bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantification and Distribution of Cerebral Emboli during Cardiopulmonary Bypass in the Swine
Authors: Plochl Walter , Cook David J. 
Published: November 2003

Background
Patients undergoing cardiac surgery have a substantial incidence of neurologic complications related to cerebral embolization during cardiopulmonary bypass. The purpose of this study was to determine if adjustments in the arterial carbon dioxide (PaCO2) level can reduce cerebral and ocular embolization.

Methods
Twenty pigs underwent cardiopulmonary bypass at 38 degrees C. At either hypercarbia (PaCO2 = 50-55 mmHg, group H, n = 10) or hypocarbia (PaCO2 = 25-30 mmHg, group L, n = 10), an embolic load of 1.2 x 10(50 67-microm orange fluorescent microspheres was injected into the aortic cannula. Before and after embolization, cerebral and ocular blood flows were determined at normocapnia using 15-microm fluorescent microspheres. After cardiopulmonary bypass was completed, the eyes were enucleated and brain tissue samples were collected. Microspheres were isolated and the fluorescence was measured.

Results
In groups H and L, the mean PaCO2 values at embolization were 52+/-3 mmHg and 27+/-2 mmHg, respectively (P < 0.0001). Total and regional embolization were significantly less in hypocapnia than in hypercapnic animals: 142% more emboli were detected in the brain in group H than in group L (P < 0.0001). Cerebral blood flow after embolization was unchanged in both groups. Similarly, fewer ocular emboli occurred in hypocapnic animals than in hypercapnic animals (P = 0.044), but in contrast to the brain, ocular blood flow decreased significantly in both groups after embolization.

Conclusions
Cerebral embolization is determined by the PaCO2 at the time of embolization. In cardiopulmonary bypass practice, reductions in PaCO2 during periods of embolic risk may reduce the risk for brain injury.
Assessment of Changes in Coagulation in Parturients with Preeclampsia Using Thromboelastography
Authors: Sharma Shiv K. , Philip John , Whitten Charles W. , Padakandla Udaya B. , Landers Dennis F. 
Published: November 2003

Background
Preeclampsia is associated with a risk of abnormal hemostasis that occurs most commonly secondary to thrombocytopenia. Thromboelastography measures whole blood coagulation and has been used to manage coagulation defects in obstetric patients. The authors conducted this investigation in a large number of preeclamptic women to assess changes in coagulation using thromboelastography.

Methods
Thromboelastography and platelet counts were performed in 52 healthy pregnant women, 140 mild preeclamptic women, and 114 severe preeclamptic women in active labor using disposable plastic cups and pins and native whole blood. In preeclamptic patients with a platelet count <100,000/mm3, conventional coagulation tests were also performed. Epidural analgesia was provided in some women when they requested pain relief.

Results
Fifteen percent of all preeclamptic women (38 of 254) and 2% (1 of 52) of healthy pregnant women had a platelet count <100,000/mm3. The incidence of thrombocytopenia <100,000/mm3 was 3% (4 of 140) and 30% (34 of 114) in mild preeclamptic patients and severe preeclamptic patients, respectively. Severe preeclamptic patients with a platelet count <100,000/mm3 were significantly hypocoagulable when compared to the other study groups. Ten severe preeclamptic women with a platelet count <100,000/mm3 had a maximum amplitude <54 mm (the lower limit of maximum amplitude in healthy pregnant women enrolled in this investigation). None of the mild preeclamptic women had a maximum amplitude <54 mm. Five severe preeclamptic women with a platelet count <100,000/mm3 had an abnormal coagulation profile, whereas all four mild preeclamptic women with a platelet count <100,000/mm3 had a normal coagulation profile.

Conclusion
This study shows that severe preeclamptic women with a platelet count <100,000/mm3 are hypocoagulable when compared to healthy pregnant women and other preeclamptic women.
Effects of Xenon on Hemodynamic Responses to Skin Incision in Humans
Authors: Nakata Yoshinori , Goto Takahisa , Morita Shigeho 
Published: November 2003

Background
The authors evaluated the hemodynamic suppressive effects of xenon in combination with sevoflurane at skin incision in patients undergoing surgery.

