bluuebunny/crossref_metadata_2025_split huggingface dataset:
Internal Jugular Vein and Carotid Artery Anatomic Relation as Determined by Ultrasonography
Authors: Troianos Christopher A. , Kuwik Richard J. , Pasqual John R. , Lim Alexander J. , Odasso David P. 
Published: November 2003

Background
Cannulation of the internal jugular vein (IJV) is associated with a 95% success rate when external landmarks are used. Anatomic variability has been implicated as the cause for difficulty in cannulation without ultrasound. In contrast to an IJV located lateral to the carotid artery (CA), an IJV overlying the CA may result in CA puncture. The authors' purpose in this study was to examine, using ultrasound, the anatomic relation of the IJV and CA as viewed from the perspective of a cannulating needle.

Methods
Ultrasound imaging was used in 1,136 patients to examine the relation between the IJV and CA. A 7.5-MHz transducer was placed in the direction of a cannulating needle on the right neck at the apex of the angle formed by the division of the sternocleidomastoid muscle. A Polaroid photograph of the image was later scored by three blinded investigators according to the percentage of the CA overlaid by the IJV (0 to 4).

Results
Of the 1,136 Polaroid photographs of the ultrasound images, 1,009 were suitable for scoring. Fifty-four percent of all patients received a score of 4, which indicated that the IJV overlies more than 75% of the CA in an imaging plane positioned in the direction of a cannulating needle. Patients older than 60 yr were more likely to have this anatomy than patients younger than 60 yr (P < 0.05). None of the other patient characteristics recorded were predictive of this anatomic relation.

Conclusions
In a majority of patients, the IJV is not lateral to the CA in an ultrasound imaging plane positioned in the direction of a cannulating needle. Instead, the IJV overlies the CA in 54% of patients overall, predisposing these patients to CA puncture if the cannulating needle traverses the IJV.
Direct Inhibitory Mechanisms of Halothane on Human Platelet Aggregation
Authors: Kohro Shinji , Yamakage Michiaki 
Published: November 2003

Background
Although halothane directly inhibits platelet aggregation, the mechanisms of this effect are still unknown. The current study aimed to clarify the inhibitory mechanisms of halothane on thrombin-induced human platelet aggregation by measuring (1) platelet-surface glycoprotein Ib expression, (2) the concentration of intracellular free Ca2+ ([Ca2+]i) measured simultaneously with aggregation, (3) the concentration of intracellular inositol 1,4,5-triphosphate, and (4) the concentration of intracellular cyclic 3',5'-adenosine monophosphate ([cAMP]i).

Methods
Washed platelet suspensions, obtained from healthy volunteers, were preincubated with halothane (0-2 mM) for 2 min and then exposed to 0.02 units/ml thrombin for 3 min. The glycoprotein Ib bound to fluorescein-labeled antibody was measured by fluorescence flow cytometry. [Ca2+]i was measured, simultaneously with aggregation, in Fura-2 (Ca2+ indicator)-loaded platelets by use of a fluorometer. Inositol 1,4,5-triphosphate and [cAMP]i were measured by radioimmunoassay.

Results
Halothane had no effect on glycoprotein Ib expression with or without thrombin. Halothane decreased the thrombin stimulated [Ca2+]i transient and inhibited platelet aggregation in a dose-dependent manner, both in the presence and in the absence of external Ca2+. Isoflurane had no apparent effect on either platelet aggregation or [Ca2+]i in the absence of external Ca2+. Halothane inhibited the increase in inositol 1,4,5-triphosphate induced by thrombin. Halothane moderately but significantly increased [cAMP]i, but the adenylate cyclase activator forskolin (which has the same inhibitory ability on aggregation as halothane) increased [cAMP]i to a much greater extent than did halothane.

Conclusions
Halothane inhibits thrombin-induced human platelet aggregation by decreasing [Ca2+]i without inhibiting agonist-receptor binding; the inhibitory effect of halothane on [Ca2+]i might be mediated by a decrease in inositol 1,4,5 triphosphate and in part by an increase in [cAMP]i.
Acetylcholine Stimulates the Release of Nitric Oxide from Rat Spinal Cord
Authors: Xu Zemin , Tong Chuanyao , Eisenach James C. 
Published: November 2003

Background
Acetylcholine causes synthesis of nitric oxide in vascular endothelium, and presumptive evidence in vivo suggests spinally released acetylcholine causes antinociception and increased sympathetic nervous system activity via a nitric oxide mechanism. The purpose of this study was to determine, using a recently described bioassay system, whether acetylcholine stimulates nitric oxide release from spinal cord tissue in vitro.

