bluuebunny/crossref_metadata_2025_split huggingface dataset:
N -Acetylcysteine Restores Isoflurane-induced Preconditioning against Myocardial Infarction during Hyperglycemia
Authors: Kehl Franz , Krolikowski John G. , Weihrauch Dorothee , Pagel Paul S. , Warltier David C. , Kersten Judy R. 
Published: November 2003

Background
Hyperglycemia generates reactive oxygen species and prevents isoflurane-induced preconditioning. The authors tested the hypothesis that scavenging reactive oxygen species with N-acetylcysteine will restore protection against myocardial infarction produced by isoflurane in vivo.

Methods
Barbiturate-anesthetized dogs (n = 45) were instrumented for measurement of systemic hemodynamics. Myocardial infarct size and coronary collateral blood flow were measured with triphenyltetrazolium staining and radioactive microspheres, respectively. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Dogs were randomly assigned to receive an infusion of 0.9% saline or 15% dextrose in water to increase blood glucose concentrations to 600 mg/dl (hyperglycemia) in the absence or presence of isoflurane (1.0 minimum alveolar concentration) with or without pretreatment with N-acetylcysteine (150 mg/kg i.v.) in six experimental groups. Isoflurane was discontinued, and blood glucose concentrations were allowed to return to baseline values before left anterior descending coronary artery occlusion.

Results
Myocardial infarct size was 27 +/- 2% (n = 8) of the left ventricular area at risk in control experiments. Isoflurane significantly (P < 0.05) decreased infarct size (13 +/- 2%; n = 7). Hyperglycemia alone did not alter infarct size (29 +/- 3%; n = 7) but abolished the protective effect of isoflurane (25 +/- 2%; n = 8). N-Acetylcysteine alone did not affect infarct size (28 +/- 2%; n = 8) but restored isoflurane-induced cardioprotection during hyperglycemia (10 +/- 1%; n = 7).

Conclusions
Acute hyperglycemia abolishes reductions in myocardial infarct size produced by isoflurane, but N-acetylcysteine restores these beneficial effects. The results suggest that excessive quantities of reactive oxygen species generated during hyperglycemia impair isoflurane-induced preconditioning in dogs.
Perflubron Emulsion in Prolonged Hemorrhagic Shock
Authors: Paxian Markus , Rensing Hauke , Geckeis Katrin , Bauer Inge , Kubulus Darius , Spahn Donat R. , Bauer Michael 
Published: November 2003

Background
Liver dysfunction as a result of impaired oxygen availability frequently occurs following hemorrhage and contributes to delayed mortality. Artificial oxygen carriers may improve oxygen supply to vital organs while avoiding the need for allogeneic transfusion.

Methods
Rats were subjected to hemorrhagic hypotension (mean arterial pressure = 35-40 mmHg for 120 min) and were subsequently resuscitated with (1) stored whole rat blood, (2) pentastarch, or (3) pentastarch combined with perflubron emulsion (PFE; 2.7 or 5.4 g/kg body weight), a second-generation artificial oxygen carrier. Recovery of liver adenosine triphosphate, hepatocellular injury, and expression of glutamine synthetase 1, a gene that is induced by exposure of hepatocytes to low partial pressure of oxygen, were studied at 4 h of resuscitation.

Results
Stored whole blood or pentastarch failed to restore liver adenosine triphosphate concentrations after prolonged shock as compared to sham controls and resulted in increased gene expression of glutamine synthetase 1. Addition of 2.7 g PFE/kg restored liver adenosine triphosphate to control, whereas 5.4 g PFE/kg resulted in adenosine triphosphate concentrations significantly above control. Improved hepatocellular oxygen supply was also confirmed by restoration of the physiologic expression pattern of glutamine synthetase 1. Serum enzyme concentrations were highest after resuscitation with stored blood, whereas addition of PFE failed to further decrease enzyme concentrations as compared to pentastarch alone.

Conclusions
Resuscitation with PFE is superior to stored blood or asanguineous resuscitation with respect to restoration of hepatocellular energy metabolism. The improved hepatocellular oxygen availability is reflected in normalization of oxygen-dependent gene expression. However, improved oxygen availability failed to affect early hepatocellular injury.
Olprinone, a Phosphodiesterase III Inhibitor, Reduces Gut Mucosal Injury and Portal Endotoxin Level during Acute Hypoxia in Rabbits
Authors: Satoh Tomoyuki , Morisaki Hiroshi , Ai Kimiaki , Kosugi Shizuko , Yamamoto Michiko , Serita Ryohei , Kotake Yoshifumi , Takeda Junzo 
Published: November 2003

Background
Preservation of gut integrity has become a therapeutic goal to obviate bacterial translocation in the critically ill. The authors examined whether olprinone, a phosphodiesterase III inhibitor, protected functional and structural integrity of gut mucosa against acute progressive hypoxia.

