bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors Affecting Perioperative Transfusion Decisions in Patients with Coronary Artery Disease Undergoing Coronary Artery Bypass Surgery
Authors: Shehata Nadine , Wilson Kumanan , Mazer C David , Tomlinson George , Streiner David , Hebert Paul , Naglie Gary 
Published: June 2006

Background
A high proportion of patients having cardiac bypass surgery receive erythrocyte transfusions. Decisions about when to transfuse patients having surgery for coronary artery disease may impact on erythrocyte utilization and patient morbidity and mortality. There are no published data about the factors that influence physicians' decisions to transfuse erythrocytes to these patients. The objectives of this study were to determine the hemoglobin concentration for transfusion and the factors that influence physicians' perioperative transfusion decisions for coronary artery bypass patients.

Methods
The authors conducted a cross-sectional study using pretested, self-administered, mailed questionnaires sent in 2004 to all cardiac surgeons and anesthesiologists in Canada who participate in coronary artery bypass surgery. The questionnaire included four intraoperative and four postoperative vignettes. Factors assessed included patient age, sex, cardiac index, and myocardial ischemia.

Results
The response rates were 70% (345 of 489) for the intraoperative and 61% (297 of 489) for the postoperative case scenarios. The mean hemoglobin concentrations for transfusion were 7.0 g/dl for the intraoperative case scenarios and 7.2 g/dl for the postoperative case scenarios. Older age, the presence of myocardial ischemia, and a low cardiac index were factors that increased the hemoglobin concentration for transfusion (P < 0.0001). Physicians ranked myocardial ischemia as the most significant factor affecting their transfusion decisions.

Conclusions
Factors such as the presence of a low cardiac index, myocardial ischemia, and older age increase the hemoglobin concentrations at which physicians transfuse coronary bypass surgery patients. Future studies are required to elucidate whether transfusions based on these variables affect patient morbidity and mortality.
Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans
Authors: Mathru Mali , Solanki Daneshvari R. , Woodson Lee C. , Funston J Sean , Ozkan Orthan , Henkel Sheryl N. , Wang Deli , Gore Dennis , Prough Donald S. 
Published: June 2006

Background
In conscious humans, reduction in hemoglobin concentration to 5 g/dl did not produce inadequate systemic oxygenation. However, systemic measures of inadequate oxygenation may not be sufficiently sensitive to detect inadequate oxygenation in individual organs such as splanchnic organs. The authors tested the hypothesis that acute normovolemic anemia to hemoglobin less than 6.0 g/dl in anesthetized humans reduces splanchnic oxygen consumption because of diminished whole body oxygen delivery.

Methods
Elective spine (n = 12) and abdominal (n = 7) surgery patients underwent acute normovolemic anemia to decrease the hemoglobin concentration close to 6.0 g/dl. The authors assessed the development of supply-dependent conditions in systemic and regional vascular beds by two primary measures before and after acute normovolemic anemia: oxygen consumption and surrogate biochemical markers of anaerobic metabolism, including plasma lactate, regional lactate kinetics, and ketone body ratio.

Results
When hemoglobin was reduced from 13.6 +/- 1.2 to 5.9 +/- 0.3 g/dl, oxygen supply dependency occurred in the splanchnic and preportal tissues but not at the systemic level. Regional supply dependency was accompanied by biochemical markers of anaerobic metabolism.

Conclusions
In anesthetized humans, a reduction in hemoglobin to 5.9 g/dl by acute normovolemic anemia diminished splanchnic and preportal whole body oxygen delivery and impaired splanchnic and preportal oxygen consumption. This was accompanied by increased plasma levels of regional lactate and an increased beta-hydroxybutyrate-to-acetoacetate ratio. These findings suggest that the risk to the gastrointestinal tract during acute normovolemic anemia may be underestimated.
Effect of Propofol Anesthesia and Continuous Positive Airway Pressure on Upper Airway Size and Configuration in Infants
Authors: Crawford Mark W. , Rohan Denise , Macgowan Christopher K. , Yoo Shi-Joon , Macpherson Bruce A. 
Published: June 2006

Background
Infants are prone to obstruction of the upper airway during general anesthesia. Continuous positive airway pressure (CPAP) is often used to prevent or treat anesthesia-induced airway obstruction. The authors studied the interaction of propofol anesthesia and CPAP on airway caliber in infants using magnetic resonance imaging.