Methods
Rat thoracolumbar spinal cord slices were incubated in a tissue chamber and perfused with Krebs-Henseleit solution. The perfusate was then passed through endotheliumdenuded rat aortic rings and their tension was measured. Vascular rings were preconstricted with phenylephrine, then were exposed to spinal cord perfusate with increasing concentrations (10(-12)-10(-4)M) of acetylcholine alone or with various antagonists.

Results
Acetylcholine perfusion of spinal tissue caused concentration-dependent relaxations of the aortic rings, an effect blocked by each of the muscarinic antagonists, atropine, pirenzepine, and AFDX-116. Acetylcholine-induced relaxation also was antagonized by an inhibitor of nitric oxide synthase (N-methyl-L-arginine), a nitric oxide scavenger (hemoglobin) and an inhibitor of guanylate cyclase (methylene blue).

Conclusions
These results demonstrate release of a vasorelaxant from spinal cord tissue by acetylcholine, which results from an action on muscarinic receptors and exhibits a pharmacology consistent with nitric oxide. Although precise anatomic localization of acetylcholine's action is not possible with this system, these results add to evidence that acetylcholine causes nitric oxide synthesis in the spinal cord.
Nitrous Oxide Depresses Spinal F Waves in Rats
Authors: Friedman Yaron , King Bryan S. , Rampil Ira J. 
Published: November 2003

Background
Evoked, recurrent electromyographic activity (F waves) reflect alpha-motor neuron excitability. Based on observations that other inhaled anesthetics do so, we hypothesized that nitrous oxide, alone or in combination with isoflurane, would depress F-wave activity and correlate with depression of movement response to tail clamp or electric stimulation.

Methods
In study 1, the authors examined the effect of nitrous oxide in combination with isoflurane in 13 normocapnic Sprague-Dawley rats anesthetized with 1.0% isoflurane (0.7 minimum alveolar concentration) in oxygen. The tibial nerve was stimulated at the popliteal fossa, and evoked electromyographic activity [M (direct neuromuscular junctional response) and F waves] were recorded from ipsilateral foot muscles. The effect of the addition of 30% or 70% nitrous oxide was measured. F-wave amplitude/M-wave amplitude ratio (F/M) was determined from each stimulus-electromyographic response pair. F/M vs. movement response to 60-s tail clamp was assessed after each recording session. F-wave amplitude/M-wave amplitude ratio at adjacent doses that permitted and prevented movement were compared. In study 2, the authors examined the effect of (hyperbaric) nitrous oxide as the sole anesthetic agent on F waves. In 11 rats anesthetized with isoflurane, stimulation and recording electrodes were placed as described above, with additional electrodes for stimulation placed in the tail. Rats were placed in a pressure chamber pressurized with nitrous oxide/oxygen to 3.4 atm. Thirty m were allowed for isoflurane washout. Electromyographic activity was evoked and recorded at 1.0, 1.6, 2.2 and 2.7 atm N2O (random order). Movement in response to 60 s of 15 V, 50-Hz tail stimulation was evaluated after each recording session.

Results
Nitrous oxide with or without isoflurane produced a dose-dependent decrease in F/M. By interpolation of this data, the authors found that 2 atm N2O alone, or 44% N2O added to 1.0% isoflurane at 1.0 atm, produced 1.0 minimum alveolar concentration anesthesia. At the deepest level of isoflurane/ nitrous oxide that permitted movement, mean F/M was 20.6 +/- 17.5%; at the lowest concentration that blocked movement, rats had a mean F/M of 13.7 +/- 13.9% (P = 0.01). At the minimal hyperbaric nitrous oxide blocking movement, rats had a mean F/M of 3.7 +/- 2.9%, whereas the F/M at the highest nitrous oxide dose that permitted movement was 4.4 +/- 2.7% (P < 0.04).

