bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of Correlation between the Reduction of Sevoflurane MAC and the Cerebellar Cyclic GMP Concentrations in Mice Treated with 7-Nitroindazole
Authors: Ichinose Fumito , Mi Wei-dong , Miyazaki Miyuki , Onouchi Tsuneko , Goto Takahisa , Morita Shigeho 
Published: November 2003

Background
Although inhibition of nitric oxide synthase (NOS) has been reported to be antinociceptive and to reduce the threshold of general anesthesia, the mechanism of action is largely unknown. Specifically, the relation between the minimum alveolar concentration (MAC)-reducing effects of NOS inhibition and cyclic guanosine monophosphate (cGMP) concentrations in the brain has not been defined. To further characterize the effects of NOS inhibition, the authors studied the relation between the MAC of sevoflurane and the cGMP concentration of the brain after acute and chronic treatment with a neuronally selective NOS inhibitor, 7-nitroindazole (7-NI).

Methods
Sevoflurane MAC and cerebellar cGMP concentrations were determined in mice after acute intraperitoneal administration or after 1, 2, 3, and 4 days of gavage feeding of 7-NI. After acute or chronic treatment with 7-NI, the mice were separated into two groups. Sevoflurane MAC was measured by a tail-clamp method in the first group, and cerebellar cGMP concentrations were measured by enzyme-linked immunosorbent assay in the second group of the mice.

Results
In mice, acute intraperitoneal administration of 7-NI dose dependently decreased sevoflurane MAC and cerebellar cGMP; and 4-day-long gavage feeding with 7-NI (500 mg/ kg, every 8 h) time dependently decreased cerebellar cGMP, but sevoflurane MAC was reduced only for the first 2 days and returned to its baseline after 3 days of 7-NI feeding.

Conclusions
Although an acute selective inhibition of neuronal NOS decreases sevoflurane MAC and cerebellar cGMP concentrations in mice, there was a dissociation between the two parameters during long-term neuronal NOS inhibition. There may be cGMP-independent compensatory mechanisms that mediate nociception when NOS is chronically inhibited.
Volatile Anesthetic Additivity and Specificity in Saccharomyces cerevisiae
Authors: Wolfe Darren , Hester Paul , Keil Ralph L. 
Published: November 2003

Background
In animals, combinations of volatile anesthetics are additive for inducing anesthesia. Furthermore, although there is a correlation between lipophilicity and anesthetic potency, not all volatile lipophilic compounds are anesthetic. Previously the authors demonstrated the effects of volatile anesthetics on the eukaryote Saccharomyces cerevisiae (yeast). To further relate anesthetic action in this organism to mammals, anesthetic additivity and effects of volatile, lipophilic nonanesthetics were studied. In addition, yeast pleiotropic drug-resistance (Pdr) mutants, which confer resistance to various lipophilic compounds, were tested to determine if they are involved in anesthetic response.

Methods
Yeast strains were grown to saturation in liquid culture, diluted, plated on various solid media, incubated, and scored for growth.

Results
Combinations of volatile anesthetics inhibit growth of wild-type (Zzz+) but not anesthetic-resistant (Zzz-) strains when additive concentrations equal 1 minimum inhibitory concentration (MIC). Two volatile, lipophilic compounds that are nonanesthetic in mammals do not inhibit yeast growth. Zzz- mutants remain sensitive to drugs used to identify yeast PDR genes. Conversely Pdr strains, which are resistant to various lipophilic compounds, remain sensitive to volatile anesthetics.