Methods
Thirty-two animals were randomly allocated to a control group (n = 12), a low-dose group (0.2 microg x kg-1 x min-1 olprinone; n = 10), or a high-dose group (0.6 microg x kg-1 x min-1 olprinone; n = 10) after preparatory surgery. Ascending aortic and portal blood flow, intramural pH of the ileum, and portal endotoxin levels were measured at normoxia and through three stages of progressive hypoxia (fraction of inspired oxygen = 0.17, 0.13, and 0.10).

Results
At normoxia, ascending aortic flow in the high-dose group was approximately 20% higher than in the control and low-dose groups. During progressive hypoxia, both ascending aortic and portal flow in the control group were depressed, whereas olprinone infusion attenuated such alterations and redistributed blood to the splanchnic area in a dose-dependent manner. On the contrary, the reduction of intramural pH of the ileum and the elevation of portal endotoxin levels observed in the control group were significantly minimized in both the low- and high-dose groups to a similar extent during acute hypoxia. Histopathologic alterations of gut mucosa observed in the control group were minimized by olprinone infusion dose-independently, accompanied by reduction of mortality rate of the animals.

Conclusions
Olprinone slows progression of intestinal mucosal acidosis and gut barrier dysfunction, concurrently with preservation of microscopic structures, through both flow-dependent and -independent mechanisms under acute hypoxia. Such properties of olprinone may serve to protect the host under insult.
Relationships between Measurement of Pain Using Visual Analog Score and Morphine Requirements during Postoperative Intravenous Morphine Titration
Authors: Aubrun Frédéric , Langeron Olivier , Quesnel Christophe , Coriat Pierre , Riou Bruno 
Published: November 2003

Background
Although intravenous morphine titration is widely used to obtain rapid and complete postoperative pain relief, the relationship between measurement of pain and morphine requirements varies, and the evolution of pain during titration is poorly understood.

Methods
Intravenous morphine titration was administered as a bolus of 2 (body weight < or = 60 kg) or 3 mg (body weight > 60 kg) during the immediate postoperative period in the PACU. The interval between each bolus was 5 min. The visual analog scale (VAS) score threshold required to administer morphine was 30, and pain relief was defined as a VAS score of 30 or less.

Results
Data from 3,045 patients were analyzed. The mean initial VAS score was 73 +/- 19 (mean +/- SD), and the mean morphine dose required to obtain pain relief was 0.17 +/- 0.10 mg/kg, i.e., a median of four boluses (range, 1-20). When patients were grouped according to several classes of initial VAS score (31-39, 40-49, 50-59, 60-69, 70-79, 80-89, 90-100), it seemed that the relationship between VAS score and morphine requirements was a sigmoid curve. A VAS score of 70 or greater predicted the need for a high (>0.15 mg/kg) morphine dose (sensitivity, 0.77; specificity, 0.54). During the pain relief process, the relationship between VAS score and time was depicted by a sigmoid curve.

Conclusion
A VAS score of 70 or greater should be considered indicative of severe pain. The relationship between the initial VAS score and morphine requirements is not linear, and the evolution of the VAS score during the pain relief process is described by a sigmoid curve.
Bilateral Intravenous Regional Anesthesia
Authors: Hartmannsgruber Maximilian W.B. , Plessmann Sabine , Atanassoff Peter G. 
Published: November 2003

Background
Ketorolac, when added to lidocaine, has been shown to reduce early tourniquet pain during intravenous regional anesthesia (i.v.RA) in patients. Although the effectiveness of ropivacaine 0.2% for i.v.RA is equal to that of lidocaine 0.5% but significantly reduces central nervous system side effects after release of the tourniquet, it provides no advantage with regard to tourniquet tolerance times. Simultaneous bilateral i.v.RA with ropivacaine 0.2% was used to test the hypothesis that ketorolac modifies tourniquet tolerance and to test whether drug combinations can be evaluated in one study session.

Methods
Ten healthy, unsedated volunteers received 30 ml of ropivacaine 0.2% in each upper arm with 2 ml of normal saline in one arm and 30 mg of ketorolac in the contralateral arm for i.v.RA. Both proximal tourniquets remained inflated for 30 min, followed by inflation of the distal tourniquets and release of the proximal ones. Verbal numeric scores for tourniquet pain were recorded for both extremities. Central nervous system side effects were graded after release of each distal tourniquet.

