bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contractility in Humans after Coronary Artery Surgery
Authors: Schmidt Christoph , Roosens Carl , Struys Michel , Deryck Yvon L. J. M. , Van Nooten Guido , Colardyn Francis , Van Aken Hugo , Poelaert Jan I. 
Published: November 2003

Background
Propofol's unique pharmacokinetic profile offers advantages for titration and rapid emergence in patients after coronary artery bypass graft (CABG) surgery, but concern for negative inotropic properties potentially limits its use in these patients. The current study analyzed the effect of various propofol plasma concentrations on left ventricular (LV) contractility by means of a single-beat contractile index based on LV maximal power (PWR(max)).

Methods
The study was conducted in 30 patients after CABG surgery. Immediately after admission to the intensive care unit (ICU), four different plasma concentrations of propofol 0.65, 1.30, 1.95, and 2.60 microg/ml were established. At each concentration level, the cardiac and vascular effects of propofol were studied by combining echocardiographic data with invasively derived aortic root pressure. Preload was characterized by LV end-diastolic dimensions. Afterload was indicated in terms of indexed systemic vascular resistance (SVRI), LV end-systolic meridional wall stress (LV-ESWS), and arterial elastance (Ea). Quantification of effects on contractility was achieved by preload-adjusted PWRmax.

Results
Myocardial contractility did not change during a fourfold increase in propofol plasma concentration. Preload-adjusted PWRmax amounted to 3.90+/-1.75 W x ml(-2) x 10(4), 3.98+/-1.69, 3.94+/-1.70, and 3.88+/-1.72, respectively (mean+/-SD). With respect to ventricular loading conditions, propofol caused a significant reduction in both pre- and afterload.

Conclusions
The current results strongly suggest that propofol lacks direct cardiac depressant effects. Nevertheless, meaningful vascular actions of propofol could be demonstrated. Significant decreases in ventricular loading conditions accounted for a marked decrease in arterial blood pressure and supported the concept that propofol in clinically relevant concentration is a vasodilator.
No Enhancement of Sensory and Motor Blockade by Neostigmine Added to Mepivacaine Axillary Plexus Block
Authors: Bouaziz Herve , Paqueron Xavier , Bur Marie Lorraine , Merle Michel , Laxenaire Marie Claire , Benhamou Dan 
Published: November 2003

Background
Intrathecal neostigmine induces analgesia but also several side effects. Recently, 500 microg neostigmine administered intraarticularly was shown to produce postoperative analgesia without side effects. The authors' goal was to determine whether 500 microg neostigmine added to mepivacaine in axillary plexus block prolongs postoperative analgesia. In addition, they wanted to determine the incidence of side effects in patients undergoing hand surgery.

Methods
Sixty-nine outpatients scheduled for carpal tunnel syndrome repair with axillary plexus block were randomly assigned to one of three groups that received saline solution in the axillary plexus and subcutaneously (group 1), 500 microg neostigmine in the axillary plexus and saline solution subcutaneously (group 2), or saline solution in the axillary plexus and 500 microg neostigmine subcutaneously (group 3). Sensory and motor block in the four hand nerve distributions were assessed every 5 min for 30 min The duration of the sensory and motor blocks were assessed after operation. Side effects were also recorded.

Results
Neostigmine had no effect on sensory and motor block in any of the four nerve distributions, nor did it increase the median duration of sensory block (215 min; range, 120-330 min) compared with group 1 (247 min; range, 190-287 min) or group 3 (236 min; range, 160-280 min). Motor block was slightly shorter (P = 0.045) in group 3 (190 min; range, 135-285 min) compared with group 1 (218 min; range, 145257 min) and group 2 (215 min; range, 105-343 min). Gastrointestinal side effects occurred in 30% of patients in both neostigmine groups but not in group 1 (P < 0.05).

Conclusions
This study suggests that 500 microg neostigmine added to mepivacaine in axillary plexus block does not prolong postoperative sensory block, but it does cause a relatively high incidence of side effects. These two findings raise doubts about the use of neostigmine associated with local anesthetics for plexus neural block.
The Mechanism of Inhibitory Actions of Propofol on Rat Supraoptic Neurons
Authors: Inoue Yoshitaka , Shibuya Izumi , Kabashima Narutoshi , Noguchi Jun , Harayama Nobuya , Ueta Yoichi , Sata Takeyoshi , Shigematsu Akio , Yamashita Hiroshi 
Published: November 2003

Background
In the perioperative period, plasma osmotic pressure, systemic blood pressure, and blood volume often change dramatically. Arginine vasopressin is a key factor in the regulation of these parameters. This study was performed to evaluate the direct and the mechanism of the actions of propofol on arginine vasopressin release from magnocellular neurosecretory neurons in the rat supraoptic nucleus.

