from national therapy-dog agencies to the patients' families. Acute care wards were 5.1 times as likely than other wards to disallow animals (95% confidence interval, 2.2-12.2;P<.001). According to the 90 dog owners included in the study, the screening protocols that dogs were required to pass to participate in their respective visitation programs were highly variable, as were the owners' infection control practices. Eighteen owners (20%) said they did not practice any infection control. Sixty-six owners (73%) allowed their dogs on patients' beds, and 71 (79%) let their dogs lick patients. Thirty-six owners (40%) were unable to name one zoonotic disease that may be transmitted from their dog.Conclusions.Although canine-visitation programs have become standard practice in nonacute human healthcare facilities, infection control and dog-screening practices are highly variable and potentially deficient. Hospital staff, visitation groups, pet owners, and veterinarians need to work together to protect both people and pets.
Increasing Antibiotic Resistance Among Isolates ofEscherichia coliRecovered From Inpatients and Outpatients in a Saudi Arabian Hospital
Authors: Al-Tawfiq Jaffar A. 
Published: June 2006

Objective.To study the pattern of antibiotic resistance amongEscherichia coliand the trend in resistance during a 6-year period in a Saudi Arabian hospital.Design.Retrospective in vitro surveillance study of the antibiotic susceptibility pattern amongE. coliisolates recovered from outpatients and from inpatients.Setting.A general hospital in Saudi Arabia.Patients.All patients with a culture positive forE. coliduring a 6-year study period.Results.A statistically significant increase in antibiotic resistance was observed among outpatient and inpatient isolates ofE, coli.Inpatient isolates were more likely to be resistant to antimicrobial agents. Among isolates from outpatients, 50% were resistant to ampicillin, 33% were resistant to trimethoprim-sulfamethoxazole (TMP-SMZ), and 14% were resistant to ciprofloxacin. Among isolates from inpatients, 63% were resistant to ampicillin, 44% were resistant to TMP-SMZ, and 33% were resistant to ciprofloxacin. There was a low rate of resistance to imipenem (0.3% of isolates), amikacin (2%), and nitrofurantoin (2.4%-6.5%). Resistance to ceftazidime was detected in 9% of outpatient isolates and 17% of inpatient isolates. Multidrug resistance was defined as resistance to 2 or more classes of antibiotics. Multidrug resistance was detected in 2.0%-28.1% of outpatient isolates and 7.4%-39.6% of inpatient isolates, depending on the combination of antimicrobials tested. More isolates were resistant to ampicillin plus TMP-SMZ than to any other combination of antimicrobials.Conclusion.The prevalence of antibiotic resistance among outpatient and inpatientE. coliisolates increased during the study period. The rates of antibiotic resistance were statistically significantly higher among inpatient isolates, compared with outpatient isolates. These findings call for wiser use of antibiotics and continued surveillance of antibiotic resistance.
Comparison of Unit-Specific and Hospital-Wide Antibiograms Potential Implications for Selection of Empirical Antimicrobial Therapy
Authors: Binkley Shawn , Fishman Neil O. , LaRosa Lori A. , Marr Ann Marie , Nachamkin Irving , Wordell David , Bilker Warren B. , Lautenbach Ebbing 
Published: June 2006

Objective.To identify differences between unit-specific and hospital-wide antibiograms and to determine the potential impact of these differences on selection of empirical antimicrobial therapy.Setting.A 625-bed tertiary care medical center.Methods.Antimicrobial susceptibility results were collected for all inpatient clinical bacterial isolates recovered over a 3-year period; isolates were categorized by the hospital location of the patient at the time of sampling and by the anatomic site from which the isolate was recovered. Antibiograms from each unit were compiled for the most commonly isolated organisms and were compared to the hospital-wide antibiogram.Results.A total of 9,970 bacterial isolates were evaluated in this study, including 2,646 enterococcal isolates, 2,806 S. aureus isolates, 2,795 E. coli isolates, and 1,723 Pseudomonas aeruginosa isolates. The percentages of bacterial isolates resistant to antimicrobials were significantly higher in the medical ICU and surgical ICU than the hospital-wide antibiogram would have predicted, whereas the percentages of isolates susceptible to antimicrobials were significantly higher in the non-ICU units, compared with the hospital overall. However, on general medicine units, the prevalence of susceptibility to levofloxacin was significantly lower than that for the hospital overall.Conclusions.Unit-specific antibiograms are important for making informed decisions about empirical antimicrobial therapy, because the hospital-wide antibiogram may mask important differences in susceptibility rates across different units. These differences may have important implications for selecting the optimal empirical antimicrobial therapy.
Interscalene Brachial Plexus Block: Can the Risk of Entering the Spinal Canal Be Reduced?
Authors: Sardesai Anand M. , Patel Roger , Denny Nicholas M. , Menon David K. , Dixon Adrian K. , Herrick Martin J. , Harrop-Griffiths Alan W. 
Published: June 2006

