bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isoflurane Blunts Electroencephalographic and Thalamic–Reticular Formation Responses to Noxious Stimulation in Goats
Authors: Antognini Joseph F. , Carstens E. 
Published: November 2003

Background
Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action.

Methods
Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC.

Results
At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus.

Conclusions
Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.
Colchicine Inhibits Isoflurane-induced Preconditioning
Authors: Ismaeil Mohamed S. , Tkachenko Igor , Hickey Robert F. , Cason Brian A. 
Published: November 2003

Background
When administered before prolonged myocardial ischemia and reperfusion, isoflurane exerts potent cardioprotective effects similar to those inferred by ischemic preconditioning. To determine whether an intact cytoskeleton is critically important in isoflurane-induced preconditioning, the authors used a rabbit model in which isoflurane-induced myocardial preconditioning decreases myocardial infarct size (IS) substantially. In this model, the authors tested whether the microtubule depolymerizing agent, colchicine, would inhibit isoflurane-induced myocardial preconditioning.

Methods
Myocardial IS was measured in four groups of propofol-anesthetized rabbits, each subjected to 30 min of anterolateral coronary occlusion followed by 3 h of reperfusion. Groups differed only in the pretreatments given, and only the control group received no pretreatment. An isoflurane-preconditioned group was pretreated with 15 min of end-tidal isoflurane, 1.1%, and then 15 min of washout. An isoflurane-plus-colchicine group was administered 2 mg/kg colchicine intravenously before isoflurane pretreatment. A colchicine-control group was administered 2 mg/kg colchicine but no isoflurane pretreatment. Myocardial IS and area at risk (AR) were defined by staining. Data were analyzed by analysis of variance or covariance.

Results
Infarct size, expressed as a percentage of AR (IS:AR) was 33.6%+/-8.8% (SD) in the control group. Isoflurane preexposure reduced myocardial IS:AR significantly, to 11.8%+/-9.1%. Colchicine pretreatment eliminated the preconditioning-like effect of isoflurane (IS:AR = 32.6%+/-8.7%). Colchicine alone did not alter IS (IS:AR = 27.6%+/-7.1%; P = not significant).

Conclusions
Colchicine abolished the preconditioning effect of isoflurane but did not increase IS when administered alone. An intact microtubular cytoskeleton is critically important in the process of volatile anesthetic-induced preconditioning.
Exposure to Cigarette Smoke Impairs Alveolar Macrophage Functions during Halothane and Isoflurane Anesthesia in Rats
Authors: Kotani Naoki , Hashimoto Hiroshi , Sessler Daniel I. , Yatsu Yuichi , Muraoka Masatoshi , Matsuki Akitomo 
Published: November 2003

Background
Smoking alters numerous alveolar macrophage functions and is an important risk factor for postoperative pulmonary complications. The authors therefore tested the hypothesis that smoke exposure impairs antimicrobial and proinflammatory responses in alveolar macrophages during halothane and isoflurane anesthesia with mechanical ventilation.

Methods
Thirty control rats and 30 rats exposed to cigarette smoke were mechanically ventilated with 1.5 minimum alveolar concentration halothane and isoflurane. Ten smoke-exposed and control animals were assigned to one of three different anesthetic durations (0, 2, and 6 h). The fraction of aggregated cells and cell distribution were determined. Opsonized and unopsonized phagocytosis was measured. Microbicidal activity was determined as the ability to kill Listeria monocytogenes. The expression of interleukin (IL)-1alpha, IL-1beta, IL-6, macrophage inflammatory protein-2, interferon-gamma, and tumor necrosis factor-alpha was measured by semiquantitative reverse-transcription polymerase chain reaction. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunosorbent assay.

Results
During both halothane and isoflurane anesthesia, the fraction of aggregated macrophages increased, whereas unopsonized and opsonized phagocytosis and microbicidal activity decreased significantly over time in both groups. Responses observed in smoke-exposed rats were almost twice as great as those observed in the control rats. Gene expression and production of all proinflammatory cytokines except IL-6 increased 2-20-fold during anesthesia. The increases in IL-1beta, interferon-gamma, and tumor necrosis factor-alpha in the control rats were 1.5-8 times greater than those in the smoke-exposed rats.