Methods
Somatodendritic arginine vasopressin release from supraoptic nucleus slice preparations was measured by radioimmunoassay. Ionic currents were measured using the whole-cell mode of the patch-clamp technique in supraoptic nucleus slice preparations or in single dissociated supraoptic nucleus neurons of the rat.

Results
Propofol at concentrations greater than 10(-5) M inhibited the arginine vasopressin release stimulated by potassium chloride (50 mM). This inhibition by propofol was not reversed by picrotoxin, a gamma-aminobutyric acid(A)(GABA(A)) receptor antagonist, whereas arginine vasopressin release induced by glutamate (10(-3) M) was also inhibited by propofol at a clinically relevant concentration (10(-6) M). The latter effect was reversed by picrotoxin. Propofol evoked Cl- currents at concentrations ranging 10(-6) to 10(-4) M. Propofol (10(-6) M) enhanced the GABA (10(-6) M)-induced current synergistically. Moreover, propofol (10(-6) M) prolonged the time constant of spontaneous GABA-mediated inhibitory postsynaptic currents. Furthermore, propofol (10(-5) M and 10(-4) M) reversibly inhibited voltage-gated Ca2+ currents, whereas it did not affect currents induced by glutamate (10(-3) M).

Conclusions
Propofol inhibits somatodendritic arginine vasopressin release from the supraoptic nucleus, and the enhancement of GABAergic inhibitory synaptic inputs and the inhibition of voltage-gated Ca2+ entry are involved in the inhibition of arginine vasopressin release.
Volatile Anesthetics Augment Expression of Proinflammatory Cytokines in Rat Alveolar Macrophages during Mechanical Ventilation
Authors: Kotani Naoki , Takahashi Satoshi , Sessler Daniel I. , Hashiba Eiji , Kubota Takeshi , Hashimoto Hiroshi , Matsuki Akitomo 
Published: November 2003

Background
Previous studies indicate that anesthesia and surgery induce an inflammatory reaction in alveolar macro phages. However,they filed to independently evaluate the relative contributions of factors including mechanical ventilation, general anesthesia, and surgical stress. Therefore, the authors tested the hypothesis that inflammatory reactions at the cellular level in alveolar macrophages are induced within 2 h of inhalation of volatile anesthetics under mechanical ventilation.

Methods
After administration of pentobarbital, rats were allocated to the nonventilated control or spontaneous or mechanical ventilation (n = 15/group) for 2 h at a fraction of inspired oxygen (FI(O2)) of 0.21. In a separate series of experiments, rats were mechanically ventilated without volatile anesthesia, or during exposure to halothane, enflurane, isoflurane, or sevoflurane (n = 15/group). Pulmonary lavage was performed, and RNA was extracted from harvested cells. The mRNA for the proinflammatory cytokines interleukin (IL)-1alpha, IL-1beta, IL-6, macrophage inflammatory protein-2 (MIP-2), interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) were measured by semiquantitative reverse transcription-polymerase chain reaction using beta-actin as an internal standard. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunoassay.

Results
The lavage cell count and cytology were similar in each series of the experiment. Gene expression of MIP-2 and TNF-alpha was greater during mechanical than spontaneous ventilation and nonventilation control However, the concentrations of cytokines except MIP-2 and TNF-alpha were less than detection levels. During exposure to volatile anesthetics, gene expression for IL-1beta, MIP-2, IFN-gamma, and TNF-alpha all increased significantly compared with mechanical ventilation alone. Significant increases in lavage concentrations of MIP-2 and TNF-alpha were also observed.

Conclusions
Gene expression of proinflammatory cytokines increase after inhalation of volatile anesthetics under mechanical ventilation. These data indicate that inhalation of volatile anesthetics under mechanical ventilation induces an inflammatory response at the transcriptional level within 2 h.
Acetaminophen Inhibits Spinal Prostaglandin E2Release after Peripheral Noxious Stimulation
Authors: Muth-Selbach Uta S. , Tegeder Irmgard , Brune Kay , Geisslinger Gerd 
Published: November 2003

Background
Prostaglandin play a pivotal role in spinal nociceptive processing. At therapeutic concentrations, acetaminophen is not a cyclooxygenase inhibitor. inhibitor. Thus, it is antinociceptive without having antiinflammatory or gastrointestinal toxic effects. This study evaluated the role of spinal prostaglandin E2 (PGE2) in antinociception produced by intraperitoneally administered acetaminophen.