Conclusions
Because nitrous oxide depressed F-wave but not M-wave activity, the data suggest a central (spinal) rather than neuromuscular junctional site of action of this agent. The direct correlation between nitrous oxide dose, F-wave amplitude depression, and surgical immobility suggests the possibility of using F-wave activity to predict the likelihood of anesthetic-induced immobility. However, the mechanism of action of nitrous oxide may differ from that of the potent inhaled agents.
Effects of Hypothermia, Pentobarbital, and Isoflurane on Postdepolarization Amino Acid Release during Complete Global Cerebral Ischemia
Authors: Nakashima Ken , Todd Michael M. 
Published: November 2003

Background
Hypothermia and anesthetics may protect the brain during ischemia by blocking the release of excitatory amino acids. The effects of hypothermia (28 degrees C), pentobarbital, and isoflurane on postischemic excitatory amino acid concentrations were compared.

Methods
Rats were anesthetized with 0.8% halothane/50% N2O, vascular catheters were placed, and a glass microelectrode and microdialysis cannula were inserted into the cerebral cortex. Experimental groups were: (1) control, pericranial, t = 38 degrees C; (2) hypothermia, t = 28 degrees C; (3) pentobarbital, t = 38 degrees C; and (4) isoflurane, t = 38 degrees C. Halothane/N2O was continued in groups 1 and 2, whereas a deep burst-suppression or isoelectric electroencephalogram was achieved with the test drugs in groups 3 and 4. Cerebral metabolic rates were similar in groups 2, 3, and 4. After a baseline dialysis sample was collected, animals were killed with potassium chloride. The time to terminal depolarization was recorded, after which three consecutive 10-min dialysate samples were collected. Glutamate, aspartate, gamma-aminobutyric acid, and glycine concentrations were measured using high-performance liquid chromatography.

Results
Times to terminal depolarization were shorter in both pentobarbital and isoflurane groups than with hypothermia (103 +/- 15 and 127 +/- 10 vs. 195 +/- 20 s respectively, mean +/- SD). However, times to terminal depolarization in all three groups were longer than in control subjects (control = 70 +/- 9s). Postdepolarization concentrations of all compounds were lower in hypothermic animals (vs. normothermic control animals), but no reductions in glutamate, aspartate, or glycine concentrations were noted in pentobarbital or isoflurane groups. gamma-Aminobutyric acid concentrations were reduced by both anesthetics, but not to the same degree as with hypothermia.

Conclusions
Pentobarbital and isoflurane prolonged the time to terminal depolarization, but did not influence the rate at which the extracellular concentrations of glutamate, aspartate, or glycine increased. By contrast, hypothermia reduced the release of all excitatory amino acids. These differences may explain the greater protective efficacy of hypothermia in the face of cerebral ischemia.
Cardiac Risk of Noncardiac Surgery in Patients with Asymmetric Septal Hypertrophy
Authors: Haering Michael J. , Comunale Mark E. , Parker Robert A. , Lowenstein Edward , Douglas Pamela S. , Krumholz Harlan M. , Manning Warren J. 
Published: November 2003

Background
Many data are available regarding cardiac risk in patients with coronary artery disease undergoing noncardiac surgery, but few data are available regarding risk for patients with hypertrophic cardiomyopathy and asymmetric septal hypertrophy.

Methods
Seventy-seven patients with asymmetric septal hypertrophy were identified in whom an echocardiogram had been performed within 24 months of noncardiac surgery. Patients' charts were reviewed for data regarding surgical operations, including length of surgery, type of anesthesia, and intravascular monitoring used. Data regarding adverse perioperative cardiac events also were gathered.

Results
Forty percent (n = 31) of patients had one or more adverse perioperative cardiac events, including one patient who had a myocardial infarction and ventricular tachycardia that required emergent cardioversion. There were no perioperative deaths. All 31 patients had minor outcomes. Of the 77 patients, perioperative congestive heart failure developed in 12 (16%). Factors associated with adverse cardiac events were increasing length of surgical time (P < 0.01) major surgery (P < 0.05), and intensity of monitoring (P < 0.05). Age, gender, resting outflow tract gradient, systolic anterior motion of the anterior mitral leaflet, prior myocardial infarction, severity of mitral regurgitation, type of anesthetic, septal thickness, and the interval between echocardiogram and surgery were not associated with the occurrence of adverse cardiac events.

