bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Randomized, Double-masked, Multicenter Comparison of the Safety of Continuous Intrathecal Labor Analgesia Using a 28-Gauge Catheter versus Continuous Epidural Labor Analgesia
Authors: Arkoosh Valerie A. , Palmer Craig M. , Yun Esther M. , Sharma Shiv K. , Bates James N. , Wissler Richard N. , Buxbaum Jodie L. , Nogami Wallace M. , Gracely Edward J. 
Published: March 2009

Background
Continuous intrathecal labor analgesia produces rapid analgesia or anesthesia and allows substantial flexibility in medication choice. The US Food and Drug Administration, in 1992, removed intrathecal microcatheters (27-32 gauge) from clinical use after reports of neurologic injury in nonobstetric patients. This study examined the safety and efficacy of a 28-gauge intrathecal catheter for labor analgesia in a prospective, randomized, multicenter trial.

Methods
Laboring patients were randomly assigned to continuous intrathecal analgesia with a 28-gauge catheter (n = 329) or continuous epidural analgesia with a 20-gauge catheter (n = 100), using bupivacaine and sufentanil. The primary outcome was the incidence of neurologic complications, as determined by masked neurologic examinations at 24 and 48 h postpartum, plus telephone follow-up at 7-10 and 30 days after delivery. The secondary outcomes included adequacy of labor analgesia, maternal satisfaction, and neonatal status.

Results
No patient had a permanent neurologic change. The continuous intrathecal analgesia patients had better early analgesia, less motor blockade, more pruritus, and higher maternal satisfaction with pain relief at 24 h postpartum. The intrathecal catheter was significantly more difficult to remove. There were no significant differences between the two groups in neonatal status, post-dural puncture headache, hemodynamic stability, or obstetric outcomes.

Conclusions
Providing intrathecal labor analgesia with sufentanil and bupivacaine via a 28-gauge catheter has an incidence of neurologic complication less than 1%, and produces better initial pain relief and higher maternal satisfaction, but is associated with more technical difficulties and catheter failures compared with epidural analgesia.
The Common Inhalational Anesthetic Isoflurane Induces Apoptosis via Activation of Inositol 1,4,5-Trisphosphate Receptors
Authors: Wei Huafeng , Liang Ge , Yang Hui , Wang Qiujun , Hawkins Brian , Madesh Muniswamy , Wang Shouping , Eckenhoff Roderic G. 
Published: March 2009

Background
Isoflurane induces cell apoptosis by an unknown mechanism. The authors hypothesized that isoflurane activates inositol 1,4,5-trisphosphate (IP3) receptors on the endoplasmic reticulum (ER) membrane, causing excessive calcium release, triggering apoptosis.

Methods
The authors determined isoflurane-induced cytotoxicity by measuring caspase-3 activity, lactate dehydrogenase release, MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) reduction, and imaging analysis of cell damage markers (annexin V and propidium iodide staining) in different cell types. The authors used the chicken B lymphocyte with a total knock-out of IP3 receptors, PC12 cells with elevated IP3 receptor activity (transfected with L286V presenilin 1), striatal cells with a knock-in of Q111 Huntingtin, and each cell line's corresponding wild-type controls. The authors also measured the isoflurane-evoked changes of calcium concentration in cytosol and/or mitochondria in these cells.

Results
Isoflurane induced apoptosis concentration- and time-dependently, and sequentially elevated cytosolic and then mitochondrial calcium in the chicken B-lymphocyte wild-type but not the IP3 receptor total knock-out cells. Thapsigargin, a calcium adenosine triphosphatase inhibitor on ER membranes, induced apoptosis and elevations of calcium in cytosol and mitochondria in both chicken B-lymphocyte wild-type and IP3 receptor total knock-out cells. Isoflurane induced significantly more neurotoxicity and greater calcium release from the ER in L286V PC12 and Q111 Huntingtin striatal cells than in their corresponding wild-type controls, both of which were significantly inhibited by the IP3 receptor antagonist xestospongin C.

Conclusion
These findings suggest that isoflurane activates the ER membrane IP3 receptor, producing excessive calcium release and triggering apoptosis. Neurons with enhanced IP3 receptor activity, as in certain cases of familial Alzheimer or Huntington disease, may be especially vulnerable to isoflurane cytotoxicity.
Postconditioning Prevents Reperfusion Injury by Activating δ-Opioid Receptors
Authors: Jang Youngho , Xi Jinkun , Wang Huihua , Mueller Robert A. , Norfleet Edward A. , Xu Zhelong 
Published: March 2009

Background
While postconditioning has been proposed to protect the heart by targeting the mitochondrial permeability transition pore (mPTP), the detailed mechanism underlying this action is unknown. The authors hypothesized that postconditioning stimulates opioid receptors, which in turn protect the heart from reperfusion injury by targeting the mPTP.