Conclusions
Yeast growth is inhibited in an additive manner by volatile anesthetics. Volatile, lipophilic compounds devoid of anesthetic activity in mammals do not inhibit yeast growth. Zzz- mutants appear to be specifically resistant to volatile anesthetics and distinct from known Pdr mutants. These results suggest that volatile anesthetics behave in a parallel manner in yeast and mammals, making yeast a useful model to investigate the molecular effects of these compounds in living cells.
Effects of Sevoflurane and Isoflurane on Renal Function and on Possible Markers of Nephrotoxicity
Authors: Higuchi Hideyuki , Sumita Shinji , Wada Hiroki , Ura Tatsuya , Ikemoto Takeshi , Nakai Tetsuji , Kanno Masuyuki , Satoh Tetsuo 
Published: November 2003

Background
Low-flow sevoflurane anesthesia is associated with increasing circuit concentrations of compound A, which is nephrotoxic in rats, but the effect of compound A and low-flow sevoflurane anesthesia on renal function in humans is unclear. The authors compared the effects of high- and low-flow sevoflurane and isoflurane anesthesia on renal function and on several possible markers of nephrotoxicity in humans.

Methods
Forty-two patients without preexisting renal disease underwent either low-flow isoflurane (1 l/min, n = 14), low-flow sevoflurane (1 l/min, n 14), or high-flow sevoflurane (6 l/min, n = 14) anesthesia for body-surface-area surgery scheduled to last at least 4 h. Twenty-four-hour urinary excretion of N-acetyl-beta-glucosaminidase (NAG), beta2-microglobulin, protein, glucose, blood urea nitrogen (BUN), and serum creatinine concentrations were measured before and after anesthesia.

Results
There were no differences in blood urea nitrogen, creatinine, and creatinine clearance among the three groups after anesthesia. Increased urinary N-acetyl-beta-glucosaminidase excretions were seen in the low-flow and high-flow sevoflurane groups, but not in the low-flow isoflurane group (P < 0.01). Ten patients in the low-flow sevoflurane group had 24-h urinary excretion of protein that exceeded the normal ranges after anesthesia, but only one patient in the isoflurane and none in the high-flow sevoflurane groups had this.

Conclusions
Low-flow sevoflurane anesthesia was associated with mild and transient proteinuria. However, the observed proteinuria was not associated with any changes in blood urea nitrogen, creatinine, and creatinine clearance in these patients with no preexisting renal disease.
Intermittent CPAP
Authors: Bratzke Edward , Downs John B. , Smith Robert A. 
Published: November 2003

Background
Airway pressure-release ventilation provides ventilation comparable to controlled mechanical ventilation (CMV), but with lower peak airway pressures and less dead-space ventilation. To obtain these advantages for patients administered general anesthesia, the authors (1) designed a mode similar to airway pressure-release ventilation, intermittent continuous positive airway pressure (CPAPI), and compared its efficiency with that of CMV; and (2) assessed the accuracy of end-tidal carbon dioxide tension (PETCO2) as a monitor of the partial pressure of carbon dioxide in arterial blood (PaCO2) during CPAPI compared with during CMV.

Methods
Twenty anesthetized, tracheally intubated patients received baseline CMV that produced a PETCO2 of approximately 35 mmHg and a pulse oximetry value > 90%. Patients were assigned to undergo alternating trials of CMV and CPAPI. During CPAPI, CPAP was applied to the airway, removed for 1 s, and reapplied at a rate equal to the ventilator rate during CMV. The difference between the carbon dioxide tension in arterial blood and end-tidal gas [P(a-ET)CO2] and the calculation of PaCO2/minute ventilation quantified the efficiency of ventilation. Data were summarized as mean +/- SD and compared using the Student's t-test.

Results
Peak airway pressure (13+/-2 vs. 23+/-5 cm H2O; P < 0.001) and minute ventilation (3.5+/-1 vs. 4.6+/-1.2 l/min; P < 0.0001) were lower during CPAPI than during CMV. The value for PaCO2/minute ventilation (11.1+/-2.9 vs. 7.9+/-2.6 mmHg x l(-1) x min(-1); P < 0.0001) was greater during CPAPI. P(a-ET)CO2 was always greater during CMV (6.3+/-1.6 vs. 1.7+/-0.9 mmHg; P < 0.0001) and was never > 3.5 mmHg during CPAPI.