Methods
The PGE2 concentrations in the dorsal horn of the spinal cord were measured after formalin was injected into the hind paw of rats. The effect of antinociceptive doses of acetaminophen (100, 200, and 300 mg/kg given intraperitoneally) on PGE2 levels and flinching behavior was monitored Spinal PGE2 and acetaminophen concentrations were obtained by microdialysis using a probe that was implanted transversely through the dorsal horn of the spinal cord at L4. Furthermore, the effects of acetaminophen on urinary prostaglandin excretion were determined.

Results
Intraperitoneal administration of acetaminophen resulted in a significant decrease in spinal PGE2 release that was associated with a significant reduction in the flinching behavior in the formalin test Acetaminophen was distributed rapidly into the spinal cord with maximum dialysate concentrations 4560 min after intraperitoneal administration. Urinary excretion of prostanoids (PGE2, PGF2alpha, and 6-keto-PGF1alpha) was not significantly altered after acetaminophen administration.

Conclusions
The data confirm the importance of PGE2 in spinal nociceptive processing. The results suggest that antinociception after acetaminophen administration is mediated, at least in part, by inhibition of spinal PGE2 release. The mechanism, however, remains unknown. The finding that urinary excretion of prostaglandins was not affected might explain why acetaminophen is antinociceptive but does not compromise renal safety.
Effects of Exogenous Surfactant on Acute Lung Injury Induced by Intratracheal Instillation of Infant Formula or Human Breast Milk in Rabbits
Authors: Nishina Kahoru , Mikawa Katsuya , Takao Yumiko , Maekawa Nobuhiro , Obara Hidefumi 
Published: November 2003

Background
An animal experimental model of acute lung injury after intratracheal instillation of acidified milk products has been recently demonstrated. Exogenous administration of surfactant has proved to be successful treatment for acute lung injury induced by many causes including acid aspiration. The authors conducted this study to investigate whether exogenous surfactant can reduce the magnitude of lung damage induced in rabbits by acidified milk products.

Methods
The lung injury was induced by intratracheal instillation of acidified human breast milk or acidified infant formula (0.8 ml/kg, pH 1.8). Thirty minutes after the insult, some animals were treated with intratracheal surfactant 100 or 200 mg/kg. Lung compliance and alveolar-to-arterial oxygen gradient were recorded during ventilation. After 4 or 12 h, the lungs were excised to determine physiologic and histologic lung damage. Albumin, interleukin-8, and eicosanoids in bronchoalveolar lavage fluid and superoxide production by neutrophils were measured.

Results
The acidified milk products increased A-aD(O2)(550+/-52 and 156+/-28 mmHg; mean+/-SD at 4 h in saline solution and infant formula groups, respectively), lung wet-to-dry weight ratio (6.6+/-0.5 and 5.6 +/- 0.2), %neutrophils in bronchoalveolar lavage fluid (84+/-4% and 8+/-20%), and decreased compliance (0.76+/-0.09 and 1.90+/-0.11 ml/cm H2O). Surfactant improved these variables in a dose-dependent manner (A-aDO2 = 363+/-50 and 237+/-55 mmHg in 100-mg/kg and 200-mg/kg surfactant groups). Surfactant attenuated extensive histologic changes caused by the milk products. Superoxide production was less in rabbits receiving surfactant than in those not receiving it.

Conclusion
Exogenous surfactant improved physiologic, histologic, and biochemical lung injury induced by acidified milk products in a dose-dependent manner. The effectiveness of surfactant may be caused, in part, by inhibition of neutrophils' sequestration and activation. These data indicate that intratracheal instillation of surfactant may be a promising therapeutic modality in acute lung injury resulting from aspiration of acidified milk products.
Ulnar Nerve Pressure
Authors: Prielipp Richard C. , Morell Robert C. , Walker Francis O. , Santos Carlos C. , Bennett Judy , Butterworth John 
Published: November 2003

Background
Although the ulnar nerve is the most frequent site of perioperative neuropathy, the mechanism remains undefined. The ulnar nerve appears particularly susceptible to external pressure as it courses through the superficial condylar groove at the elbow, rendering it vulnerable to direct compression and ischemia However, there is disagreement among major anesthesia textbooks regarding optimal positioning of the arm during anesthesia.