Background
Spinal cord damage during interscalene brachial plexus block has been attributed to needle entry into the spinal canal. The purpose of this study was to identify the angles and depths of needle insertion that increase the likelihood of such an event, using the traditional classic interscalene approach and two more proximal entry points.

Method
Magnetic resonance images of the neck from 10 healthy volunteers were used to obtain the three-dimensional spatial coordinates of three skin markers and the right-sided cervical nerves at the exiting neural foramina. The distance of the intervertebral foramina from the skin markers and the angles of the needle vector and the foramina were calculated.

Results
The distance from the skin to the intervertebral foramen may be as short as 2.5 cm with the classic approach. A caudal angulation greater than 50 degrees seemed to eliminate the risk of needle entry through the foramen.

Conclusion
With the classic approach to the interscalene block, there is a greater possibility of the needle passing through the intervertebral foramen if the needle is advanced too deeply. More proximal entry points and techniques that use a more steeply angled needle may reduce the risk of entry into the spinal space.
Cerebral State Index during Propofol Anesthesia
Authors: Jensen Erik W. , Litvan Hector , Revuelta Miren , Rodriguez Bernardo E. , Caminal Pere , Martinez Pablo , Vereecke Hugo , Struys Michel M. R. F. 
Published: June 2006

Background
The objective of this study was to prospectively test the Cerebral State Index designed for measuring the depth of anesthesia. The Cerebral State Index is calculated using a fuzzy logic combination of four subparameters of the electroencephalographic signal. The performance of the Cerebral State Index was compared with that of the Bispectral Index and the A-Line ARX Index.

Methods
This study applied raw data from two previously published clinical protocols. The patients in protocol 1 were given a continuous propofol infusion, 300 ml/h, until 80% of burst suppression occurred. In protocol 2, a stepwise increased target-controlled infusion of propofol was administered to patients until loss of response to noxious stimuli while the Observer's Assessment of Alertness and Sedation was registered every 4 min. The Cerebral State Index was calculated off-line from the recorded electroencephalographic data. The Spearman rank correlation coefficient between electronic indices and the effect site concentration of propofol was calculated along with the prediction probability of each index to predict the Observer's Assessment of Alertness and Sedation level.

Results
The Spearman rank correlation coefficients between the Cerebral State Index, Bispectral Index, and A-Line ARX Index and the propofol effect site concentration were -0.94, -0.89, and -0.82, respectively, in protocol 1, whereas the prediction probability values between the Cerebral State Index, Bispectral Index, and A-Line ARX Index and the Observer's Assessment of Alertness and Sedation score in protocol 2 were 0.92, 0.93, and 0.91, respectively.

Conclusion
The Cerebral State Index detects well the graduated levels of propofol anesthesia when compared with the propofol effect site concentration and the Observer's Assessment of Alertness and Sedation score.
Naloxone Reversal of Buprenorphine-induced Respiratory Depression
Authors: van Dorp Eveline , Yassen Ashraf , Sarton Elise , Romberg Raymonda , Olofsen Erik , Teppema Luc , Danhof Meindert , Dahan Albert 
Published: June 2006

Background
The objective of this investigation was to examine the ability of the opioid antagonist naloxone to reverse respiratory depression produced by the mu-opioid analgesic, buprenorphine, in healthy volunteers. The studies were designed in light of the claims that buprenorphine is relatively resistant to the effects of naloxone.

Methods
In a first attempt, the effect of an intravenous bolus dose of 0.8 mg naloxone was assessed on 0.2 mg buprenorphine-induced respiratory depression. Next, the effect of increasing naloxone doses (0.5-7 mg, given over 30 min) on 0.2 mg buprenorphine-induced respiratory depression was tested. Subsequently, continuous naloxone infusions were applied to reverse respiratory depression from 0.2 and 0.4 mg buprenorphine. All doses are per 70 kg. Respiration was measured against a background of constant increased end-tidal carbon dioxide concentration.