Methods
Forty patients were assigned randomly to receive one of the following four anesthetics: 1.3 minimum alveolar concentration (MAC) sevoflurane, 0.7 MAC xenon with 0.6 MAC sevoflurane, 1 MAC xenon with 0.3 MAC sevoflurane, or 0.7 MAC nitrous oxide with 0.6 MAC sevoflurane (n = 10 each group). Systolic blood pressure and heart rate were measured before anesthesia, before incision, and approximately 1 min after incision.

Results
The changes in hemodynamic variables in response to incision were less with sevoflurane in combination with xenon and nitrous oxide than with sevoflurane alone. Changes in heart rate (in beats/min) were 19+/-11 (+/- SD) for sevoflurane alone, 11+/-6 for 0.7 MAC xenon-sevoflurane, 4+/-4 for 1 MAC xenon-sevoflurane, and 8+/-7 for nitrous oxide-sevoflurane. Changes in systolic blood pressure were 35+/-18 mmHg for sevoflurane alone, 18+/-8 mmHg for 0.7 MAC xenon-sevoflurane, 16+/-7 mmHg for 1 MAC xenon-sevoflurane, and 14+/-10 mmHg for nitrous oxide-sevoflurane.

Conclusions
Xenon and nitrous oxide in combination with sevoflurane can reduce hemodynamic responses to skin incision compared with sevoflurane alone. One probable explanation may be that xenon has analgesic properties similar to those of nitrous oxide, although the exact mechanism is yet to be determined.
Molar Potency Is Predictive of the Speed of Onset of Neuromuscular Block for Agents of Intermediate, Short, and Ultrashort Duration
Authors: Kopman Aaron F. , Klewicka Monica M. , Kopman David J. , Neuman George G. 
Published: November 2003

Background
The times to peak effect of rocuronium, vecuronium, cisatracurium, mivacurium, and succinylcholine were evaluated to confirm that the correlation between potency and onset time observed for long-acting relaxants also held for drugs of intermediate and short duration.

Methods
The authors recruited 99 patients classified as American Society of Anesthesiologists physical status score 1 or 2 for the study. After anesthesia was induced, tracheal intubation was accomplished without relaxants. Anesthesia was maintained with nitrous oxide and 3% or 4% end-tidal desflurane plus intravenous narcotic supplementation. The evoked electromyographic response to single stimuli administered at 0.10 Hz was recorded continuously. Drug doses were selected to produce approximately 95% twitch depression. If peak twitch depression did not fall in the range of 90% to 98%, the patient was excluded from the study. The time to 50% to 90% of peak effect was plotted as a function of the administered dose.

Results
There was no difference in the onset profiles of mivacurium and vecuronium, or in the time to 50% of peak effect between succinylcholine and rocuronium. For all other parameters, onset times ranked as follows: succinylcholine < rocuronium < vecuronium-mivacurium < cisatracurium (P < 0.05). When the log of the ED95 in micromoles per kilogram for all five drugs was plotted against the log of onset time to 50% peak effect, the R2 value for the best fit line was more than 0.98.

Conclusions
The inverse correlation between the molar potency and speed of onset previously described for agents of long duration also applies to nondepolarizing agents of intermediate and short duration. The onset time of succinylcholine also appears to be compatible with this relation.
Immunochemical Evidence against the Involvement of Cysteine Conjugate β-lyase in Compound A Nephrotoxicity in Rats
Authors: Njoku Dolores B. , Pohl Lance R. , Sokoloski Edward A. , Marchick Michael R. , Borkowf Craig B. , Martin Jackie L. 
Published: November 2003

Background
Compound A, a degradation product of sevoflurane, causes renal corticomedullary necrosis in rats. Although the toxicity of this compound was originally hypothesized to result from the biotransformation of its cysteine conjugates into toxic thionoacyl halide metabolites by renal cysteine conjugate beta-lyase, recent evidence suggests that alternative mechanisms may be responsible for compound A nephrotoxicity. The aim of this study was to evaluate these issues by determining whether mercapturates and glutathione conjugates of compound A could produce renal corticomedullary necrosis in rats, similar to compound A, and whether renal covalent adducts of the thionacyl halide metabolite of compound A could be detected immunochemically.