Conclusions
During CPAPI, less ventilation was necessary to produce a PaCO2 comparable to that during CMV. This represents a significant reduction in dead-space ventilation, improved efficiency of ventilation, and a lower value for P(a-ET)CO2. Compared with CMV, CPAPI also improves the accuracy of PETCO2 as a monitor of PaCO2.
A Comparison of Left Ventricular Performance Indices Measured by Transesophageal Echocardiography with Automated Border Detection
Authors: Declerck Christ , Hillel Zak , Shih Henry , Kuroda Maxine , Connery Cliff P. , Thys Daniel M. 
Published: November 2003

Background
Automated border detection (ABD) allows semiautomated measurement of left ventricular (LV) areas. They can be combined with left ventricular pressure signals to generate pressure-area loops and pressure-dimension indices of contractility. This study compared conventional indices of ventricular performance (fractional area change [FAC] and circumferential fiber shortening [Vcfc]) with pressure-dimension indices of contractility. A secondary aim was to compare the effects of volatile anesthetics on the indices.

Methods
Using transesophageal echocardiography with automated border detection, FAC and Vcfc were obtained in 23 patients after cardiopulmonary bypass. Left ventricular pressures were obtained with a left ventricular catheter. Preload reduction by inferior vena caval occlusion was used to obtain end-systolic elastance (Ees), preload recruitable stroke force (PRSF), and dP/dtmax x EDA(-1) (EDA = end-diastolic area). In 11 patients, the measurements were repeated at 1 end-tidal minimum alveolar concentration of halothane or isoflurane. The results are expressed as mean +/- SD.

Results
After cardiopulmonary bypass, FAC was 31.1+/-7.9%, Vcfc was 0.6+/-0.2 circ x s(-1), Ees was 25.8+/-11.6 mmHg x cm(-2), PRSF was 60.8+/-26.6 mmHg, and dP/dtmax x EDA(-1) was 245+/-123.4 mmHg x s(-1) x cm(-2). At 1 minimum alveolar concentration of a volatile anesthetic agent, FAC, Vcfc, and dP/dtmax x EDA(-1) remained unchanged. Significant decreases in Ees (19%) and PRSF (28%) were observed.

Conclusions
The association between pressure-dimension indices and Vcfc or FAC was weak or nonexistent. A reduction in myocardial contractility induced by the administration of volatile anesthetic agents was detected by Ees and PRSF, but not by FAC, Vcfc, or dP/dtmax x EDA(-1). After myocardial revascularization, Ees and PRSF appear more sensitive than FAC or Vcfc for measuring changes in contractility.
Intraoperative Determination of Cardiac Output Using Multiplane Transesophageal Echocardiography
Authors: Perrino Albert C. , Harris Stephen N. , Luther Martha A. 
Published: November 2003

Background
Limitations in the imaging views that can be obtained with transesophageal echocardiography (TEE) have hindered development of a widely adopted Doppler method for cardiac output (CO) monitoring. The authors evaluated a CO technique that combines steerable continuous-wave Doppler with the imaging capabilities of two-dimensional multiplane TEE.

Methods
From the transverse plane transgastric, short-axis view of the left ventricle, the imaging array was rotated to view the left ventricular outflow tract (LVOT) and ascending aorta. Steerable continuous-wave Doppler was subsequently used to measure aortic blood flow velocities. Aortic valve area was determined using a triangular orifice model. Matched thermodilution and Doppler CO measurements were obtained serially during surgery.

Results
The left ventricular outflow tract was imaged in 32 of 33 patients (97%). Data analysis reveal a mean difference between techniques of -0.01 l/min, and a standard deviation of the differences of 0.56 l/min. Multiple regression showed a correlation of r = 0.98 between intrasubject changes in CO. Multiplane TEE correctly tracked the direction of 37 of 38 serial changes in thermodilution CO but with a modest 14% underestimation of the magnitude of these changes.