Methods
Rat hearts (both in vivo and in vitro) were subjected to 30 min of ischemia and 2 h of reperfusion. Postconditioning was elicited by six cycles of 10-s reperfusion and 10-s ischemia. To measure nitric oxide concentration, cardiomyocytes loaded with 4-amino-5-methylamino-2',7'-difluorofluorescein were imaged using confocal microscopy. Mitochondrial membrane potential was determined by loading cardiomyocytes with tetramethylrhodamine ethyl ester.

Results
In open chest rats, postconditioning reduced infarct size, an effect that was reversed by both naloxone and naltrindole. The antiinfarct effect of postconditioning was also blocked by the mPTP opener atractyloside. In isolated hearts, postconditioning reduced infarct size. Morphine mimicked postconditioning to reduce infarct size, which was abolished by both naltrindole and atractyloside. N-nitro-l-arginine methyl ester and guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one blocked the action of morphine. Further experiments showed that morphine produces nitric oxide in cardiomyocytes by activating delta-opioid receptors. Moreover, morphine could prevent hydrogen peroxide-induced collapse of mitochondrial membrane potential in cardiomyocytes, which was reversed by naltrindole, N-nitro-l-arginine methyl ester, and the protein kinase G inhibitor KT5823.

Conclusions
Postconditioning protects the heart by targeting the mPTP through activation of delta-opioid receptors. The nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway may account for the effect of postconditioning on the mPTP opening.
Intermitted Pharmacologic Pretreatment by Xenon, Isoflurane, Nitrous Oxide, and the Opioid Morphine Prevents Tumor Necrosis Factor α–induced Adhesion Molecule Expression in Human Umbilical Vein Endothelial Cells
Authors: Weber Nina C. , Kandler Jennis , Schlack Wolfgang , Grueber Yvonne , Fräßdorf Jan , Preckel Benedikt 
Published: March 2009

Background
The barrier properties of the endothelium are of critical importance during pathophysiologic processes. These barrier properties depend on an intact cytoskeleton and are regulated by cell adhesion molecules. Tumor necrosis factor alpha (TNF-alpha) is known to induce cell adhesion molecule expression. In myocardium, the protective effect by xenon and isoflurane preconditioning was found to be linked to the cytoskeleton. The authors investigated the impact of different anesthetics and morphine on TNF-alpha-induced endothelial cell adhesion molecule expression.

Methods
Human umbilical vein endothelial cells were isolated from three different preparations. Cells were either left untreated or pretreated with xenon, nitrous oxide, isoflurane (each 0.43 minimum alveolar concentration), or morphine (100 ng/ml) and stimulated with 10 ng/ml TNF-alpha. Reverse-transcription polymerase chain reaction and fluorescence-activated cell sorting of intracellular cell adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin were performed. Transcriptional activity of nuclear factor kappaB was assessed by infrared electrophoretic mobility shift assay.

Results
Tumor necrosis factor alpha significantly induced messenger RNA (mRNA) and protein expression of cell adhesion molecules as well as transcriptional activity of nuclear factor kappaB. All four agents prevented TNF-alpha-induced mRNA and protein expression of intracellular cell adhesion molecule 1. Vascular cell adhesion molecule 1 expression was only blocked by the inhalational anesthetics and not by morphine. None of the four agents had an effect on TNF-alpha induced E-selectin expression. TNF-alpha-induced transcriptional activity of nuclear factor kappaB was decreased by all four agents.

Conclusion
These results suggest a protective effect of anesthetics on TNF-alpha-induced endothelial cell damage.
Effect of Dexmedetomidine on Cerebral Blood Flow Velocity, Cerebral Metabolic Rate, and Carbon Dioxide Response in Normal Humans
Authors: Drummond John C. , Dao Andrew V. , Roth David M. , Cheng Ching-Rong , Atwater Benjamin I. , Minokadeh Anushirvan , Pasco Leonardo C. , Patel Piyush M. 
Published: March 2009

Background
Dexmedetomidine reduces cerebral blood flow (CBF) in humans and animals. In animal investigations, cerebral metabolic rate (CMR) was unchanged. Therefore, the authors hypothesized that dexmedetomidine would cause a decrease in the CBF/CMR ratio with even further reduction by superimposed hyperventilation. This reduction might be deleterious in patients with neurologic injuries.