Results
There was no difference between the two upper extremities with regard to surgical anesthesia and tourniquet tolerance. Total tourniquet tolerance was a median of 58.5 min (range, 45-90 min) and 60.5 min (39-79 min) in the normal saline and ketorolac groups, respectively. After release of the distal tourniquets, 5 of 10 volunteers experienced mild dizziness.

Conclusions
The addition of ketorolac to ropivacaine does not improve tourniquet tolerance. Minimal central nervous system side effects after tourniquet release suggest that a total of 60 ml ropivacaine 0.2% for bilateral i.v.RA is a useful model for comparison of i.v.RA drug combinations.
Comparison of the Parasacral Approach and the Posterior Approach, with Single- and Double-Injection Techniques, to Block the Sciatic Nerve
Authors: Cuvillon Philippe , Ripart Jacques , Jeannes Pascal , Mahamat Aba , Boisson Christophe , L'Hermite Joel , Vernes Eric , de La Coussaye Jean Emmanuel 
Published: November 2003

Background
The purpose of this study was to compare parasacral and Winnie's single- or double-injection approaches for sciatic nerve block.

Methods
One hundred fifty adults scheduled to undergo lower limb surgery were randomized to receive on the sciatic nerve 20 ml ropivacaine, 0.75%: single bolus for parasacral and Winnie's single injection. For Winnie's double injection, the peroneal and tibial nerves received separately 10 ml plus 10 ml. Blocks were performed with the use of nerve stimulator (intensity < 0.5 mA, 1 Hz). For the parasacral method, a line was drawn between the posterior superior iliac spine and the ischial tuberosity; needle entry was at 6 cm inferior to the posterior superior iliac spine.

Results
The groups were similar. Time to perform the block was 2 (1-5) min for the parasacral method, with no difference from Winnie's single injection (3 [1-10] min), but was shorter with double injection (5.5 [2-15] min) (P = 0.0001). Onset of sensory block was similar in the parasacral (25 [7.5-50] min) and Winnie single-injection groups (25 [5-50] min) but significantly longer in the double-injection group (15 [5-50] min). Success rates for complete block were similar in the parasacral (66%) and Winnie's double-injection groups (68%) after 30 min but higher in the Winnie's single-injection group for tibial sensory and motor block (48%) (P < 0.017).

Conclusion
Time to perform a parasacral block was short, and the parasacral approach had a high success rate and a short onset time. Therefore, this block might be a useful alternative to Winnie's modification for sciatic nerve block.
Overestimation of Bispectral Index in Sedated Intensive Care Unit Patients Revealed by Administration of Muscle Relaxant
Authors: Vivien Benoît , Di Maria Sophie , Ouattara Alexandre , Langeron Olivier , Coriat Pierre , Riou Bruno 
Published: November 2003

Background
Electromyographic activity has previously been reported to elevate the Bispectral Index (BIS) in patients not receiving neuromuscular blockade while under sedation in the intensive care unit. This study aimed to investigate the magnitude of the decrease of BIS following administration of muscle relaxant in sedated intensive care unit patients.

Methods
The authors prospectively investigated 45 patients who were continuously sedated with midazolam and sufentanil to achieve a Sedation-Agitation Scale value equal to 1 and who required administration of muscle relaxant. BIS (BIS version 2.10), electromyography, and acceleromyography at the adductor pollicis muscle were recorded simultaneously before and after neuromuscular blockade. Sixteen of these 45 patients were also studied simultaneously with the new BIS XP.

Results
After administration of a muscle relaxant, BIS (67 +/- 19 vs. 43 +/- 10, P < 0.001) and electromyographic activity (37 +/- 9 vs. 27 +/- 3 dB, P < 0.001) significantly decreased. Multiple regression analysis showed that the decrease of BIS following administration of myorelaxant was significantly correlated to BIS and electromyographic baseline values. Using standard BIS range guidelines, the number of patients under light or deep sedation versus general anesthesia or deep hypnotic state was markedly overestimated before administration of myorelaxant (53 vs. 2%, P < 0.001).