Methods
Nine infants undergoing elective magnetic resonance imaging of the brain were studied. Head position was standardized. Spin echo magnetic resonance images of the airway were acquired at the level of the soft palate, base of the tongue, and tip of the epiglottis. Four sets of images were acquired in sequence: (1) during light propofol anesthesia at an infusion rate of 80 microg . kg(-1) . min(-1), (2) after increasing the depth of propofol anesthesia by administering a bolus dose (2.0 mg/kg) and increasing the infusion rate to 240 microg . kg(-1) . min(-1), (3) during continued infusion of 240 microg . kg(-1). min propofol and application of 10 cm H2O CPAP, and (4) after removal of CPAP and continued infusion of 240 microg . kg(-1). min propofol.

Results
Increasing depth of propofol anesthesia decreased airway caliber at each anatomical level, predominantly due to anteroposterior narrowing. Application of CPAP completely reversed the propofol-induced decrease in airway caliber, primarily by increasing the transverse dimension.

Conclusions
Airway narrowing with increasing depth of propofol anesthesia results predominantly from a reduction in anteroposterior dimension, whereas CPAP acts primarily to increase the transverse dimension. Although airway caliber during deep propofol anesthesia and application of CPAP was similar to that during light propofol anesthesia, there were significant configurational differences.
Antagonistic Actions of Halothane and Sevoflurane on Spontaneous Ca2+Release in Rat Ventricular Myocytes
Authors: Graham Mark D. , Hopkins Philip M. , Harrison Simon M. 
Published: June 2006

Background
Halothane has been reported to sensitize Ca(2+) release from the sarcoplasmic reticulum (SR), which is thought to contribute to its initial positive inotropic effect. However, little is known about whether isoflurane or sevoflurane affect the SR Ca(2+) release process, which may contribute to the inotropic profile of these anesthetics.

Methods
Mild Ca(2+) overload was induced in isolated rat ventricular myocytes by increase of extracellular Ca(2+) to 2 mM. The resultant Ca(2+) transients due to spontaneous Ca(2+) release from the SR were detected optically (fura-2). Cells were exposed to 0.6 mM anesthetic for a period of 4 min, and the frequency and amplitude of spontaneous Ca(2+) transients were measured.

Results
Halothane caused a temporary threefold increase in frequency and decreased the amplitude (to 54% of control) of spontaneous Ca(2+) transients. Removal of halothane inhibited spontaneous Ca release before it returned to control. In contrast, sevoflurane initially inhibited frequency of Ca(2+) release (to 10% of control), whereas its removal induced a burst of spontaneous Ca(2+) release. Isoflurane had no significant effect on either frequency or amplitude of spontaneous Ca(2+) release on application or removal. Sevoflurane was able to ameliorate the effects of halothane on the frequency and amplitude of spontaneous Ca(2+) release both on application and wash-off.

Conclusions
Application of halothane and removal of sevoflurane sensitize the SR Ca(2+) release process (and vice versa on removal). Sevoflurane reversed the effects of halothane, suggesting they may act at the same subcellular target on the SR.
Flumazenil Mimics whereas Midazolam Abolishes Ischemic Preconditioning in a Rabbit Heart Model of Ischemia–Reperfusion
Authors: Rivo Julia , Raphael Jacob , Drenger Benjamin , Berenshtein Eduard , Chevion Mordechai , Gozal Yaacov 
Published: June 2006

Background
The goal of the current study was to assess the effects of flumazenil, a benzodiazepine receptor antagonist, in limiting infarct size and in reducing hydroxyl free radical production.

Methods
After intravenous salicylate (100 mg/kg) administration, rabbits were subjected to 40 min of regional myocardial ischemia and 2 h of reperfusion. In one group, flumazenil (0.05 mg/kg) and, in another, midazolam (0.05 mg/kg) was administered 15 min before 40 min of ischemia. Ischemic preconditioning (IP) was elicited by 5 min of ischemia followed by 10 min of reperfusion (before the 40-min ischemia period). In two other groups, midazolam was added to flumazenil and IP. Infarct size was determined using triphenyl tetrazolium chloride staining. The authors quantified the hydroxyl-mediated conversion of salicylate to its 2,3- and 2,5-dihydroxybenzoate derivatives during reperfusion by high-performance liquid chromatography coupled with electrochemical detection. Results are expressed as mean +/- SEM.