Methods
Middle cerebral artery velocity (CBFV) was recorded continuously in six volunteers. CBFV, jugular bulb venous saturation (Sjvo2), CMR equivalent (CMRe), and CBFV/CMRe ratio were determined at six intervals before, during, and after administration of dexmedetomidine: (1) presedation; (2) presedation with hyperventilation; at steady state plasma levels of (3) 0.6 ng/ml and (4) 1.2 ng/ml; (5) 1.2 ng/ml with hyperventilation; and (6) 30 min after discontinuing dexmedetomidine. The slope of the arterial carbon dioxide tension (Paco2)-CBFV relation was determined presedation and at 1.2 ng/ml.

Results
CBFV and CMRe decreased in a dose-related manner. The CBFV/CMRe ratio was unchanged. The CBFV response to carbon dioxide decreased from 1.20 +/- 0.2 cm.s.mm Hg presedation to 0.40 +/- 0.15 cm.s.mm Hg at 1.2 ng/ml. Sjvo2 was statistically unchanged during hyperventilation at 1.2 ng/ml versus presedation (50 +/- 11 vs. 43 +/- 5%). Arousal for hyperventilation at 1.2 ng/ml resulted in increased CBFV (30 +/- 5 to 38 +/- 4) and Bispectral Index (43 +/- 10 to 94 +/- 3).

Conclusions
The predicted decrease in CBFV/CMRe ratio was not observed because of an unanticipated reduction of CMRe and a decrease in the slope of the Paco2-CBFV relation. CBFV and Bispectral Index increases during arousal for hyperventilation at 1.2 ng/ml suggest that CMR-CBF coupling is preserved during dexmedetomidine administration. Further evaluation of dexmedetomidine in patients with neurologic injuries seems justified.
Concentration–Effect Relations, Prediction Probabilities (Pk), and Signal-to-noise Ratios of Different Electroencephalographic Parameters during Administration of Desflurane, Isoflurane, and Sevoflurane in Rats
Authors: Ihmsen Harald , Schywalsky Michael , Plettke Regina , Priller Michael , Walz Florian , Schwilden Helmut 
Published: March 2009

Background
The authors investigated the suitability of different electroencephalographic parameters to quantify the anesthetic effect of desflurane, isoflurane, and sevoflurane in rats.

Methods
Ten male Sprague-Dawley rats were anesthetized in a randomized crossover design with maximum values of 11% desflurane, 2.1% isoflurane, and 3.5% sevoflurane. The electroencephalogram was recorded with implanted electrodes and a wireless telemetry system. Concentration-effect relations and signal-to-noise ratios were determined for the approximate entropy and for the median frequency and the spectral edge frequency, which were modified to account for spikes and burst suppression. The prediction probability Pk with respect to the response to a painful stimulus was determined.

Results
All drugs produced deep anesthesia with burst suppression and no response at the highest concentrations. The occurrence of spikes and burst suppression made a modification of median frequency and spectral edge frequency necessary to obtain Pk values greater than 0.5 and monotonic sigmoid concentration-effect relations. The Pk values were between 0.89 and 0.98, with significantly higher values for modified median frequency and spectral edge frequency during desflurane and sevoflurane. The signal-to-noise ratios were between 3.0 and 6.4 dB, with significantly better values for modified spectral edge frequency and approximate entropy during sevoflurane.

Conclusions
If modified for spikes and burst suppression, median frequency and spectral edge frequency as well as the unmodified approximate entropy were able to assess the anesthetic effect of desflurane, isoflurane, and sevoflurane in rats. For sevoflurane, the modified spectral edge frequency was best with regard to signal-to-noise ratio and prediction probability.
Brain Maturation of Preterm Newborn Babies: New Insights
Authors: Ramenghi Luca A , Fumagalli Monica , Bassi Laura , Groppo Michela , De Carli Agnese , Fanaro Silvia , Mosca Fabio 
Published: March 2009