Conclusion
Patients with asymmetric septal hypertrophy undergoing noncardiac surgery have a high incidence of adverse cardiac events, frequently manifested as congestive heart failure. However, irreversible cardiac morbidity and mortality was extremely low. Important independent risk factors for adverse outcome in all patients include major surgery and increasing duration of surgery.
Epidural Meperidine after Cesarean Section
Authors: Ngan Kee Warwick D. , Lam Kwok K. , Chen Phoon P. , Gin Tony 
Published: November 2003

Background
Epidural meperidine is effective for postoperative analgesia, but the optimum dose has not been evaluated.

Methods
Five doses of epidural meperidine (12.5, 25, 50, 75, and 100 mg) given at the first request for analgesia after cesarean section were compared. Visual analog pain scores, duration of analgesia as defined by time to first patient-controlled epidural analgesia demand, plasma concentrations of meperidine, side effects, and subsequent 24-h consumption of meperidine were evaluated.

Results
All doses were effective, but patients took longer to become pain-free after 12.5 mg (median 30 min) compared with 25 mg (median 12 min, P = 0.038), and duration of analgesia was shorter after 12.5 mg (median 83 min) compared with 25 mg (median 165 min, P = 0.0005). Increasing dose to more than 25 mg did not improve onset or duration of analgesia. Plasma concentrations of meperidine were less than minimum effective analgesia concentration for all doses except 100 mg. There was more frequent nausea (P = 0.004) and dizziness (P = 0.0002) after 100 mg compared with smaller doses.

Conclusions
Epidural meperidine provides effective postoperative analgesia, although of relatively short duration. A single dose of 25 mg is superior to 12.5 mg, but there is no benefit from increasing the dose to 50 mg or greater.
Acute Pain and Central Nervous System Arousal Do Not Restore Impaired Hypoxic Ventilatory Response during Sevoflurane Sedation
Authors: Sarton Elise , Dahan Albert , Teppema Luc , van den Elsen Maarten , Olofsen Erik , Berkenbosch Aad , van Kleef Jack 
Published: November 2003

Background
To quantify the effects of acute pain on ventilatory control in the awake and sedated human volunteer, the acute hypoxic ventilatory response was studied in the absence and presence of noxious stimulation before and during 0.1 minimum alveolar concentration sevoflurane inhalation.

Methods
Step decreases in end-tidal partial pressure of oxygen from normoxia into hypoxia (approximately 50 mmHg) were performed in 11 healthy volunteers. Four acute hypoxic ventilatory responses were obtained per subject: one in the absence of pain and sevoflurane (C), one in the absence of sevoflurane with noxious stimulation in the form of a 1-Hz electrical current applied to the skin over the tibial bone (C + P), one in the absence of pain during the inhalation of 0.1 minimum alveolar concentration sevoflurane (S), and one during 0.1 minimum alveolar concentration sevoflurane with noxious stimulation (S + P). The end-tidal partial pressure of carbon dioxide was held constant at a value slightly greater than baseline (44 mmHg). To assess the central nervous system arousal state, the bispectral index of the electroencephalogram was monitored. Values are mean +/- SE.

Results
Pain caused an increase in prehypoxic baseline ventilation before and during sevoflurane inhalation: C = 13.7 +/- 0.9 l.min-1, C + P = 16.0 +/- 1.0 l.min-1 (P < 0.05 vs. C and S), S = 12.7 +/- 1.2 l.min-1, and S + P = 15.9 +/- 1.1 l.min-1 (P < 0.05 vs. C and S). Sevoflurane decreased the acute hypoxic ventilatory response in the absence and presence of noxious stimulation: C = 0.69 +/- 0.20 l.min-1 (% change in arterial hemoglobin-oxygen saturation derived from pulse oximetry [SpO2])-1, C + P = 0.64 +/- 0.13 l.min-1.%SpO2(-1), S = 0.48 +/- 0.15 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P) and S + P = 0.46 +/- 0.21 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P). The bispectral indexes were C = 96.2 +/ 0.7, C + P = 97.1 +/- 0.4, S = 86.3 +/- 1.3 (P < 0.05), and S + P = 95.0 +/- 1.0.