Methods
To determine which arm position (supination, neutral orientation, or pronation) minimizes external pressure applied to the ulnar nerve, we studied 50 awake, normal volunteers using a computerized pressure sensing mat. An additional group of 15 subjects was tested on an operating table with their arm in 30 degrees, 60 degrees, and 90 degrees of abduction, as well as in supination, neutral orientation, and pronation. To determine the onset of clinical paresthesia compared to the onset and severity of somatosensory evoked potential (SSEP) electrophysiologic changes, we studied a separate group of 16 male volunteers while applying intentional pressure directly to the ulnar nerve. Data are presented as mean (median; range).

Results
Supination minimizes direct pressure over the ulnar nerve at the elbow (2 mmHg [0; 0-23]; n = 50), compared with both neutral forearm orientation (69 mmHg [22; 0-220]; P < 0.0001), as well as pronation (95 mmHg [61; 0-220]; P < 0.0001). Neutral forearm orientation also results in significantly less pressure over the ulnar nerve compared to pronation (P < or = 0.04). The estimated contact area of the ulnar nerve with the weight-bearing surface was significantly (P < 0.0001) smaller in the supine position (2.2 cm2 [0.5; 0-9]; n = 50) compared with both neutral orientation (5.5 cm2 [5.0; 0-13]) and pronation (5.8 cm2 [6; 0-12]). With the forearm in neutral orientation, ulnar nerve pressure decreased significantly (P < or = 0.01; n = 15) as the arm was abducted at the shoulder from 0 degrees to 90 degrees. In the 16 male subjects tested, notable alterations in ulnar nerve SSEP signals (decrease > or = 20% in N9-N9' amplitude) were detected in 15 of 16 awake males during application of intentional pressure to the ulnar nerve. However, eight of these subjects did not perceive a paresthesia, even as SSEP waveform amplitudes were decreasing 23-72%. Two of these eight subjects manifested severe decreases in SSEP amplitude (> or = 60%).

Conclusions
Extrapolating these results to the clinical setting, the supinated arm position is likely to minimize pressure over the ulnar nerve. With the forearm in neutral orientation, pressure over the ulnar nerve decreases as the arm is abducted between 30 degrees and 90 degrees. In addition, up to one half of male patients may fail to perceive or experience clinical symptoms of ulnar nerve compression sufficient to elicit SSEP changes.
Platelet-activated Clotting Time Does Not Measure Platelet Reactivity during Cardiac Surgery
Authors: Shore-Lesserson Linda , Ammar Tameshwar , DePerio Marietta , Vela-Cantos Frances , Fisher Cherie , Sarier Kaya 
Published: November 2003

Background
Platelet dysfunction is a major contributor to bleeding after cardiopulmonary bypass (CPB), yet it remains difficult to diagnose. A point-of-care monitor, the platelet-activated clotting time (PACT), measures accelerated shortening of the kaolin-activated clotting time by addition of platelet activating factor. The authors sought to evaluate the clinical utility of the PACT by conducting serial measurements of PACT during cardiac surgery and correlating postoperative measurements with blood loss.

Methods
In 50 cardiac surgical patients, blood was sampled at 10 time points to measure PACT. Simultaneously, platelet reactivity was measured by the thrombin receptor agonist peptide-induced expression of P-selectin, using flow cytometry. These tests were temporally analyzed. PACT values, P-selectin expression, and other coagulation tests were analyzed for correlation with postoperative chest tube drainage.

Results
PACT and P-selectin expression were maximally reduced after protamine administration. Changes in PACT did not correlate with changes in P-selectin expression at any time interval. Total 8-h chest tube drainage did not correlate with any coagulation test at any time point except with P-selectin expression after protamine administration (r = -0.4; P = 0.03).