Methods
Male Wistar rats were administered, intraperitoneally, N-acetylcysteine conjugates (mercapturates) of compound A (90 or 180 micromol/kg) or glutathione conjugates of compound A (180 micromol/kg) with or without intraperitoneal pretreatments with aminooxyacetic acid (500 micromol/kg) or acivicin (250 micromol/kg). Rats were killed after 24 h, and kidney tissues were analyzed for toxicity by histologic examination or for protein adducts by immunoblotting or immunohistochemical analysis, using antisera raised against the covalently bound thionoacyl halide metabolite of compound A.

Results
Mercapturates and glutathione conjugates of compound A both produced renal corticomedullary necrosis similar to that caused by compound A. Aminooxyacetic acid, an inhibitor of renal cysteine conjugate beta-lyase, did not inhibit the toxicity of the mercapturates, whereas acivicin, an inhibitor of gamma-glutamyltranspeptidase, potentiated the toxicity of both classes of conjugates. No immunochemical evidence for renal protein adducts of the thionacyl halide metabolite was found in rats 24 h after the administration of the mercapturates of compound A or in the kidneys of rats, obtained from a previous study, 5 and 24 h after the administration of compound A.

Conclusion
The results of this study are consistent with the idea that a mechanism other than the renal cysteine conjugate beta-lyase pathway of metabolic activation is responsible for the nephrotoxicity of compound A and its glutathione and mercapturate conjugates in male Wistar rats.
Nitrous Oxide Produces Antinociceptive Response via α2Band/or α2CAdrenoceptor Subtypes in Mice
Authors: Guo Tian-Zhi , Davies Frances M. , Kingery Wade S. , Patterson Andrew J. , Limbird Lee E. , Maze Mervyn 
Published: November 2003

Background
Opiate receptors in the periaqueductal gray region and alpha2 adrenoceptors in the spinal cord of the rat mediate the antinociceptive properties of nitrous oxide (N2O). The availability of genetically altered mice facilitates the detection of the precise protein species involved in the transduction pathway. In this study, the authors establish the similarity between rats and mice in the antinociceptive action of N2O and investigate which alpha2 adrenoceptor subtypes mediate this response.

Methods
After obtaining institutional approval, antinociceptive dose-response and time-course to N2O was measured in wild-type and transgenic mice (D79N), with a nonfunctional alpha2A adrenoceptor using tail-flick latency. The antinociceptive effect of N2O was tested after pretreatment systemically with yohimbine (nonselective alpha2 antagonist), naloxone (opiate antagonist), L659,066 (peripheral alpha2-antagonist) and prazosin (alpha2B- and alpha2C-selective antagonist). The tail-flick latency to dexmedetomidine (D-med), a nonselective alpha2 agonist, was tested in wild-type and transgenic mice.

Results
N2O produced antinociception in both D79N transgenic and wild-type litter mates, although the response was less pronounced in the transgenic mice. Antinociception from N2O decreased over time with continuing exposure, and the decrement was more pronounced in the transgenic mice. The antinociceptive response could be dose dependently antagonized by opiate receptor and selective alpha2B-/alpha2C-receptor antagonists but not by a central nervous system-impermeant alpha2 antagonist (L659,066). Whereas dexmedetomidine exhibited no antinociceptive response in the D79N mice, the robust antinociceptive response in the wild-type litter mates could not be blocked by a selective alpha2B-/alpha2C-receptor antagonist.

Conclusion
These data confirm that the antinociceptive response to an exogenous alpha2-agonist is mediated by an alpha2A adrenoceptor and that there appears to be a role for the alpha2B- or alpha2C-adrenoceptor subtypes, or both, in the analgesic response to N2O.
Effects of Temperature and Volatile Anesthetics on GABAAReceptors
Authors: Jenkins Andrew , Franks Nicholas P. , Lieb William R. 
Published: November 2003

Background
Potentiation of the activity of the gamma-aminobutyric acid type A (GABA(A)) receptor channel by volatile anesthetic agents is usually studied in vitro at room temperature. Systematic variation of temperature can be used to assess the relevance of this receptor to general anesthesia and to characterize the modulation of its behavior by volatile agents at normal body temperature.