Results
An intravenous naloxone dose of 0.8 mg had no effect on respiratory depression from buprenorphine. Increasing doses of naloxone given over 30 min produced full reversal of buprenorphine effect in the dose range of 2-4 mg naloxone. Further increasing the naloxone dose (doses of 5 mg or greater) caused a decline in reversal activity. Naloxone bolus doses of 2-3 mg, followed by a continuous infusion of 4 mg/h, caused full reversal within 40-60 min of both 0.2 and 0.4 mg buprenorphine-induced respiratory depression.

Conclusions
Reversal of buprenorphine effect is possible but depends on the buprenorphine dose and the correct naloxone dose window. Because respiratory depression from buprenorphine may outlast the effects of naloxone boluses or short infusions, a continuous infusion of naloxone may be required to maintain reversal of respiratory depression.
Selective γ-Aminobutyric Acid Type A Receptor Antagonism Reverses Isoflurane Ischemic Neuroprotection
Authors: Elsersy Hazem , Mixco Javier , Sheng Huaxin , Pearlstein Robert D. , Warner David S. 
Published: June 2006

Background
Isoflurane provides protection against severe forebrain ischemia in the rat. The authors hypothesized that this is attributable to interaction with the gamma-aminobutyric acid type A (GABAA) receptor resulting in altered time to onset of ischemic hippocampal depolarization.

Methods
Organotypic hippocampal slices were subjected to oxygen-glucose deprivation in the presence of isoflurane and combinations of GABAA (bicuculline) and GABAB (phaclofen) receptor antagonists. Cell death was measured. Rats were subjected to severe forebrain ischemia while anesthetized with fentanyl-nitrous oxide or 1.4% isoflurane. In the isoflurane group, rats also received intravenous bicuculline (0, 1, or 2 mg/kg). Neurologic and histologic outcomes and time to depolarization were assessed.

Results
In slices, 2% isoflurane caused near-complete protection against oxygen-glucose deprivation. This was unaffected by coadministration of phaclofen but largely reversed by bicuculline. The GABAA agonist muscimol was also protective, having an effect equivalent to 1% isoflurane. In rats, isoflurane (0 mg bicuculline) improved neurologic and histologic outcome versus fentanyl-nitrous oxide (CA1 percentage of alive neurons: fentanyl-nitrous oxide, 15 +/- 7; isoflurane, 61 +/- 24). The isoflurane effect was reversed in a dose-dependent manner by bicuculline (CA1 percentage alive: 1 mg/kg, 44 +/- 22; 2 mg/kg, 21 +/- 15). Time to depolarization was delayed with isoflurane versus fentanyl-nitrous oxide (137 vs. 80 s) but was not affected by bicuculline (149 s). In contrast, postischemic time to repolarization was more rapid with fentanyl-nitrous oxide or isoflurane plus bicuculline versus isoflurane alone.

Conclusions
These studies are consistent with the hypothesis that the GABAA receptor serves as a major site of action for isoflurane neuroprotection both in vitro and in vivo. However, the mechanism by which this interaction confers in vivo protection cannot be attributed to effects on the duration of ischemic depolarization.
Biologically Variable Ventilation Improves Oxygenation and Respiratory Mechanics during One-lung Ventilation
Authors: McMullen Michael C. , Girling Linda G. , Graham M Ruth , Mutch W Alan C. 
Published: June 2006

Background
Hypoxemia is common during one-lung ventilation (OLV). Atelectasis contributes to the problem. Biologically variable ventilation (BVV), using microprocessors to reinstitute physiologic variability to respiratory rate and tidal volume, has been shown to be advantageous over conventional monotonous control mode ventilation (CMV) in improving oxygenation during the period of lung reinflation after OLV in an experimental model. Here, using a porcine model, the authors compared BVV with CMV during OLV to assess gas exchange and respiratory mechanics.

Methods
Eight pigs (25-30 kg) were studied in each of two groups. After induction of anesthesia-tidal volume 12 ml/kg with CMV and surgical intervention-tidal volume was reduced to 9 ml/kg. OLV was initiated with an endobronchial blocker, and the animals were randomly allocated to either continue CMV or switch to BVV for 90 min. After OLV, a recruitment maneuver was undertaken, and both lungs were ventilated for a further 60 min. At predetermined intervals, hemodynamics, respiratory gases (arterial, venous, and end-tidal samples) and mechanics (airway pressures, static and dynamic compliances) were measured. Derived indices (pulmonary vascular resistance, shunt fraction, and dead space ventilation) were calculated.