Conclusion
Antimicrobial and proinflammatory responses of alveolar macrophages during anesthesia were markedly suppressed by smoke exposure. Our data suggest that smoke exposure reduces the efficacy of immune defenses during anesthesia.
Different Ventilation Strategies Affect Lung Function but Do Not Increase Tumor Necrosis Factor-α and Prostacyclin Production in Lavaged Rat Lungs In Vivo
Authors: Verbrugge Serge J. C. , Uhlig Stefan , Neggers Sebastian J. C. M. M. , Martin Christian , Held Heinz-Dieter , Haitsma Jack J. , Lachmann Burkhard 
Published: November 2003

Background
Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma.

Methods
In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls.

Results
Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls.

Conclusions
Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.
Tissue Factor Expression in Vital Organs during Murine Traumatic Shock
Authors: Armstead Valerie E. , Opentanova Irina L. , Minchenko Alexander G. , Lefer Allan M. 
Published: November 2003

Background
Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats.

Methods
Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1.

Results
TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively).

Conclusions
These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.
Effects of Halothane and Enflurane on Ventricular Conduction, Refractoriness, and Wavelength
Authors: Aya Antoine G. , de La Coussaye Jean E. , Robert Emmanuelle , Ripart Jacques , Lefrant Jean-Yves , Fabbro-Péray Pascale , Eledjam Jean-Jacques 
Published: November 2003

Background
Effects of halothane and enflurane on ventricular conduction, anisotropy, duration and dispersion of refractory periods, and wavelengths were studied, and putative antiarrhythmic or arrhythmogenic properties on ventricles were discussed.

Methods
High-resolution epicardial mapping system was used to study the effects of 1, 3, and 5 vol% halothane and enflurane in 30 isolated rabbit hearts. Ten hearts were kept intact to study the effects on spontaneous sinus cycle length (RR interval), perfusion pressure, and the occurrence of spontaneous dysrhythmias. In 20 other hearts, a thin epicardial layer was obtained (frozen hearts) to study ventricular conduction velocity, ventricular effective refractory period (VERP in four sites) and wavelengths.

Results
Halothane induced a concentration-dependent lengthening of RR interval, whereas enflurane did not. Both agents slowed longitudinal and transverse ventricular conduction velocity with no anisotropic change. Ventricular effective refractory period was prolonged at 1 vol% and was shortened at higher concentrations, with no significant increase in dispersion. Ventricular longitudinal and transverse wavelengths decreased in a concentration-dependent manner. Although changes in wavelengths could express proarrhythmic effects of volatile anesthetics, no arrhythmia occurred in spontaneously beating hearts or in frozen hearts.

Conclusions
The ventricular electrophysiologic effects of halothane and enflurane were slight, suggesting that both agents are unable per se to induce functional conduction block and therefore reentrant ventricular arrhythmias.
Incidence of Venous Air Embolism during Craniectomy for Craniosynostosis Repair
Authors: Faberowski Lisa W. , Black Susan , Mickle J. Parker 
Published: November 2003

Background
Investigations to determine the incidence of venous air embolism in children undergoing craniectomy for craniosynostosis repair have been limited, although venous air embolism has been suspected as the cause of hemodynamic instability and sometimes death. A precordial Doppler ultrasonic probe is an accepted method for detection of venous air embolism and is readily available at most institutions.

Methods
A prospective study was conducted using a precordial Doppler ultrasonic probe in children undergoing craniectomy for craniosynostosis repair. The Doppler signal was continuously monitored intraoperatively for characteristic changes of venous air embolism. A recording was made of the precordial Doppler probe pulses, which was later reviewed by a neuroanesthesiologist, blinded to the intraoperative events. This information was correlated with the intraoperative events and episodes of venous air embolism were graded.

Results
Twenty-three patients were enrolled in the study during the 2-yr study period. Nineteen patients (82.6%) demonstrated 64 episodes of venous air embolism; six patients (31.6%) had hypotension associated with venous air embolism. Thirty-two episodes of hypotension were demonstrated in eight patients (34.7%). None of the patients developed cardiovascular collapse.