Results
Flumazenil, like IP, significantly decreased infarct size (23 +/- 4 and 22 +/- 5%, respectively, vs. 57 +/- 6% in control group; P < 0.01). Midazolam inhibited the effects of flumazenil and IP. Flumazenil and IP significantly limited the increase in the normalized concentrations of 2,3- and 2,5-dihydroxybenzoic acids. With midazolam, however, the increase was comparable to that of the control group. 5-Hydroxydecanoate, a selective mitochondrial adenosine triphosphate-sensitive K channel blocker, given with flumazenil, abolished the protection obtained with the latter.

Conclusions
Flumazenil mimics preconditioning to decrease infarct size and hydroxyl radical production during reperfusion. Midazolam, however, abolishes these effects. Blockade of benzodiazepine receptors is upstream to the mitochondrial adenosine triphosphate-sensitive K channels in the preconditioning cascade.
Noninvasive, Automated and Continuous Cardiac Output Monitoring by Pulmonary Capnodynamics
Authors: Peyton Philip J. , Venkatesan Yagnaprabhu , Hood Sally G. , Junor Paul , May Clive 
Published: June 2006

Background
Cardiac output monitoring is most important where cardiovascular stability is potentially threatened, such as during major surgery and in critically ill patients. However, continuous monitoring of cardiac output is still not performed routinely during anesthesia and critical care, because of invasiveness, expense, and inaccuracy of available technologies.

Methods
A technique termed the capnodynamic method was tested for breath-to-breath measurement of pulmonary blood flow from lung carbon dioxide mass balance, using measured carbon dioxide elimination and end-tidal concentration. A prototype measurement system was constructed for a feasibility study in six anesthetized sheep. Large and rapid fluctuations in cardiac output were generated by repeated dobutamine and esmolol challenge. Measurements were compared with an indwelling ultrasonic flow probe placed on the ascending aorta or pulmonary artery.

Results
Cardiac output measured by the flow probe varied between zero and 8.67 l/min, with a mean of 3.50 l/min. Overall mean bias [SD of the difference] between the methods (capnodynamic - flow probe) was -0.25 [0.94] l/min, r = 0.79 (P < 0.001). During periods of stability in cardiac output of 5 min or more, mean bias was -0.20 [0.55] l/min. The method successfully indicated two cardiac arrest events, which were induced in one of the animals.

Conclusions
The method satisfactorily tracked wide fluctuations in cardiac output in real time. The capnodynamic method may have potential for continuous noninvasive cardiac output monitoring in patients undergoing anesthesia for major surgery, and in critical care, on a routine basis.
Midazolam Inhibits Proinflammatory Mediators in the Lipopolysaccharide-activated Macrophage
Authors: Kim Seon Nyo , Son Soo Chang , Lee Sang Mook , Kim Cuk Seong , Yoo Dae Goon , Lee Sang Ki , Hur Gang Min , Park Jin Bong , Jeon Byeong Hwa 
Published: June 2006

Background
Midazolam, a benzodiazepine, has a hypnotic effect and is widely used as a sedative. The role of midazolam in activation of macrophages during sepsis is not known. The aim of this study was to evaluate the antiinflammatory actions of midazolam in cultured macrophages.

Methods
Using a macrophage cell line, RAW264.7 cells, the effect of midazolam on proinflammatory mediators and activation of mitogen-activated protein kinase was measured by Western blot. Nuclear factor-kappaB (NF-kappaB) activation and translocation of p65 subunit of NF-kappaB was measured using luciferase assay and immunocytochemistry. Superoxide production was measured by lucigenin chemiluminescence.

Results
Midazolam significantly inhibited lipopolysaccharide-induced up-regulation of both cyclooxygenase 2 and inducible nitric oxide synthase in a dose-dependent manner (approximately 3-30 microm). IkappaB-alpha degradation and NF-kappaB transcriptional activity induced by lipopolysaccharide were also suppressed by the midazolam. Nuclear translocation of the p65 subunit of NF-kappaB was inhibited by midazolam. Furthermore, midazolam suppressed phosphorylation of p38 mitogen-activated protein kinase and also inhibited lipopolysaccharide-induced superoxide production in macrophages.