Results
By 15 min of OLV, arterial oxygen tension was greater in the BVV group (group x time interaction, P = 0.003), and shunt fraction was lower with BVV from 30 to 90 min (group effect, P = 0.0004). From 60 to 90 min, arterial carbon dioxide tension was lower with BVV (group x time interaction, P = 0.0001) and dead space ventilation was less from 60 to 90 min (group x time interaction, P = 0.0001). Static compliance was greater by 60 min of BVV and remained greater during return to ventilation of both lungs (group effect, P = 0.0001).

Conclusions
In this model of OLV, BVV resulted in superior gas exchange and respiratory mechanics when compared with CMV. Improved static compliance persisted with restoration of two-lung ventilation.
Distinct Roles for Sarcolemmal and Mitochondrial Adenosine Triphosphate-sensitive Potassium Channels in Isoflurane-induced Protection against Oxidative Stress
Authors: Marinovic Jasna , Bosnjak Zeljko J. , Stadnicka Anna 
Published: June 2006

Background
Cardiac preconditioning, including that induced by halogenated anesthetics, is an innate protective mechanism against ischemia-reperfusion injury. The adenosine triphosphate-sensitive potassium (K(ATP)) channels are considered essential in preconditioning mechanism. However, it is unclear whether K(ATP) channels are triggers initiating the preconditioning signaling, and/or effectors responsible for the cardioprotective memory and activated during ischemia-reperfusion.

Methods
Adult rat cardiomyocytes were exposed to oxidative stress with 200 microM H(2)O(2) and 100 microM FeSO4. Myocyte survival was determined based on morphologic characteristics and trypan blue exclusion. To induce preconditioning, the myocytes were pretreated with isoflurane. The involvement of sarcolemmal and mitochondrial K(ATP) channels was investigated using specific inhibitors HMR-1098 and 5-hydroxydecanoic acid. Data are expressed as mean +/- SD.

Results
Oxidative stress induced cell death in 47 +/- 14% of myocytes. Pretreatment with isoflurane attenuated this effect to 26 +/- 8%. Blockade of the sarcolemmal K(ATP) channels abolished the protection by isoflurane pretreatment when HMR-1098 was applied throughout the experiment (50 +/- 21%) or only during oxidative stress (50 +/- 12%), but not when applied during isoflurane pretreatment (29 +/- 13%). Inhibition of the mitochondrial K(ATP) channels abolished cardioprotection irrespective of the timing of 5-hydroxydecanoic acid application. Cell death was 42 +/- 23, 45 +/- 23, and 46 +/- 22% when 5-hydroxydecanoic acid was applied throughout the experiment, only during isoflurane pretreatment, or only during oxidative stress, respectively.

Conclusion
The authors conclude that both sarcolemmal and mitochondrial K(ATP) channels play essential and distinct roles in protection afforded by isoflurane. Sarcolemmal K(ATP) channel seems to act as an effector of preconditioning, whereas mitochondrial K(ATP) channel plays a dual role as a trigger and an effector.
Low-dose Intravenous Ketamine Potentiates Epidural Analgesia after Thoracotomy
Authors: Suzuki Manzo , Haraguti Syuji , Sugimoto Kikuzo , Kikutani Takehiko , Shimada Yoichi , Sakamoto Atsuhiro 
Published: June 2006

Background
Ketamine potentiates intravenous or epidural morphine analgesia. The authors hypothesized that very-low-dose ketamine infusion reduces acute and long-term postthoracotomy pain.

Methods
Forty-nine patients scheduled to undergo open thoracotomy were randomly assigned to receive one of two anesthesia regimens: continuous epidural infusion of ropivacaine and morphine, along with intravenous infusion of ketamine (0.05 mg . kg(-1) . h(-1) [approximately 3 mg/h], ketamine group, n = 24) or placebo (saline, control group, n = 25). Epidural analgesia was continued for 2 days after surgery, and infusion of ketamine or placebo was continued for 3 days. Pain was assessed at 6, 12, 24, and 48 h after surgery. Patients were asked about their pain, abnormal sensation on the wound, and inconvenience in daily life at 7 days and 1, 3, and 6 months after surgery.