Conclusions
The BIS in sedated intensive care unit patients may be lower with paralysis for an equivalent degree of sedation because of high muscular activity. The magnitude of BIS overestimation is significantly correlated to both BIS and electromyographic activity before neuromuscular blockade. The authors conclude that clinicians who determine the amount of sedation in intensive care unit patients only from BIS monitoring may expose them to unnecessary oversedation.
Narcotrend Monitoring Allows Faster Emergence and a Reduction of Drug Consumption in Propofol–Remifentanil Anesthesia
Authors: Kreuer Sascha , Biedler Andreas , Larsen Reinhard , Altmann Simone , Wilhelm Wolfram 
Published: November 2003

Background
The Narcotrend is a new electroencephalographic monitor designed to measure depth of anesthesia, based on a six-letter classification from A (awake) to F (increasing burst suppression) including 14 substages. This study was designed to investigate the impact of Narcotrend monitoring on recovery times and propofol consumption in comparison to Bispectral Index (BIS) monitoring or standard anesthetic practice.

Methods
With institutional review board approval and written informed consent, 120 adult patients scheduled to undergo minor orthopedic surgery were randomized to receive a propofol-remifentanil anesthetic controlled by Narcotrend, by BIS(R), or solely by clinical parameters. Anesthesia was induced with 0.4 micro x kg-1 x min-1 remifentanil and a propofol target-controlled infusion at 3.5 microg/ml. After intubation, remifentanil was reduced to 0.2 micro x kg-1 x min-1, whereas the propofol infusion was adjusted according to clinical parameters or to the following target values: during maintenance to D(0) (Narcotrend) or 50 (BIS); 15 min before the end of surgery to C(1) (Narcotrend) or 60 (BIS). Recovery times were recorded by a blinded investigator, and average normalized propofol consumption was calculated from induction and maintenance doses.

Results
The groups were comparable for demographic data, duration of anesthesia, and mean remifentanil dosages. Compared with standard practice, patients with Narcotrend or BIS monitoring needed significantly less propofol (standard practice, 6.8 +/- 1.2 mg x kg-1 x h-1 vs. Narcotrend, 4.5 +/- 1.1 mg x kg-1 x h-1 or BIS(R), 4.8 +/- 1.0 mg x kg-1 x h-1; P < 0.001), opened their eyes earlier (9.3 +/- 5.2 vs. 3.4 +/- 2.2 or 3.5 +/- 2.9 min), and were extubated sooner (9.7 +/- 5.3 vs. 3.7 +/- 2.2 or 4.1 +/- 2.9 min).

Conclusions
The results indicate that Narcotrend and BIS monitoring are equally effective to facilitate a significant reduction of recovery times and propofol consumption when used for guidance of propofol titration during a propofol-remifentanil anesthetic.
Evaluation of a New Point-of-care Celite-activated Clotting Time Analyzer in Different Clinical Settings
Authors: Paniccia Rita , Fedi Sandra , Carbonetto Fiorella , Noferi Daniela , Conti Paolo , Bandinelli Brunella , Giusti Betti , Evangelisti Lucia , Pretelli Paola , Palmarini Mara F.G. , Abbate Rosanna , Prisco Domenico 
Published: November 2003

Background
Activated clotting time (ACT) is used to monitor heparin therapy during cardiopulmonary bypass, interventional cardiology, and hemodialysis. Traditionally, ACT is performed by use of the Hemochron system. Recently, a new device, the i-STAT system, has been introduced to measure ACT. The aim of this study was to correlate the performances of these two systems and to compare ACT values with heparin levels.

Methods
One hundred sixty-five samples from 29 patients undergoing cardiopulmonary bypass or hemodialysis were assayed in duplicate with two Hemochron and two i-STAT devices. Heparin levels were determined by anti-factor Xa assay.

Results
The Hemochron ACT ranged from 88 to 1,028 s, and the i-STAT ACT ranged from 80 to 786 s. Heparin plasma levels ranged from 0.01 to 10.8 U/mL. Bland-Altman analysis showed a mean difference between the two methods of 24 +/- 101 s. Strong relationships between anti-factor Xa activity and Hemochron ACTs (r2 = 0.69, P < 0.001) and i-STAT ACTs (r2 = 0.79, P < 0.001) were observed. During cardiac surgery, significant correlations were found: Hemochron, r2 = 0.61, P < 0.001 and i-STAT, r2 = 0.74, P < 0.001. During hemodialysis, relationships between anti-factor Xa activity and ACTs were found: Hemochron, r2 = 0.62, P < 0.001 and i-STAT, r2 = 0.55, P < 0.001.