Methods
Potentiation of the GABA(A) receptor by halothane, sevoflurane, isoflurane, and methoxyflurane was studied at six temperatures in the range 10-37 degrees C using the whole-cell patch-clamp technique and mouse fibroblast cells stably transfected with defined GABA(A) receptor subunits.

Results
Control GABA concentration-response plots showed small and physically reasonable changes in the GABA concentration required for a half-maximal effect, the Hill coefficient, and maximal response over the range 10-30 degrees C. Potentiations of GABA (1 microM) responses by aqueous minimum alveolar concentrations of the volatile anesthetic agents decreased with increasing temperature from 10-37 degrees C in an agent-specific manner (methoxyflurane > isoflurane > sevoflurane > halothane) but tended to equalize at normal body temperature (37 degrees C). These findings are in line with published results on the temperature dependence of anesthetic potencies in animals.

Conclusions
These results are consistent with direct binding of volatile anesthetic agents to the GABA(A) receptor channel playing an important role in general anesthesia. The finding that the degree of anesthetic potentiation was agent-specific at low temperatures but not at 37 degrees C emphasizes the importance of doing in vitro experiments at normal body temperature.
Intrathecal Clonidine Alleviates Allodynia in Neuropathic Rats
Authors: Pan Hui-Lin , Chen Shao-Rui , Eisenach James C. 
Published: November 2003

Background
Intrathecally administered clonidine increases release of spinal acetylcholine, which may be related to its analgesic action in neuropathic pain. The current study determined the role of spinal muscarinic and nicotinic receptors in the antiallodynic effect of intrathecally administered clonidine in spinal nerve-ligated rats.

Methods
Allodynia was produced in rats by ligation of the left L5-L6 spinal nerves. Mechanical allodynia was determined by application of von Frey filaments to the left hindpaw. The effect of intrathecal injection of saline, two muscarinic receptor antagonists (atropine and scopolamine), and two nicotinic receptor antagonists (mecamylamine and hexamethonium) on the antiallodynic action produced by intrathecal administration of 20 microg clonidine was assessed in six groups of animals. Each group consisted of six to eight rats.

Results
Intrathecal injection of saline or muscarinic or nicotinic receptor antagonists did not alter the withdrawal thresholds. The antiallodynic effect produced by intrathecally administered clonidine was attenuated in a dose-dependent manner by intrathecal treatment with muscarinic and nicotinic antagonists. Although nicotinic receptor antagonists only partially attenuated the effect of clonidine, blockade of spinal muscarinic receptors almost abolished the antiallodynic effect of clonidine.

Conclusions
These results demonstrate that the analgesic effect of intrathecally administered clonidine on neuropathic pain is mediated by spinal muscarinic and nicotinic receptors. Therefore, this study provides functional evidence that spinally released acetylcholine plays a role in the antiallodynic effect of intrathecally administered clonidine in neuropathic pain.
Effects of Xenon on the Performance of Various Respiratory Flowmeters
Authors: Goto Takahisa , Saito Hayato , Nakata Yoshinori , Uezono Shoichi , Ichinose Fumito , Uchiyama Masanori , Morita Shigeho 
Published: November 2003

Background
The anesthetic gas xenon has distinctly different physical properties compared with air, nitrous oxide, or oxygen. This led us to predict that xenon would affect the performance of commercially available flowmeters.

Methods
Flow was generated by an anesthesia ventilator connected to a lung simulator via a semiclosed breathing circuit. With the system filled with air or with various concentrations of xenon or nitrous oxide in a balance of oxygen, the tidal volume was measured with two rotating vanes, a Pitot tube, a variable-orifice flowmeter, and two constant-temperature hot-wire flowmeters.

Results
Although xenon minimally affected both rotating vane flowmeters, it caused the Pitot tube and the variable-orifice flowmeters to overread in proportion to the square root of the density of the gas mixture used (xenon is 4.6 times more dense than air). In contrast, the hot-wire anemometers underread with xenon; for example, their readings in the presence of 45% and 70% xenon were less than 10% of those displayed when air was used. Nitrous oxide minimally affected all the flowmeters except the variable-orifice device. The Pitot flowmeter was also affected, but only when its gas analyzer port was open to the ambient air so that it no longer corrected its readings for changes in gas composition. In these cases, nitrous oxide produced overreadings in the same manner as did xenon.