Conclusions
These results indicate that multiplane TEE can provide an alternative method for the intraoperative measurement of CO. The ability of the rotatable imaging array to align with the left ventricular outflow tract and the need for only minimal adjustments in probe position advance the utility of intraoperative TEE.
Transnasal Butorphanol Is Effective for Postoperative Pain Relief in Children Undergoing Myringotomy
Authors: Bennie Ruth E. , Boehringer Leigh A. , Dierdorf Stephen F. , Hanna Mark P. , Means Lyn J. 
Published: November 2003

Background
More than 70% of children require analgesics after bilateral myringotomy and tube placement (BMT). Because anesthesia for BMT is generally provided by face mask without placement of an intravenous catheter, an alternative route for analgesia administration is needed. Transnasal butorphanol is effective in relieving postoperative pain in adults and children. The effectiveness of transnasal butorphanol for postoperative pain management in children undergoing BMT was studied.

Methods
This double-blinded, placebo-controlled study compared the postoperative analgesic effects of transnasal butorphanol administered after the induction of anesthesia. Sixty children classified as American Society of Anesthesiologists physical status 1 or 2 who were aged 6 months or older and scheduled for elective BMT were randomized to receive transnasal placebo or 5, 15, or 25 microg/kg butorphanol. Postoperative pain was assessed using the Children's Hospital of Eastern Ontario Pain Scale (CHEOPS) on arrival in the postanesthesia care unit and at 5, 10, 15, 30, 45, and 60 min.

Results
The CHEOP scores were significantly less in the 25 microg/kg transnasal butorphanol group compared with controls. Significantly fewer children received rescue analgesia in the 25 microg/kg transnasal butorphanol group compared with controls (n = 1 and 8, respectively; P = 0.02).

Conclusions
Transnasal butorphanol given in a dose of 25 microg/kg after induction of anesthesia provided adequate postoperative pain relief in children undergoing BMT.
Volatile Anesthetics Do Not Alter Bradykinin-induced Release of Nitric Oxide or L-Citrulline in Crystalloid Perfused Guinea Pig Hearts
Authors: Fujita Satoshi , Roerig David L. , Chung Wynda W. , Bosnjak Zeljko J. , Stowe David F. 
Published: November 2003

Background
Nitric oxide (NO) and L-citrulline (L-cit) are released by endothelial NO synthase (eNOS) to induce vasodilation via guanylyl cyclase and cyclic guanosine monophosphate (cGMP). Volatile anesthetics directly reduce vascular muscle tone, but their effects on the eNOS cGMP pathway is controversial. The aim of this study was to examine the effects of anesthetics on bradykinin-induced increases in flow, NO, and L-cit in isolated hearts.

Methods
Guinea pig hearts were isolated, perfused at 55 mmHg with a crystalloid or erythrocyte perfusate at 37 degrees C, and heart rate, left ventricular pressure, coronary flow (CF), effluent pH, and oxygen tension were monitored. Effluent [NO] was measured by a Clark-type electrode (sensitivity > or = 1 nM = 3 pA) with a selectively permeable membrane. Effluent [L-cit] was measured by chromatography. Before, during, and after exposure to halothane, isoflurane, or sevoflurane, hearts were infused with as much as 100 nM bradykinin to induce increases in CF and effluent release of NO and L-cit.

Results
In crystalloid-perfused hearts, 10 nm bradykinin produced maximal concentration-dependent increases in CF (87+/-2%), [NO] (24+/-4 nM), NO release (128+/-18 pmol x g(-1) x min(-1)), and [L-cit] (58+/-8 nM). Isoflurane slightly increased CF but not NO. Anesthetics did not alter the bradykinin-induced CF, NO slope relationship, or change [L-cit]. In erythrocyte-perfused hearts, isoflurane also did not alter the bradykinin-induced increase in CF and decrease in percentage of oxygen extracted.