ABSTRACTPreterm birth still results in a high number of neurodevelopmental sequelae, although major forms of brain lesions—such as periventricular leukomalacia and intraventricular hemorrhage—are significantly reduced in this population of babies compared with a few years ago. This paper focuses on the possible reasons for this phenomenon. Some brain lesions, such as those affecting the periventricular white matter and the cerebellum, may be underestimated if magnetic resonance imaging is not used. In addition, a functional neurological consequence is not necessarily due to a recognized brain lesion, but may simply derive from an abnormally or suboptimally developed brain structure. The quality of nutrition given to a preterm baby could play a crucial role in such cases. In fact, nutrition is known to affect brain function; a case in point is the improvement in visual function resulting from dietary essential fatty acids. Finally, research in this area should aim at both reducing potential hazards and improving the quality of perinatal care, including the quality of nutrition.
Protective Effects of L‐Arginine on Rat Terminal Ileum Subjected to Ischemia/Reperfusion
Authors: Sayan Hale , Ozacmak V Haktan , Altaner Semsi , Aktas R Gulhan , Arslan S Oktay 
Published: March 2009

ABSTRACTObjectives:Studies have shown that nitric oxide (NO) may play a major role in sustaining mucosal integrity; however, NO has been also implicated in the pathogenesis of ischemia/reperfusion (I/R)–related tissue injury. We investigated the effects of L‐arginine andNG‐nitro L‐arginine methyl ester (L‐NAME) on the acetylcholine‐induced contractile response of ileum and the levels of malondialdehyde (MDA) and reduced glutathione (GSH). Histopathological changes were also evaluated in ileal preparations.Materials and Methods:Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3 hours). Four groups were designed: sham‐operated control; I/R; I/R and L‐arginine pretreatment; and I/R and L‐NAME pretreatment. After reperfusion, ileum specimens were collected to determine the parameters mentioned above.Results:Following reperfusion, a significant decrease in acetylcholine‐induced contractile response, an increase in lipid peroxidation, a decrease in GSH content, and mucosal damage of the ileal preparations were observed. We showed that decreased contractility, increased lipid peroxidation, and reduced GSH content have been reversed by L‐arginine but not by L‐NAME. Mucosal injury was significantly lowered in the L‐arginine group.Conclusions:Treatment with L‐arginine exerted a protective effect in intestinal I/R injury, which was mediated in part by regulating MDA and GSH levels, consequently ameliorating impaired contractile response and mucosal injury.
Pilot Evaluation of an Instrument to Measure Quality of Life in British Children With Inflammatory Bowel Disease
Authors: Ogden Cassandra Anne , Abbott Janice , Aggett Peter , Derkx Bert H , Maity Santanu , Thomas Adrian G 
Published: March 2009

ABSTRACTThe IMPACT questionnaire was developed in Canada to measure quality of life in children with inflammatory bowel disease (IBD). In the present study, 20 children with IBD completed 2 versions of the IMPACT questionnaire with a Likert scale or visual analog scale (VAS), 5 of whom expressed problems with language or phrasing. Difficult words included “restrictions,” “moderate,” “diarrhea,” “school break,” and the abbreviation “IBD.” Fifteen children preferred the Likert scale to the VAS (χ2 = 20, P < 0.01). Rewording the difficult words and using a Likert scale should facilitate completion of the IMPACT questionnaire in the United Kingdom. Further validation is needed to ensure that the instrument is reliable and valid.
Quantitation of the Effect of Nitrous Oxide on Rocuronium Infusion Requirements Using Closed-loop Feedback Control
Authors: Illman Hanna , Antila Heikki , Olkkola Klaus T. 
Published: March 2009

Background
Nitrous oxide has a minor effect on the effective dose 50% values of bolus doses of rocuronium. The authors have studied the effect of nitrous oxide on the infusion requirements of rocuronium using closed-loop feedback control of rocuronium infusion.

Methods
The authors obtained institutional approval and informed consent to study 70 patients. The patients were given total intravenous anesthesia with propofol and remifentanil by target-controlled infusion and were randomly assigned to one of two groups, one receiving nitrous oxide with 30% oxygen (n = 35) and the other group receiving air with 30% oxygen (n = 35). The possible interaction of rocuronium with nitrous oxide was quantitated by determining the asymptotic steady state rate of infusion of rocuronium necessary to produce a constant 90% neuromuscular block. This was accomplished by applying nonlinear curve fitting to data on the cumulative dose requirement during the initial 90-min period after bolus administration of rocuronium.