Conclusion
Among the four types of flowmeters studied, only the rotating-vane type is sufficiently accurate for use during anesthesia with xenon.
Increased Reading Speed for Stories Presented during General Anesthesia
Authors: Munte Sinikka , Kobbe Isabelle , Demertzis Avra , Lullwitz Ekkehard , Munte Thomas F. , Piepenbrock Siegfried , Leuwer Martin 
Published: November 2003

Background
In the absence of explicit memories such as the recall and recognition of intraoperative events, memory of auditory information played during general anesthesia has been demonstrated with several tests of implicit memory. In contrast to explicit memory, which requires conscious recollection, implicit memory does not require recollection of previous experiences and is evidenced by a priming effect on task performance. The authors evaluated the effect of a standardized anesthetic technique on implicit memory, first using a word stem completion task, and then a reading speed task in a subsequent study.

Methods
While undergoing lumbar disc surgery, 60 patients were exposed to auditory materials via headphones in two successive experiments. A balanced intravenous technique with propofol and alfentanil infusions and a nitrous oxide-oxygen mixture was used to maintain adequate anesthesia. In the first experiment, 30 patients were exposed randomly to one of the two lists of 34 repeated German nouns; in the second experiment, 30 patients were exposed to one of two tapes containing two short stories. Thirty control patients for each experiment heard the tapes without receiving anesthesia. All patients were tested for implicit memory 6-8 h later: A word stem completion task for the words and a reading speed task for the stories were used as measures of implicit memory.

Results
The control group completed the word stems significantly more often with the words that they had heard previously, but no such effect was found in the anesthetized group. However, both the control and patient groups showed a decreased reading time of about 40 ms per word for the previously presented stories compared with the new stories. The patients had no explicit memory of intraoperative events.

Conclusions
Implicit memory was demonstrated after anesthesia by the reading speed task but not by the word stem completion task. Some methodologic aspects, such as using low frequency words or varying study and test modalities, may account for the negative results of the word stem completion task. Another explanation is that anesthesia with propofol, alfentanil, and nitrous oxide suppressed the word priming but not the reading speed measure of implicit memory. The reading speed paradigm seems to provide a stable and reliable measurement of implicit memory.
Effects of Anticholinergics on Postoperative Vomiting, Recovery, and Hospital Stay in Children Undergoing Tonsillectomy with or without Adenoidectomy
Authors: Chhibber Ashwani K. , Lustik Stewart J. , Thakur Rajbala , Francisco David R. , Fickling Kenneth B. 
Published: November 2003

Background
Nausea and vomiting are the most frequent problems after minor ambulatory surgical procedures. The agents used to induce and maintain anesthesia may modify the incidence of emesis. When neuromuscular blockade is antagonized with anticholinesterases, atropine or glycopyrrolate is used commonly to prevent bradycardia and excessive oral secretions. This study was designed to evaluate the effect of atropine and glycopyrrolate on postoperative vomiting in children.

Methods
Ninety-three patients undergoing tonsillectomy with or without adenoidectomy were studied. After inhalation induction of anesthesia with nitrous oxide, oxygen, and halothane, anesthesia was maintained with a nitrous oxide-oxygen mixture, halothane, morphine, and atracurium. Patients were randomized to receive, in a double-blinded manner, either 15 microg/kg atropine or 10 microg/kg glycopyrrolate with 60 microg/kg neostigmine to reverse neuromuscular blockade. Patient recovery, the incidence of postoperative emesis, antiemetic therapy, and the duration of postoperative hospital stay were assessed.

Results
There were no significant differences in age, gender, weight, or discharge time from the postanesthesia care unit or the hospital between the groups. Twenty-four hours after operation, the incidence of vomiting in the atropine group (56%) was significantly less than in the glycopyrrolate group (81%; P<0.05). There was no significant difference between the atropine and glycopyrrolate groups in the number of patients who required antiemetics or additional analgesics.

Conclusions
In children undergoing tonsillectomy with or without adenoidectomy, reversal of neuromuscular blockade with atropine and neostigmine is associated with a lesser incidence of postoperative emesis compared with glycopyrrolate and neostigmine.