Conclusion
The incidence of venous air embolism in our study of 23 children undergoing craniectomy for craniosynostosis was 82.6%. Though most episodes of venous air embolism during craniosynostosis repair are without hemodynamic consequences, the preemptive placement of a precordial Doppler ultrasonic probe is a noninvasive, economic, and safe method for the detection of venous air embolism. Prompt recognition may allow for the early initiation of therapy, thereby decreasing morbidity and mortality rates related to venous air embolism.
Hemodynamic Effects of Synchronized High-frequency Jet Ventilation Compared with Low-frequency Intermittent Positive-pressure Ventilation after Myocardial Revascularization
Authors: Romand Jacques-Andre , Treggiari-Venzi Miriam M. , Bichel Thierry , Suter Peter M. , Pinsky Michael R. 
Published: November 2003

Background
The purpose of this prospective study was to examine the effect on cardiac performance of selective increases in airway pressure at specific points of the cardiac cycle using synchronized high-frequency jet ventilation (sync-HFJV) delivered concomitantly with each single heart beat compared with controlled mechanical ventilation in 20 hemodynamically stable, deeply sedated patients immediately after coronary artery bypass graft.

Methods
Five 30-min sequential ventilation periods were used interspersing controlled mechanical ventilation with sync-HFJV twice to control for time and sequencing effects. Sync-HFJV was applied using a driving pressure, which generated a tidal volume resulting in gas exchanges close to those obtained on controlled mechanical ventilation and associated with the maximal mixed venous oxygen saturation. Hemodynamic variables including cardiac output, mixed venous oxygen saturation and vascular pressures were recorded at the end of each ventilation period.

Results
The authors found that in 20 patients, hemodynamic changes induced by controlled mechanical ventilation and by sync-HFJV were similar. Cardiac index did not change (mean +/- SD for controlled mechanical ventilation: 2.6 +/- 0.7 l x min(-1) x m(-2); for sync-HFJV: 2.7 +/- 0.7 l x min(-1) x m(-2); P value not significant). This observation persisted after stratification according to baseline left-ventricular contractility, as estimated by ejection fraction.

Conclusions
The authors conclude that after coronary artery bypass graft, if gas-exchange values are maintained within normal range, sync-HFJV does not result in more favorable hemodynamic support than controlled mechanical ventilation. These findings contrast with the beneficial effects of sync-HFJV, resulting in marked hypocapnia, on cardiac performance observed in patients with terminal left-ventricular failure.
Left-molar Approach Improves the Laryngeal View in Patients with Difficult Laryngoscopy
Authors: Yamamoto Ken , Tsubokawa Tsunehisa , Ohmura Shigeo , Itoh Hironori , Kobayashi Tsutomu 
Published: November 2003

Background
The molar approach of laryngoscopy is reported to improve glottic view in sporadic cases of difficult laryngoscopy. The authors studied the effect of molar approaches and optimal external laryngeal manipulation (OELM) using the Macintosh blade.

Methods
A series of 1,015 adult patients who underwent general anesthesia and tracheal intubation was studied. Laryngoscopy was carried out using a Macintosh no. 3 or 4 standard blade. Three consecutive trials of direct laryngoscopy using the midline and left- and right-molar approaches were carried out under full muscle relaxation with optimal head and neck positioning. The best glottic views were recorded for each approach with and without OELM.

Results
Difficult laryngoscopy with a midline approach accounted for 6.5% (66 cases) before OELM and 1.97% (20 cases) after OELM. A left-molar approach with OELM further reduced difficult laryngoscopy to seven cases (P < 0.001 vs. midline approach with OELM); a right-molar approach with OELM reduced difficult laryngoscopy to 18 cases (P = 0.48).