Conclusions
During cardiopulmonary bypass procedure and hemodialysis, i-STAT provides measurements of clotting time quite similar to Hemochron ACT, which were significantly correlated with heparin levels.
Protection with Antibody to Tumor Necrosis Factor Differs with Similarly Lethal Escherichia coli versus Staphylococcus aureus Pneumonia in Rats
Authors: Karzai Waheedullah , Cui Xizhong , Mehlhorn Bjoern , Straube Eberhard , Hartung Thomas , Gerstenberger Eric , Banks Steven M. , Natanson Charles , Reinhart Konrad , Eichacker Peter Q. 
Published: November 2003

Background
Differing factors may alter the effects of antibody to tumor necrosis factor (TNF) in infection and sepsis. The authors tested whether bacteria type or treatment route alters antibody to TNF in a rat model of bacterial pneumonia.

Methods
Rats (n = 231) received similarly lethal doses of either intratracheal Escherichia coli or Staphylococcus aureus followed by treatment with either intratracheal or intraperitoneal antibody to TNF or control serum. Animals received antibiotics (cefotiam daily dose, 100 mg/kg) starting 4 h after inoculation and were studied for up to 96 h.

Results
Compared with S. aureus, E. coli increased serum TNF and interleukin-6 concentrations, lung lavage TNF concentrations, neutrophil counts, and alveolar-to-arterial oxygen gradients and decreased circulating neutrophils and lymphocytes (P > or = 0.05 for all). Compared with controls, with both bacteria, except for lung lavage TNF concentrations (which decreased with intratracheal but not with intraperitoneal antibody to TNF), treatment route did not alter the effects of antibody to TNF on any parameter (P = not significant for all). Antibody to TNF reduced mortality rates (relative risk of death +/- SEM) with both E. coli (-1.6 +/- 0.6; P = 0.006) and S. aureus (-0.5 +/- 0.04; P = 0.185), but these reductions were greater with E. coli than with S. aureus in a trend approaching statistical significance (P = 0.09). Compared with controls, similarly (P = not significant) with both bacteria, antibody to TNF decreased lung lavage and tissue bacteria concentrations (both P < 0.05) and serum TNF concentration (P < 0.09) and increased circulating neutrophils and lymphocytes (both P < or = 0.01). Compared with S. aureus, with E. coli antibody to TNF decreased alveolar-to-arterial oxygen gradients (P = 0.04) and increased serum interleukin-6 concentrations (P = 0.003).

Conclusion
Antibody to TNF improved host defense and survival rates with both lethal E. coli and S. aureus pneumonia, but protection was greater with E. coli, where TNF concentrations were higher than with S. aureus. The efficacy of antiinflammatory agents in sepsis may be altered by bacteria type.
Uterine Cervical Distension Induces cFos Expression in Deep Dorsal Horn Neurons of the Rat Spinal Cord
Authors: Tong Chuanyao , Ma Weiya , Shin Sang-Wook , James Robert L. , Eisenach James C. 
Published: November 2003

Background
Uterine cervical distension underlies labor pain, yet its neurophysiology and pharmacology of inhibition remain unexplored. The authors examined uterine cervical distension-evoked cFos immunoreactivity in rat spinal cords, and the inhibitory effect of spinal cyclo-oxygenase inhibition on cFos expression.

Methods
Female rats were anesthetized with halothane, and pairs of metal rods were inserted in each cervical os through a mid-line laparotomy. A submaximal distension force (75 g) was applied for either 30 or 60 min, or, in control animals, no force was applied. Other animals received cervical lidocaine infiltration prior to uterine cervical distension. At the end of the experiments, the spinal cord at T12 to L2 levels was harvested and immunostained for cFos protein. Other animals received intrathecal ketorolac (0, 5, 25, and 50 microg; n = 5-6 for each group) prior to uterine cervical distension.

Results
Uterine cervical distension significantly increased cFos immunoreactivity in the spinal cord from T12 to L2, with most cFos expression in the deep dorsal and central canal regions. Surgical preparation alone without uterine cervical distension resulted in minimal cFos expression, primarily in the superficial dorsal horn. Uterine cervical distension-evoked cFos expression was prevented by prior infiltration of lidocaine into the cervix. Intrathecal ketorolac produced a dose-dependent inhibition of uterine cervical distension-induced cFos expression.

Conclusion
The present study demonstrates that uterine cervical distension results in a similar pattern of spinal cord neuronal activation as seen with other noxious visceral stimuli. The inhibition of cFos expression by intrathecal ketorolac suggests that spinal cyclo-oxygenase plays a role in uterine cervical distension-induced nociception.