P Pu ur rp po os se e: : To compare the influence of a longer duration of intraperitoneal CO 2 insufflation with head-up tilt on electrocardiogram indices during laparoscopic cholecystectomy between elderly and younger patients.M Me et th ho od ds s: : Twelve elderly and 12 younger patients were studied. In all patients, intraperitoneal CO 2 insufflation was performed for more than 150 min in the head-up position. RR interval, QT interval, the rate-corrected QT (QTc) interval, QT dispersion (QTD) and the rate-corrected QTD (QTcD) were measured.
Purpose: To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.Methods: Forty gerbils were randomly assigned to five groups: Group I, control, sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg·kg -1 propofol; Group IV, ischemia/reperfusion treated with 100 mg·kg -1 propofol; Group V, ischemia /reperfusion treated with 150 mg·kg -1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N 2 O/O 2 /halothane anesthesia after propofol or PSS. Five days later, the cerebrum was removed and each forebrain was cut into two including the hippocampus. Lipid peroxidation was determined using the production of malondialdehyde (MDA), and histopathological changes in the hippocampal CA1 subfield were examined.Results: In group II, the pyramidal cells were atrophic and pycnotic; vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. Degenerative ratios of pyramidal cells were: Group I: 4.9 ± 2.3, Group II: 94.1 ± 4.5 (P < 0.01), Group III: 12.5 ± 5.7, Group IV: 11.0 ± 4.6, Group V: 9.6 ± 4.9%. Production of MDA was: Group I: 83 ± 22, Group II: 198 ± 25 (P < 0.01), Group III: 153 ± 39, Group IV: 113 ± 34, Group V: 106 ± 27 nmol·g -1 wet tissue.Conclusion: Propofol attenuated delayed neuronal death by preventing lipid peroxidation induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.Objectif : Vérifier si le propofol empêche la peroxydation lipidique qui survient à la mort neuronale différée induite par une ischémie transitoire du prosencéphale, dans le sous-champ CA1 de l'hippocampe chez des gerbilles.Méthode : On a réparti au hasard 40 gerbilles en cinq groupes : dans le groupe 1, témoin, elles ont subi une opération fictive traitée avec une solution physiologique salée (SPS); dans le groupe II, une ischémie/reperfusion traitée avec une SPS; dans le groupe III, une ischémie/reperfusion traitée avec 50 mg·kg -1 de propofol; dans le groupe IV, une ischémie/reperfusion traitée avec 100 mg·kg -1 de propofol et dans le groupe V, une ischémie/reperfusion traitée avec 150 mg·kg -1 de propofol. L'ischémie transitoire du cerveau antérieur a été induite par l'occlusion bilatérale des artères carotides communes pendant quatre minutes sous anesthésie au N 2 O/O 2 /halothane après l'administration de propofol ou de SPS. Cinq minutes plus tard, le cerveau a été retiré et chaque prosencéphale a été coupé en deux, incluant l'hippocampe. La peroxydation lipidique a été déterminée en utilisant la production de malondialdéhyde (MDA), et les changements histopathologiques du sous-champ CA1 de l'hippocampe ont été examinés.Résultats : Dans le groupe II, les cellules pyramidales étaient atrophiques et pycnotiques; une rupture vacuolaire et stru...
This study compared the effect of intraperitoneal CO2 insufflation with abdominal wall lift on RR interval, QT interval, the rate-corrected QT (QTc) interval, QT dispersion (QTD), and the rate-corrected QTD (QTcD) using computerized measurement during laparoscopic cholecystectomy. Thirty patients scheduled for laparoscopic cholecystectomy were randomly assigned to 2 groups: intraperitoneal CO2 insufflation (CO2 group) or abdominal wall lift (lift group). A 12-lead electrocardiogram was monitored to measure parameters. The RR interval, QT interval, and QTc interval did not change significantly during the study in both groups. The QTD and QTcD in the CO2 group increased significantly during CO2 insufflation, and were significantly higher than those of the lift group. Statistically significant increases of QTD and QTcD, which are associated with an increased risk of arrhythmias and cardiac events, occur during CO2 insufflation, and QTD and QTcD in the CO2 group were significantly higher than those of the lift group.