Conclusions
These results suggest that midazolam has an antiinflammatory action by inhibiting inducible nitric oxide synthase and cyclooxygenase-2 expression, possibly through suppression of NF-kappaB and p38 mitogen-activated protein kinase activation.
Different Brain Activation Patterns to Pain and Pain-related Unpleasantness during the Menstrual Cycle
Authors: Choi Jae Chan , Park Sang Kyu , Kim Yun-Hee , Shin Yong-Wook , Kwon Jun Soo , Kim Jin Soo , Kim Ji-Woong , Kim Soon Yul , Lee Sang Gyu , Lee Moo Sam 
Published: June 2006

Background
The changes in the functional magnetic resonance imaging signal during anticipation, pain stimulation, and the poststimulation periods were investigated to determine whether changes in sex hormones affect brain activity.

Methods
Eighteen participants were examined twice, once in the follicular phase and once in the luteal phase. Half the participants were tested first during the follicular phase, and the other half were tested first in the luteal phase.

Results
The pain and unpleasantness ratings were significantly higher in the luteal phase than in the follicular. During the anticipation of pain, the prefrontal cortices were activated during the follicular phase, whereas the parahippocampal gyrus and amygdala were activated during the luteal phase. During the pain stimulation, putamen and cerebellum and precentral gyrus involving motor preparation and defense mechanism related to antinociceptive behavior were activated during the follicular phase, whereas the thalamus was activated during the luteal phase. During the poststimulation periods, the prefrontal cortices were activated during the follicular phase, whereas parahippocampal gyrus was activated during the luteal phase. The temporal pole was activated during the anticipation, pain stimulation, and poststimulation periods of the luteal phase.

Conclusions
During surgical and medical procedures, requirements of anesthetic and analgesic and anxiolytic drugs may be reduced during the follicular phase and increased during the luteal phase. These results highlight the need to consider the effects of the sex hormones in women when designing clinical or neuroimaging studies or when treating patients for pain and pain-related unpleasantness.
Effects of Bupivacaine and Tetrodotoxin on Carrageenan-induced Hind Paw Inflammation in Rats (Part 1)
Authors: Beloeil Hélène , Ababneh Zaid , Chung Richard , Zurakowski David , Mulkern Robert V. , Berde Charles B. 
Published: June 2006

Background
Local anesthetics exert antiinflammatory actions. To elucidate potential mechanisms, the authors examined effects of bupivacaine or tetrodotoxin, administered to rats by ipsilateral or contralateral sciatic blockade or systemically, on carrageenan-induced hind paw hyperalgesia, edema, and stimulated cytokine production in circulating blood cells.

Methods
Twelve groups of rats (n = 9-12) received injections in three sites: (1) right or left hind paw (carrageenan or saline), (2) left sciatic block, and (3) systemically (subcutaneously in the upper back). Sciatic and systemic injections were performed with epinephrine plus bupivacaine, tetrodotoxin, or saline; injections were repeated 6 h later. Fifteen hours later, hyperalgesia and/or sensory and motor block were assessed behaviorally, and paw edema was quantified by magnetic resonance imaging. Stimulated production of tumor necrosis factor alpha, interleukin 10, and interleukin 1beta in whole blood cultures was measured by enzyme-linked immunosorbent assay.

Results
Either ipsilateral or contralateral sciatic blocks using either bupivacaine or tetrodotoxin reduced carrageenan-induced edema and hyperalgesia. Systemic bupivacaine and tetrodotoxin were ineffective in preventing edema and hyperalgesia. Bupivacaine was effective in suppressing systemic tumor necrosis factor alpha and interleukin 1beta by all three routes, whereas tetrodotoxin was ineffective by all three routes.

Conclusion
Bupivacaine and tetrodotoxin, via a contralateral or ipsilateral sciatic block, attenuate local inflammatory edema and hyperalgesia induced by hind paw injection of carrageenan in rats. Mechanisms underlying contralateral effects of sciatic blockade remain unexplained. Bupivacaine inhibits carrageenan-evoked systemic cytokine production by a mechanism not shared by tetrodotoxin; this action may involve tetrodotoxin-resistant sodium channels or a variety of non-sodium-channel targets.
Permeability of Injured and Intact Peripheral Nerves and Dorsal Root Ganglia
Authors: Abram Stephen E. , Yi Johnny , Fuchs Andreas , Hogan Quinn H. 
Published: June 2006

Background
Nerve injury that produces behavioral changes of allodynia and hyperalgesia in animals is associated with electrophysiologic changes in dorsal root ganglion (DRG) cells. The introduction of drugs into the DRG or the peripheral nerve that alter calcium, sodium, or potassium channel activity may be of therapeutic benefit after nerve injury. For this reason, the authors sought to determine whether drugs that do not ordinarily cross the blood-nerve barrier will enter the DRG after intravenous or regional injection and to determine whether nerve injury alters drug access to DRGs or peripheral nerves.