Conclusions
This is the first study to simultaneously measure CF with bradykinin-induced changes in [NO] and [L-cit] in the presence of halothane, isoflurane, and sevoflurane in intact hearts. The study shows for the first time that volatile anesthetics do not alter the CF to NO relationship and suggests that NO production, NO release, and NO vasodilatory effects mediated by the eNOS cGMP pathway are not significantly affected by anesthetics in crystalloid or erythrocyte-perfused guinea pig hearts.
Nitric Oxide Inhibits Neutrophil Adhesion during Experimental Extracorporeal Circulation
Authors: Chello Massimo , Mastroroberto Pasquale , Marchese Antonietta R. , Maltese Giovanni , Santangelo Ermenegildo , Amantea Bruno 
Published: November 2003

Background
Myocardial and pulmonary injuries often occur after cardiopulmonary bypass, mediated in part by neutrophil activation and adhesion to endothelial cells. The effects of nitric oxide (NO) administration on neutrophil adhesion to endothelial cells after simulated extracorporeal circulation were investigated.

Methods
Two identical extracorporeal circulation circuits were primed with fresh human blood and circulated for 2 h at 37 degrees C. Nitric oxide at a 40-ppm concentration was added to one of the oxygenators in each pair. Neutrophil CD11b/CD18 expression and their adhesion to human umbilical vein endothelial cell monolayers were assayed in leukocytes isolated from samples drawn from the circuit 30, 60, 90, and 120 min after circulation began. In another series of experiments, blocking monoclonal antibodies to both neutrophil CD11b and CD18 were incubated with polymorphonuclear leukocytes after removal from the circuit before the adhesion assay.

Results
After 60 min of circulation, the neutrophils from NO-treated circuits showed significantly reduced CD11b/CD18 surface expression compared with the control group. There was also a significant reduction in neutrophil-endothelial adhesion in the NO group after 120 min of circulation. Monoclonal antibodies to both CD11b and CD18 significantly inhibited the adhesion of polymorphonuclear leukocytes at endothelial cells after 120 min of circulation.

Conclusions
These results confirm that neutrophil activation occurs during cardiopulmonary bypass. The addition of NO to the circuits of extracorporeal circulation significantly affects neutrophil adhesion to endothelial cells.
Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation
Authors: Blobner Manfred , Bogdanski Ralph , Kochs Eberhard , Henke Julia , Findeis Alexander , Jelen-Esselborn Sabine 
Published: November 2003

Background
Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared.

Methods
Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation.

Results
During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures.

Conclusions
In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure < or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.
Intrathecal Neostigmine, but Not Sympathectomy, Relieves Mechanical Allodynia in a Rat Model of Neuropathic Pain
Authors: Lavand'homme Patricia , Pan Hui-Lin , Eisenach James C. 
Published: November 2003

Introduction
Pain resulting from a usually nonpainful stimulus (allodynia) is a common characteristic of neuropathic pain. Among animal models of allodynia, tight ligature of lumbar spinal nerves has been of special interest because it has been reported to be relieved by sympathectomy. The purpose of this study was to determine whether spinal analgesic agents, which have opposite effects on sympathetic nervous system activity (clonidine decreases it and neostigmine increases it), have differing efficacy in this model.

Methods
Male Sprague-Dawley rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. At least 2 weeks later, a lumbar intrathecal or jugular intravenous catheter was inserted. Withdrawal threshold to mechanical stimulation of the hind paw was determined by application of von Frey filaments before surgery; after surgery; after intrathecal injection of clonidine, neostigmine, or their combination; after intravenous injection of phentolamine or guanethidine; and after surgical sympathectomy.

Results
Spinal nerve ligation reduced withdrawal threshold ipsilateral to the lesion. This allodynia was relieved by clonidine (50% block of allodynia at 20+/-1.2 microg and neostigmine (50% block of allodynia at 2+/-0.1 microg, and they interacted synergistically to block allodynia. Neither chemical nor surgical sympathectomy altered allodynia.

Discussion
These results disagree with previous observations that mechanical allodynia in this animal model depends on sympathetic nervous system activity. Therefore, intrathecally administered analgesic agents, one that reduces sympathetic outflow from the spinal cord (clonidine) and one that increases it (neostigmine), were similarly effective in this model.