Shinsuke Hamaguchi

Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Purpose: To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CAI 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 N2O/O2/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 CAI 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 CAI subfield in gerbils.RésuméObjectif: Vérfier 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 CAI de l’hippocampe chez des gerbilles.Méthode: On a réparti au hasard 40 gerbilles en cinq groupes: dans le groupe I, 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 N2O/O2/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, induant l’hippocampe. La peroxydation lipidique a été déterminée en utilisant la production de malondialdéhyde (MDA), et les changements histopathologiques du sous-champ CAI de l’hippocampe ont été examinés.Résultats: Dans le groupe II, les cellules pyramidales étaient atrophiques et pycnotiques; une rupture vacuolaire et structurale de la zone radiale striée a été observée. Dans les autres groupes, ces changements n’ont pas été notés. Les taux de cellules pyramidales dégénératives ont été: groupe I: 5,8±2,5 %, groupe II: 94,1±4,5 (P<0,01), groupe III: 12,5±5,7 %, group IV: 11,0±4,6 %, groupe V: 9,4±6,6 %. La production de MDA a été dans le groupe I: 83±22, II: 198±25 (P<0,01), III: 153±39, IV: 113±34 et V: 106±27 nmol·g−1 de tissu.Conclusion: Le propofol a réduit la mort neuronale différée en empêchant la peroxydation lipidique induite par l’ischémie transitoire du prosencéphale dans le sous-champ CAI de l’hippocampe de gerbilles.

Superoxide radical generation and histopathological changes in hippocampal CA1 after ischaemia/ reperfusion in gerbils

PurposeWe investigated the relationship between the generation of Superoxide radicals and histopathological changes on delayed neuronal death in the hippocampal CA1 subfield.MethodsSeventy 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 twenty-four 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.ResultsIn the I/R group, Superoxide radicals increased on the 3rd and 5th days compared with the sham group (16.1 ±3.4vs3.2± 1.0 on the third day (P < 0.0001 ); 10.9 ± 1.9 vs 3.3 ± 0.8 on the 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 day (P < 0.05); 6.2 ± 1.5 vs 95.0 ± 1.3 on the seventh day (P < 0.05)).ConclusionThere is a correlation between the generation of Superoxide radicals and histopathological changes of the pyramidal cells in the hippocampal CAI subfield.RésuméObjectifInvestiguer la relation entre la production des radicaux superoxydes et les changements histopathologiques sur le décès neuronal retardé dans le champ hippocampique CAL.MéthodesSoixante-dix gerbilles ont été aléatoirement réparties en 2 groupes, un groupe contrôle et un groupe ischémie/reperfusion (I/R). Dans le groupe I/R, une ischémie transitoire du prosencéphale était induite par l’occlusion bilatérale des carotides communes pour quatre minutes. Après reperfusion, le cerveau était retiré de l’animal après une minute de même qu’à six, douze et vingt-quatre heures ainsi qu’à trois, cinq et sept jours. Chaque prosencéphale était coupé en deux parties incluant l’hippocampe. La quantité de radicaux superoxydes était mesurée par chemiluminescence et les changements histopathologiques dans le champ hippocampique CAI étaient observés.RésultatsDans le groupe I/R, les radicaux superoxydes ont augmenté aux jours 3 et 5 comparativement au groupe témoin (16,1 ±3,4 vs 3,2± 1,0 au jour 3 (P< 0,000l); 10,9 ± 1,9 vs 3,3 ± 0,8 au jour 5 (P< 0,000l)). Dans le groupe I/R, les cellules pyramidales étaient atrophiques et picnotiques; du 3e au 7e jour, on a observé de la vacuolisation et de la destruction structurale de la zone striée radiaire, et ces changements n’ont pas été retrouvés dans le groupe témoin. On a observé des différences dans le pourcentage dégénératif des cellules pyramidales entre les deux groupes à partir du jour 3 au jour 7 (5,6 ± 2,0 vs 80,9 ± 3,3 au jour 3 (P< 0,05); 6,9 ± 0,4 vs 93,6 ± 2,4 au jour 5 (P< 0,05); 6,2 ± 1,5vs 95,0 ± 1,3 au jour 7 (P< 0,05)).ConclusionIl y a une corrélation entre la production de radicaux superoxydes et les changements histopathologiques des cellules pyramidales du champ CAI de l’hippocampe.

A combination of heparin and an intermittent pneumatic compression device may be more effective to prevent deep-vein thrombosis in the lower extremities after laparoscopic cholecystectomy

BackgroundThe purpose of this study was to clarify the effect of a combination of heparin and an intermittent pneumatic compression device on thrombogenesis and platelet activation in the upper and lower extremities after laparoscopy.MethodsA blinded study was performed on 30 patients. Patients were randomly injected with either heparin or physiological saline solution (PSS) subcutaneously. The intermittent compression boot was used during surgery. Plasma D-dimer (D-D), a, marker of thrombogenesis, and β-thromboglobulin (β-TG), a marker of platelet activation, were measured in the upper and lower extremities.ResultsIn the heparin group, D-Ds in the upper and lower extremities increased significantly 24 h after surgery, but they were significantly lower than those of the PSS group. β-TG in the low-r extremities of patients in the PSS group increased significantly 24 h after surgery.ConclusionA combination of low-molecular-weight heparin and intermittent pneumatic compression may be more effective to prevent deep-vein thrombosis in the legs.