Results
The visual analog scale scores for pain at rest and on coughing 24 and 48 h after thoracotomy were lower in the ketamine group than in the control group (pain at rest, 9 +/- 11 vs. 25 +/- 20 and 9 +/- 11 vs. 18 +/- 13; pain on coughing, 26 +/- 16 vs. 50 +/- 17 and 30 +/- 18 vs. 43 +/- 18, mean +/- SD; P = 0.002 and P = 0.01, P < 0.0001 and P = 0.02, respectively). The numerical rating scale scores for baseline pain 1 and 3 months after thoracotomy were significantly lower in the ketamine group (0.5 [0-4] vs. 2 [0-5] and 0 [0-5] vs. 1.5 [0-6], median [range], respectively; P = 0.02). Three months after surgery, a higher number of control patients were taking pain medication (2 vs. 9; P = 0.03).

Conclusions
Very-low-dose ketamine (0.05 mg . kg(-1) . h(-1)) potentiated morphine-ropivacaine analgesia and reduced postthoracotomy pain.
Effects of Bupivacaine and Tetrodotoxin on Carrageenan-induced Hind Paw Inflammation in Rats (Part 2)
Authors: Beloeil Hélène , Ji Ru-Rong , Berde Charles B. 
Published: June 2006

Background
The authors previously showed that bupivacaine and tetrodotoxin via contralateral or ipsilateral sciatic block, but not systemically, attenuate local edema and hyperalgesia induced by carrageenan hind paw injection in rats. Bupivacaine, by all three routes, suppressed systemic cytokine activation, whereas tetrodotoxin was ineffective by all three routes. In the current study, the authors examined cytokine and p38 mitogen-activated protein kinase (MAPK) activation in lumbar dorsal root ganglia (DRGs) and spinal cord after carrageenan paw injections and sciatic blocks with either bupivacaine or tetrodotoxin.

Methods
Ten groups of rats (n = 3-5) received injections in the following sites: right or left hind paw or right forepaw (carrageenan or saline) and left sciatic block (with epinephrine plus bupivacaine, tetrodotoxin, or saline; repeated 6 h later). Fifteen hours later, tumor necrosis factor alpha, interleukin 1beta, p38 MAPK, and phosphorylated p38 MAPK were measured by enzyme-linked immunosorbent assay in DRGs and in the spinal cord.

Results
Carrageenan-induced hind paw inflammation enhanced tumor necrosis factor-alpha and interleukin-1beta production in bilateral DRGs and spinal cord and enhanced p38 MAPK activation in bilateral DRGs. These pathways were not activated after forepaw injection of carrageenan, suggesting a segmental mechanism. Neither bupivacaine nor tetrodotoxin inhibited cytokine and p38 MAPK activation after carrageenan injection.

Conclusion
Ipsilateral or contralateral sciatic blockade using either bupivacaine or tetrodotoxin does not inhibit carrageenan-induced activation of cytokines and p-38 MAPK in spinal cord and DRGs. Possible explanations may include incomplete degrees of conduction blockade or afferent signaling via saphenous nerves.
Cerebrospinal Fluid and Spinal Cord Distribution of Baclofen and Bupivacaine during Slow Intrathecal Infusion in Pigs
Authors: Bernards Christopher M. 
Published: June 2006

Background
Increasing numbers of patients are receiving chronic intrathecal infusions of local anesthetics, baclofen, opioids, and other analgesics via implanted pumps. These infusions typically deliver drugs at rates measured in microliters per hour. However, to date, there have been no studies aimed at characterizing drug distribution within cerebrospinal fluid (CSF) and spinal cord during these slow infusion rates. Therefore, this study was designed to address this knowledge gap.

Methods
Anesthetized pigs were instrumented with eight intrathecal microdialysis probes placed at multiple points along the neuroaxis in both the anterior and posterior intrathecal space to permit continuous CSF sampling for measurement of bupivacaine and baclofen concentrations. Animals were divided into three groups and received bupivacaine and baclofen infusions at 20 or 1,000 microl/h or as a 1,000-microl bolus over 5 min every hour. Drug administration continued for 8 h, at which time the animals were killed, and the spinal cord was removed and divided into 1-cm-long sections that were further divided into anterior and posterior portions for measurement of bupivacaine and baclofen concentrations.

Results
In all groups, drug concentration in CSF and spinal cord decreased rapidly as a function of distance from the site of administration, with most drug found within a few centimeters. In addition, there were significant anterior-posterior differences in both CSF and spinal cord drug concentrations.

Conclusions
During slow intrathecal infusion, drug distribution in CSF and spinal cord is severely limited in all groups, although significantly more so in the 20-microl/h infusion group.