Results
Patient characteristics and controller performance, i.e., the ability of the controller to maintain the neuromuscular block constant at the set point, did not differ significantly between the groups. The administration of nitrous oxide did not affect rocuronium infusion requirements. The mean steady state rates of infusion were 33.0 +/- 9.8 and 36.9 +/- 13.2 mg/h in the nitrous oxide-total intravenous anesthesia and air-total intravenous anesthesia groups, respectively.

Conclusions
Nitrous oxide does not affect the infusion requirements of rocuronium to a clinically significant degree.
Transient Hyperglycemia Affects the Extent of Ischemia-Reperfusion-induced Renal Injury in Rats
Authors: Hirose Ryutaro , Xu Fengyun , Dang Kim , Liu Tao , Behrends Matthias , Brakeman Paul R. , Wiener-Kronish Jeanine , Niemann Claus U. 
Published: March 2009

Background
Chronic hyperglycemia is known to increase renal injury, particularly during ischemia-reperfusion episodes. The goal of this study was to examine whether transient hyperglycemia during or after renal ischemia-reperfusion increased renal dysfunction.

Methods
Male Lewis rats underwent sham operations or unilateral nephrectomies followed by contralateral renal ischemia-reperfusion. Hyperglycemic rats were given 25% dextrose to induce transient hyperglycemia lasting throughout the duration of ischemia (PI rats) or beginning 2 h after initiation of reperfusion (PR rats). Additional vehicle control rats received saline and underwent ischemia-reperfusion surgery as with PI and PR rats. Twenty-five minutes of mild renal ischemia followed by 24 h of reperfusion was induced by occluding the renal artery and vein.

Results
Terminal serum creatinine concentrations were significantly higher in the PI rats when compared with the PR or vehicle control rats. Histology demonstrated significantly increased necrosis in the PI rats relative to PR and control animals. Tissue analyses demonstrated significantly higher heat shock protein 70, heat shock protein 32, and cleaved caspase-3 protein levels in the PI rats. Oxidative stress generated through the xanthine pathway in the PI group was significantly increased compared with the oxidative stress in the PR and vehicle control rats. In contrast, vascular endothelial growth factor and erythropoietin were significantly decreased in the PI rats compared with the PR rats and controls.

Conclusions
Hyperglycemia that occurred during renal ischemia-reperfusion resulted in severe functional injury compared with normoglycemia or with hyperglycemia that occurred after reperfusion. Investigated molecular pathways are more profoundly affected by hyperglycemia that occurs before renal ischemia-reperfusion.
Alteration of the Piglet Diaphragm Contractility In Vivo and Its Recovery after Acute Hypercapnia
Authors: Jaber Samir , Jung Boris , Sebbane Mustapha , Ramonatxo Michèle , Capdevila Xavier , Mercier Jacques , Eledjam Jean-Jacques , Matecki Stefan 
Published: March 2009

Background
The effects of hypercapnic acidosis on the diaphragm and its recovery to normocapnia have been poorly evaluated. The authors studied diaphragmatic contractility facing acute variations of arterial carbon dioxide tension (Paco2) and evaluated the contractile function at 60 min after normocapnia recovery.

Methods
Thirteen piglets weighing 15-20 kg were anesthetized, ventilated, and separated into two groups: a control group (n = 5) evaluated in normocapnia (time-control experiments) and a hypercapnia group (n = 8) in which animals were acutely and shortly exposed to five consecutive ranges of Paco2 (40, 50, 70, 90, and 110 mmHg). Then carbon dioxide insufflation was stopped. Diaphragmatic contractility was assessed by measuring transdiaphragmatic pressure variations obtained after bilateral transjugular phrenic nerve pacing at increased frequencies (20-120 Hz). For each level of arterial pressure of carbon dioxide, pressure-frequency curves were obtained in vivo by phrenic nerve pacing.

Results
In the hypercapnia group, mean +/- SD transdiaphragmatic pressure significantly decreased from 41 +/- 3 to 29 +/- 3 cm H2O (P < 0.05) between the first (40 mmHg) and fifth (116 mmHg) stages of capnia at the frequency of 100 Hz stimulation. The observed alteration of the contractile force was proportional to the level of Paco2 (r = 0.61, P < 0.01). Normocapnia recuperation allowed a partial recovery of the diaphragmatic contractile force (80% of the baseline value) at 60 min after carbon dioxide insufflation interruption.

Conclusion
A short exposure to respiratory acidosis decreased diaphragmatic contractility proportionally to the degree of hypercapnia, and this alteration was only partially reversed at 60 min after exposure.