Toshimitsu Kitajima MDPurpose: We investigated the relationship between the generation of superoxide radicals and histopathological changes on delayed neuronal death in the hippocampal CA I subfield. Methods: Seventy gerbils were randomly assigned to two groups, a sham group and an ischaemia/reperfusion (I/R) group. In the I/R group, transient forebrain ischaemia was induced by occluding the bilateral common carotid arteries for four minutes. The cerebrum was removed after reperfusion at intervals of one minute, six, twelve and twentyfour hr and at three, five and seven days. Each forebrain was cut into two portions including the hippocampus. The quantity of superoxide radicals was measured by using chemiluminescence, and histopathological changes in the hippocampal CAI subfield were examined. Results: In the I/R group, superoxide radicals increased on the 3rd and 5th days compared with the sham group (16.1 ___ 3.4 vs 3.2 ___ 1.0 onthe third day(P < 0.0001); 10.9 + 1.9 vs 3.3 ___ 0.8 onthe fifth day (P < 0.0001)). In the I/R group, the pyramidal cells were atrophic and pycnotic; vacuolation, and structural disruption of the radial striated zone were observed from the third through the seventh day. In the sham group, these changes were not observed. There were differences of degenerative ratios in the pyramidal cells between the two groups from the third to seventh days (5.6 • 2.0 vs 80.9 +_ 3.3 on the third day (P < 0.05); 6.9 +--0.4 vs 93.6 ---2.4 on the fifth clay (P < 0.05); 6.2 _ 1.5 vs 95.0 ___ 1.3 on the seventh day (P < 0.05)). Condusion: There is a correlation between the generation of superoxide radicals and histopathological changes of the pyramidal cells in the hippocampal CAI subfield.Objectif: Investiguer la relation entre la production des radicaux superoxydes et les changements histopathologiques sur led&& neuronal retard~ darts le champ hippocampique CAl. M&hodes : Soixante-dix gerbilles ont ~t~ al6atoirement r~parties en 2 groupes, un groupe contr61e et un groupe isch~mie/reperfusion (I/R). Darts le groupe I/R, une isch~mie transitoire du prosenc6phale 6tait induite par rocclusion bilat&ale des carotides communes pour quatre minutes. Apr~s reperfusion, le cerveau ~tait retir~ de l'animal apr~s une minute de m~.me qu'~ six, douze et vingt-quatre heures ainsi qu'~ trois, cinq et sept jours. Chaque prosenc~phale ~tait coup~ en deux parties incluant l'hippocampe. La quantit6 de radicaux superoxydes &ait mesur& par chemiluminescence et les changements histopathologiques dans le champ hippocampique C.AI ~taient observ&. R&ultats : Darts le groupe I/R, les radicaux superoxydes ont augment~ aux jours 3 et 5 comparativement au groupe t~moin (I 6, I ---3,4 vs 3,2 + 1,0 au jour 3 (P<0,0001); 10,9 + 1,9 vs 3,3 ---0,8 au jour 5 (m<0,0001)). Darts le groupe I/R, les cellules pyramidales ~taient atrophiques et picnotiques; du 3e au 7e jour, on a observ~ de la vacuolisation et de la destruction structurale de la zone stri~e radiaire, et ces changements n'ont pas &6 retrouv& darts le groupe t~moin. On a observ~ ...
Significant increases of QT interval, QTc interval, and QTcD, which are associated with an increased risk of ventricular arrhythmias and cardiac events, occur immediately after head-up tilt in right SGB. However, head-up tilt does not induce increases of QT interval, QTc interval, QTD, and QTcD in left SGB.
A combination of low-molecular-weight heparin and intermittent pneumatic compression may be more effective to prevent deep-vein thrombosis in the legs.
The QTc interval, QTD, and QTcD, which were associated with increased risks of ventricular arrhythmias, increased significantly before anesthetic induction in patients with major depression. Electrical stimulus during ECT induced further increases of the QTD and QTcD.
The A11 dopaminergic cell group is the only group among the A8-A16 dopaminergic cell groups that includes neurons innervating the spinal cord, and a decrease in dopaminergic transmission at the spinal cord is thought to contribute to the pathogenesis of restless legs syndrome. However, the mechanisms regulating the neuronal activity of A11 dopaminergic neurons remain to be elucidated. Unraveling the neuronal composition, distribution and connectivity of A11 neurons would provide insights into the mechanisms regulating the spinal dopaminergic system. To address this, we performed immunohistochemistry for calcium-binding proteins such as calbindin (Calb) and parvalbumin (PV), in combination with the retrograde tracer Fluorogold (FG) injected into the spinal cord. Immunohistochemistry for Calb, PV, or tyrosine hydroxylase (TH), a marker for dopaminergic neurons, revealed that there were at least three types of neurons in the A11 region: neurons expressing Calb, TH, or both TH and Calb, whereas there were no PV-immunoreactive (IR) cell bodies. Both Calb- and PV-IR processes were found throughout the entire A11 region, extending in varied directions depending on the level relative to bregma. We found retrogradely labeled FG-positive neurons expressing TH, Calb, or both TH and Calb, as well as FG-positive neurons lacking both TH and Calb. These findings indicate that the A11 region is composed of a variety of neurons that are distinct in their neurochemical properties, and suggest that the diencephalospinal dopamine system may be regulated at the A11region by both Calb-IR and PV-IR processes, and at the terminal region of the spinal cord by Calb-IR processes derived from the A11 region.
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