Effects of head-up tilt after stellate ganglion block on QT interval and QT dispersion.

Background and Objectives The aim of this study is to examine the effects of head-up tilt (70°) 30 minutes after right or left stellate ganglion block (SGB) on RR interval, QT interval, the rate-corrected QT (QTc) interval, QT dispersion (QTD), and the rate-corrected QT dispersion (QTcD) using computerized measurement. Methods Ten healthy volunteers underwent both right and left SGBs using 7 mL 1% mepivacaine with a 7-day interval between the two blocks. A 12-lead electrocardiogram was monitored to measure parameters before SGB; 30 minutes after SGB (before head-up tilt); and immediately, 5, 10, and 15 minutes after head-up tilt. Results Right SGB induced significant increases in QT interval, QTc interval, QTD, and QTcD from 30 minutes after the block through 15 minutes after head-up tilt. There were significant increases of QT interval, QTc interval, and QTcD between before and immediately after head-up tilt in right SGB. Left SGB induced significant decreases of QT interval and QTc interval from 30 minutes after SGB through 15 minutes after head-up tilt. Left SGB also induced a significant decrease of QTD from immediately after through 10 minutes after head-up tilt. Conclusions 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.

Comparison between intraperitoneal CO2 insufflation and abdominal wall lift on QT dispersion and rate-corrected QT dispersion during laparoscopic cholecystectomy.

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.

Addition of clonidine increases duration and magnitude of vasodilative effect induced by sympathetic block with mepivacaine in dogs.

Background and Objectives The aim of this study is to examine the duration and magnitude of vasodilative effect induced by sympathetic block with the addition of clonidine to mepivacaine. Methods We measured mean arterial pressure (MAP), heart rate (HR), and right and left brachial artery blood flow (BABF) before and after stellate ganglion block (SGB) in dogs. The experimental protocol was designed as follows: (1) left SGB using 1.0 mL 0.5% mepivacaine (n = 6) and (2) left SGB using the addition of clonidine 0.5 μg to 1.0 mL 0.5% mepivacaine (n = 6). Results MAP and HR did not change significantly throughout the study in either group. Left SGB with mepivacaine increased left BABF significantly from 10 minutes through 50 minutes after SGB (baseline, 100%; peak at 10 minutes after SGB, 176% ± 28%; P < .01). Left SGB with the addition of clonidine to mepivacaine induced a significant increase of left BABF from 10 minutes through 70 minutes after SGB (baseline, 100%; peak at 10 minutes after SGB, 223% ± 42%; P < .01). The values of left BABF after SGB with the addition of clonidine to mepivacaine were significantly higher than those of SGB with mepivacaine alone from 10 minutes through 80 minutes after SGB (P < .05). Right BABF decreased significantly after SGB throughout the study in both groups. Conclusions The addition of clonidine increases both duration and magnitude of the vasodilative effect induced by sympathetic block over that caused by mepivacaine alone.

Assessment of Qt Interval and Qt Dispersion During Electroconvulsive Therapy Using Computerized Measurements

Background: Electroconvulsive therapy (ECT) used in the treatment of severe psychiatric disorders induces stimulation of the autonomic nervous system with initial parasympathetic outflow immediately followed by a sympathetic response. These responses induce an initial bradycardia, arrhythmias, and hypertension. QT dispersion (QTD), defined as maximal QT interval minus minimal QT interval on 12 leads of the surface electrocardiogram, reflects regional heterogeneity of ventricular repolarization. The effects of electrical stimulus due to ECT on QT interval and QTD are of considerable interest. Objective: This study was designed to investigate the effects of electrical stimulation caused by ECT on RR interval, QT interval, the rate-corrected QT (QTc) interval, QTD, and the rate-corrected QTD (QTcD) under general anesthesia using computerized measurements. Methods: Thirty psychiatric patients scheduled for ECT were studied under propofol anesthesia. A 12-lead electrocardiogram was monitored to measure parameters. Muscle paralysis was achieved by administering succinylcholine 1 mg/kg intravenously, and the efficacy of ECT was determined by the tourniquet technique. Results: The RR interval and QT interval decreased significantly immediately after electrical stimulus, and returned to the baseline level 1 minute after electrical stimulus. In 25 out of 30 patients, the baseline value of QTc interval was higher than the normal limits, and the QTc interval decreased significantly for 2 minutes after electrical stimulus. In 27 out of 30 patients, the baseline values of QTD and QTcD were higher than the normal limits, and the QTD and QTcD increased significantly from immediately after electrical stimulus to 5 minutes after electrical stimulus. Conclusions: 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.