Methods
Both intact and spinal nerve-ligated rats were injected with sodium fluorescein by intravenous, intrathecal, peri-DRG, perisciatic, and epidural routes. DRG, sciatic nerve, and spinal cord tissues were harvested and frozen, and histologic sections were analyzed quantitatively for tissue fluorescence.

Results
In both intact and nerve-injured animals, fluorescein accumulated in DRGs after intravenous, peri-DRG, and epidural injection. There was accumulation in the proximal portion of the ganglion after intrathecal injection. Minimal amounts of fluorescein were found in the sciatic nerve in intact animals after intravenous or perineural injection, but substantial amounts were found in some nerve fascicles in nerve-injured animals after both intravenous and perineural injection. There was almost no fluorescein found in the spinal cord except after intrathecal administration.

Conclusions
In both intact and nerve-injured animals, fluorescein accumulates freely in the DRG after intravenous, epidural, or paravertebral injection. The sciatic nerve is relatively impermeable to fluorescein, but access by either systemic or regional injection is enhanced after nerve injury.
Increased Prostaglandin E2Release and Activated Akt/β-Catenin Signaling Pathway Occur after Opioid Withdrawal in Rat Spinal Cord
Authors: Dunbar Stuart A. , Karamian Ivan , Roberts Lou , Zhang Jiahui 
Published: June 2006

Background
Prostaglandin E(2) is an important spinal modulator of nociception. However, the effects of chronic opioid administration and withdrawal on prostaglandin E(2) release and associated signaling pathways in the spinal cord are generally unknown.

Methods
This study sought to examine these effects using a spinal microdialysis technique in a model of chronic morphine administration and withdrawal in the rat.

Results
The authors found that spinal prostaglandin E(2) release was unaffected by chronic morphine treatment but was significantly increased during withdrawal. Recurrent withdrawal did not further enhance this release. The authors also found up-regulation of cyclooxygenase-2 expression and phosphorylation of protein kinase Akt at Ser-473 in response to opioid withdrawal. In addition, they demonstrated that beta-catenin, a transcription factor downstream of Akt, was induced during morphine withdrawal, particularly during recurrent withdrawal.

Conclusions
These results suggest that opioid withdrawal activates signaling pathways associated with neuronal survival and transcriptional control, two processes implicated in neuronal development and synaptic plasticity.
Painful Peripheral Nerve Injury Decreases Calcium Current in Axotomized Sensory Neurons
Authors: McCallum J Bruce , Kwok Wai-Meng , Sapunar Damir , Fuchs Andreas , Hogan Quinn H. 
Published: June 2006

Background
Reports of Ca(2+) current I(Ca) loss after injury to peripheral sensory neurons do not discriminate between axotomized and spared neurons. The spinal nerve ligation model separates axotomized from spared neurons innervating the same site. The authors hypothesized that I(Ca) loss is a result of neuronal injury, so they compared axotomized L5 dorsal root ganglion neurons to spared L4 neurons, as well as neurons from rats undergoing skin incision alone.

Methods
After behavioral testing, dissociated neurons from L4 and L5 dorsal root ganglia were studied in both current and voltage patch clamp modes. The biophysical consequence of I(Ca) loss on the action potential was confirmed using selective I(Ca) antagonists. Data were grouped into small, medium, and large cells for comparison.

Results
Reduced I(Ca) was predominantly a consequence of axotomy (L5 after spinal nerve ligation) and was most evident in small and medium neurons. ICa losses were associated with action potential prolongation in small and medium cells, whereas the amplitude and duration of after hyperpolarization was reduced in medium and large neurons. Blockade with Ca(2+) channel antagonists showed that action potential prolongation and after hyperpolarization diminution were alike, attributable to the loss of I(Ca).

Conclusion
Axotomy is required for I(Ca) loss. I(Ca) loss correlated with changes in the biophysical properties of sensory neuron membranes during action potential generation, which were due to I(Ca) loss leading to decreased outward Ca(2+)-sensitive K currents. Taken together, these results suggest that neuropathic pain may be mediated, in part, by loss of I(Ca) and the cellular processes dependent on Ca(2+).