Conclusions
The left-molar approach with OELM improves the laryngeal view in patients with difficult laryngoscopy.
Concentration–Effect Relationship of Intravenous Lidocaine on the Allodynia of Complex Regional Pain Syndrome Types I and II
Authors: Wallace Mark S. , Ridgeway Beri M. , Leung Albert Y. , Gerayli Afshin , Yaksh Tony L. 
Published: November 2003

Background
Several lines of evidence suggest that neuropathic pain (including Complex Regional Pain Syndrome [CRPS] I and CRPS II) is mediated in part by an increase in the density of voltage-sensitive sodium channels in injured axons and the dorsal root ganglion of injured axons. This study sought to characterize the effects of intravenous lidocaine (a sodium channel blocker) on acute sensory thresholds within the painful area and the size of the painful area in patients suffering from CRPS I and II.

Methods
This study used a randomized, double-blind, placebo-controlled design in 16 subjects suffering from CRPS I and II with a prominent allodynia. Each subject received an intravenous infusion of lidocaine and diphenhydramine separated by 1 week. A computer-controlled infusion pump targeted stair-step increases in plasma levels of lidocaine of 1, 2, and 3 microg/ml. At baseline and at each plasma level, spontaneous and evoked pain scores and neurosensory testing within the painful area were measured. The neurosensory testing consisted of thermal thresholds, tactile thresholds and the area of allodynia to punctate, and stroking and thermal stimuli.

Results
Intravenous lidocaine and diphenhydramine had no significant effect on the cool, warm, or cold pain thresholds. However, lidocaine caused a significant elevation of the hot pain thresholds in the painful area. Intravenous lidocaine caused a significantly decreased response to stroking and cool stimuli in the allodynic area. There was also a significant decrease in pain scores to cool stimuli at all plasma levels and the spontaneous pain at the highest plasma level.

Conclusions
This study demonstrates that intravenous lidocaine affects pain in response to cool stimuli more than mechanical pain in subjects with neuropathic pain. There is a lesser effect on spontaneous pain and pain induced by stroking stimuli and no effect on the pain induced by punctate stimuli.
Stellate Ganglion Block Modifies the Distribution of Lymphocyte Subsets and Natural-killer Cell Activity
Authors: Yokoyama Masataka , Nakatsuka Hideki , Itano Yoshitaro , Hirakawa Masahisa 
Published: November 2003

Background
Recent investigations suggest that the sympathetic nervous system affects the immune system. This study examined whether stellate ganglion block (SGB) affects the immune response, specifically the distribution of lymphocyte subsets and natural-killer (NK) cell activity.

Methods
Ten volunteers received three different treatments in random order at 7-day intervals: (1) SGB with 7 ml of 1% lidocaine; (2) an identical volume of normal saline injected at the same site as SGB; and (3) an identical volume of 1% lidocaine injected intramuscularly. Blood samples were drawn before and 30 min after treatment. The distribution of lymphocyte subsets was analyzed, and NK cell activity was measured. Plasma concentrations of epinephrine, norepinephrine, adrenocorticotropic hormone, and cortisol were measured.

Results
Any value in the normal saline and intramuscular treatments did not change significantly. After SGB, the plasma concentrations of epinephrine and norepinephrine decreased significantly (P < 0.01), but adrenocorticotropic hormone and cortisol values were unchanged. Increases were observed in the proportion of B cells (from 18.4 +/- 3.0% to 20.0 +/- 3.8%; P < 0.01) and T cells (from 64.2 +/- 4.1% to 67.1 +/- 4.2%; P < 0.01). A decrease in the proportion of NK cells was observed (from 13.4 +/- 2.7% to 9.8 +/- 2.2%; P < 0.01). The proportion of CD4+ cells increased (P < 0.01), and that of CD8+ cells decreased (P < 0.01), so that the CD4+ cell/CD8+ cell ratio increased (P < 0.01). The proportion of CD29+ (helper-inducer T) cells increased (P < 0.05), but that of CD45RA+ (suppressor-inducer T) cells did not change. NK cell activity decreased significantly (from 33.6 +/- 8.3% to 29.1 +/- 7.6%; P < 0.01).

Conclusions
A small but significant alteration in lymphocyte subsets and in NK cell activity by SGB indicates that local sympathetic nerve block may modulate the immune response.