Comparison of 0.25% levobupivacaine, 0.25% bupivacaine, and 0.125% bupivacaine for duration and magnitude of action in peripheral arterial blood flow induced by sympathetic block in dogs.

Background and Objectives: The aim of this study is to compare 0.25% levobupivacaine with 0.25% bupivacaine and 0.125% bupivacaine to examine the duration and magnitude of vasodilative effect induced by sympathetic block. Methods: We measured mean arterial pressure (MAP), heart rate (HR), and right and left brachial-artery blood flow (BABF) before and after cervicothoracic sympathetic block in 24 dogs. The experimental protocol was designed as follows: (1) left cervicothoracic sympathetic block with 1.0 mL of 0.25% levobupivacaine (n = 8), (2) left cervicothoracic sympathetic block with 1.0 mL of 0.25% bupivacaine (n = 8), and (3) left cervicothoracic sympathetic block with 1.0 mL of 0.125% bupivacaine (n = 8). Results: MAP and HR did not change significantly throughout the study in either group. Left cervicothoracic sympathetic block with 0.25% levobupivacaine increased left BABF significantly from 5 minutes through 80 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 185 ± 35%; P <.01). Left cervicothoracic sympathetic block with 0.25% bupivacaine increased left BABF significantly from 5 minutes through 100 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 251 ± 47%; P < .01). Left cervicothoracic sympathetic block with 0.125% bupivacaine increased left BABF significantly from 5 minutes through 80 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 155 ± 20%; P < .01). Conclusions: 0.25% Levobupivacaine may have a lower potency compared with 0.25% bupivacaine in sympathetic block in dogs.

QT interval and QT dispersion increase in the elderly during laparoscopic cholecystectomy: a preliminary study

PurposeTo compare the influence of a longer duration of intraperitoneal CO2 insufflation with head-up tilt on electrocardiogram indices during laparoscopic cholecystectomy between elderly and younger patients.MethodsTwelve elderly and 12 younger patients were studied. In all patients, intraperitoneal CO2 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.ResultsThe QT interval and the QTc interval increased significantly from 120 to 150 min after CO2 insufflation in the elderly. The QTD and QTcD increased significantly during CO2 insufflation in both groups. Those were significantly greater in the elderly than in younger patients from 120 to 150 min after CO2 insufflation.ConclusionLonger duration of CO2 insufflation with head-up tilt is associated with a prolongation of the QT interval and the QTD in elderly patients. The clinical significance of these findings remains to be determined.RésuméObjectifComparer l’influence d’une insufflation intrapéritonéale prolongée de CO2 en position de Fowler, sur les indices de l’électrocardiogramme pendant la cholécystectomie laparoscopique, entre les patients âgés et de jeunes patients.MéthodeDouze patients âgés et douze jeunes patients ont participé à l’étude, L’insufflation de CO2 a été réalisée pendant plus de 150 min en position de Fowler chez tous les patients. L’intervalle RR, l’intervalle QT, l’intervalle QT corrigé pour la fréquence (QTc), la dispersion QT (QTd) et la QTd corrigée pour la fréquence (QTcD) ontété mesurés.RésultatsL’intervalle QT et l’intervalle QTc ont augmenté significativement de 120 à 150 min après l’insufflation de CO2 chez les patients âgés. Le QTD et le QTcD ont augmenté de façon significative pendant l’insufflation de CO2 chez tous les patients. Ces résultats ont été plus élevés chez les patients âgés comparés aux jeunes patients, entre 120 et 150 min après l’insufflation de CO2.ConclusionUne insufflation prolongée de CO2 en position de Fowler est associée à des intervalles QT et QTD également prolongés chez les patients âgés. La portée clinique de ces résultats demeure indéterminée.

Does hypertonic saline have preventive effects against delayed neuronal death in gerbil hippocampus

This experiment was conducted to ascertain whether or not hypertonic saline solution (HSS) has preventive effects on delayed neuronal death in the hippocampal CA1 subfield of the gerbil. Twenty-eight gerbils were anesthetized with 1% halothane and 50% nitrous oxide during the experimental period. Their common carotid arteries were occluded bilaterally for 2.5 min, immediately after which 2 mL/kg of 10% NaCl was infused via the tail vein. Two mL/kg of physiological saline solution (PSS) was used for the control group in the same manner. 5 days later, after the cerebrum was removed, the hippocampus was stained with hematoxylin-eosin, and histopathological changes in the CA1 subfield were observed under the light microscope. Degenerative or necrotic pyramidal cells were compared among groups. The degeneration rates of the pyramidal cells were as follows; after sham operation with PSS, 4.2 ± 1.8%; after sham operation with HSS, 6.5 ± 3.3%; on ischemia-reperfusion with PSS, 95.6 ± 1.6%; on ischemia-reperfusion with HSS, 7.1 ± 3.0%. This study suggested that hypertonic saline might prevent delayed neuronal death in the hippocampal CA1 subfield of gerbils subjected to cerebral ischemia-reperfusion.