Conclusions
The observation that acute pain caused an increase in baseline ventilation with no effect on the acute hypoxic ventilatory response indicates that acute pain interacted with ventilatory control without modifying the effect of low-dose sevoflurane on the peripheral chemoreflex loop. Acute pain increased the level of arousal significantly during sevoflurane inhalation but did not restore the approximately 30% depression of the acute hypoxic ventilatory response by sevoflurane. The central nervous system arousal state per se did not contribute to the impairment of the acute hypoxic ventilatory response by sevoflurane.
Density of Lumbar Cerebrospinal Fluid in Pregnant and Nonpregnant Humans
Authors: Richardson Michael G. , Wissler Richard N. 
Published: November 2003

Background
Dextrose-free local anesthetics and opioids, alone and in combinations, are being used increasingly to provide subarachnoid anesthesia and analgesia. These dextrose-free drugs have been described as hypobaric by some and isobaric by others. To accurately classify anesthetics with regard to baricity, the density of cerebrospinal fluid (CSF) must be known. The authors sought to determine the exact density of human CSF, and determine whether CSF density is altered by pregnancy.

Methods
Density measurements accurate to 0.00001 g/ml were made at 37.00 degrees C, using a mechanical oscillation resonance frequency density meter. Cerebrospinal fluid samples were obtained from 44 patients during spinal anesthesia. Five groups were studied: men, and premenopausal, postmenopausal, term pregnant, and postpartum women.

Results
Mean CSF densities in men (1.00064 +/- 0.00012 g/ ml), postmenopausal women (1.00070 +/- 0.00018 g/ml), and nonpregnant premenopausal women (1.00049 +/- 0.00004 g/ ml) were significantly greater than in term pregnant (1.00030 +/- 0.00004 g/ml) and postpartum (1.00034 +/- 0.00005 g/ml) women. Cerebrospinal fluid density did not correlate with age.

Conclusions
Mean CSF density varies in different patient subpopulations. Pregnancy and the immediate postpartum period are associated with the lowest CSF densities. In addition, the cutoff values defining hypobaricity (mean CSF density minus three standard deviations) are greater than previously reported. Accurate CSF density values should be used when considering baricity as a mechanism for clinical observations of dextrose-free intrathecal local anesthetics and opioids. Gestational status also should be considered.
Phenylephrine Increases Cerebral Blood Flow during Low-flow Hypothermic Cardiopulmonary Bypass in Baboons
Authors: Schwartz Arthur E. , Minanov Oktavijan , Stone Gilbert J. , Adams David C. , Sandhu Aqeel A. , Pearson Mark E. , Kwiatkowski Pawel , Young William L. , Michler Robert E. 
Published: November 2003

Background
Although low-flow cardiopulmonary bypass (CPB) has become a preferred technique for the surgical repair of complex cardiac lesions in children, the relative hypotension and decrease in cerebral blood flow (CBF) associated with low flow may contribute to the occurrence of postoperative neurologic injury. Therefore, it was determined whether phenylephrine administered to increase arterial blood pressure during low-flow CPB increases CBF.

Methods
Cardiopulmonary bypass was initiated in seven baboons during fentanyl, midazolam, and isoflurane anesthesia. Animals were cooled at a pump flow rate of 2.5 l.min-1.m-2 until esophageal temperature decreased to 20 degrees C. Cardiopulmonary bypass flow was then reduced to 0.5 l.min-1.m-2 (low flow). During low-flow CPB, arterial partial pressure of carbon dioxide (Pco2) and blood pressure were varied in random sequence to three conditions: (1) Pco2 30-39 mmHg (uncorrected for temperature), control blood pressure; (2) Pco2 50-60 mmHg, control blood pressure; and (3) Pco2 30-39 mmHg, blood pressure raised to twice control by phenylephrine infusion. Thereafter, CPB flow was increased to 2.5 l.min-1.m-2, and baboons were rewarmed to normal temperature. Cerebral blood flow was measured by washout of intraarterial 133Xe before and during CPB.

Results
Phenylephrine administered to increase mean blood pressure from 23 +/- 3 to 46 +/- 3 mmHg during low-flow CPB increased CBF from 14 +/- 3 to 31 +/- 9 ml.min-1.100 g-1, P < 0.05. Changes in arterial Pco2 alone during low flow bypass produced no changes in CBF.

Conclusions
Although low-flow CPB resulted in a marked decrease in CBF compared with prebypass and full-flow bypass, phenylephrine administered to double arterial pressure during low-flow bypass produced a proportional increase in CBF.