Conclusions
The platelet dysfunction associated with CPB may be a result of depressed platelet reactivity, as shown by thrombin receptor activating peptide-induced P-selectin expression. Changes in PACT did not correlate with blood loss or with changes in P-selectin expression suggesting that PACT is not a specific measure of platelet reactivity.
Diaphragmatic Activity after Laparoscopic Cholecystectomy
Authors: Sharma Rajiv R. , Axelsson Hans , Oberg Ake , Jansson Erica , Clergue Francois , Johansson Goran , Reiz Sebastian 
Published: November 2003

Background
Laparoscopic cholecystectomy is presumed to induce a reduction in diaphragmatic activity. Indirect indices of diaphragmatic function based on tidal changes in pressures and cross-section area measurements can be unreliable in the postoperative phase. The present study evaluates diaphragmatic activity by directly recording diaphragmatic EMG (EMGdia) data, along with indirect indices.

Methods
Thirteen adult patients (American Society of Anesthesiologists physical status I or II) undergoing laparoscopic cholecystectomy were examined preoperatively for inspiratory tidal changes in gastric (Pgas-insp) and esophageal (Peso-insp) pressures, and tidal changes in ribcage (Vthor) and abdominal (Vabd) cross-section areas and then again at 1, 6, and 24 h postoperatively combined with EMGdia recordings. Variations in inspiratory gastric (deltaPgas-insp) and inspiratory transdiaphragmatic (deltaPdi-insp) pressures were derived from the above.

Results
Laparoscopic cholecystectomy induced a significant reduction in mean deltaPgas-insp, mean deltaPdi-insp, and mean Vabd indicating a reduction of diaphragmatic activity postoperatively. DeltaPdi-insp decreased from 11.8+/-4.0 cm H2O preoperatively to 5.7+/-5.7 cm H2O at 1 h and 6.6+/-5.1 cm H2O at 6 h postoperatively (mean +/- SD; P < 0.05). Vabd decreased from 327.0+/-113.0 ml preoperatively to 174.0+/-65.0 ml at 1 h and 175.0+/-98.0 ml at 6 h postoperatively (mean +/- SD; P < 0.05). These values had partially recovered at 24 h.

Conclusion
The direct and indirect indices of diaphragmatic activity taken together confirm the presence of reduction in diaphragmatic activity after laparoscopic cholecystectomy followed by its partial recovery at 24 h.
Morphine-sparing Effect of Acetaminophen in Pediatric Day-case Surgery
Authors: Korpela Reijo , Korvenoja Pekka , Meretoja Olli A. 
Published: November 2003

Background
Postoperative pain is a major problem in day-case surgery in children. Nonsteroidal antiinflammatory drugs have gained popularity in management of pediatric surgical patients to reduce the need for opioids. The aim of this study was to evaluate the efficacy of different doses of rectal acetaminophen in day-case surgery in children.

Methods
A randomized, double-blinded, placebo-controlled study design was used. Patients (n = 120) were randomized to receive a single dose of 0, 20, 40, or 60 mg/kg of rectal acetaminophen after induction of anesthesia. General anesthesia was induced by mask ventilation with sevoflurane (7%) in nitrous oxide and oxygen and maintained with 2.5-4.0% end-tidal sevoflurane. Opioids or local anesthetics were not used. Postoperative pain was evaluated by behavioral assessment and physiologic measurements every 10 min after arrival at the postanesthesia care unit. The pain intensity was scored using a 0-100 visual analog scale used in the authors' clinic. The need for rescue medication, intravenous morphine 0.1 mg/kg, was decided by the nurse, who was unaware of the rectal acetaminophen dose. The parents were interviewed by phone after 24 h regarding pain and its treatment, nausea, and vomiting. Rescue analgesia at home was rectal ibuprofen, 10 mg/kg.

Results
In the postanesthesia care unit pain scores were significantly lower in the 40- and 60-mg/kg groups compared with placebo and 20-mg/kg groups. Acetaminophen resulted in a dose-related reduction in the number of children who required postoperative rescue opioid, with significance reached with 40 or 60 mg/kg doses. Calculated dose of acetaminophen at which 50% of the children not requiring a rescue opioid was 35 mg/kg. The need for rescue analgesia at home during the first 24 h after surgery was also significantly less in patients in the 40- or 60-mg/kg groups than in the 0- or 20-mg/kg groups (20-17 vs. 80-63%). Thirty-three percent of patients receiving placebo had postoperative nausea and vomiting, compared with 0-3% in groups receiving 40 or 60 mg/kg acetaminophen.

Conclusions
A single dose of 40 or 60 mg/kg of rectal acetaminophen has a clear morphine-sparing effect in day-case surgery in children if administered at the induction of anesthesia. Moreover, children with adequate analgesia with acetaminophen have less postoperative nausea and vomiting.