Relationship between serum biotin concentration and moisture content of the sole horn in cows with clinical laminitis or sound hooves.
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Animal Nutritional Physiological Phenomena↗
Biomedical subjects
H Higuchi
Publications and source records attributed to H Higuchi.
Halothane decreases impulse-dependent but not cytoplasmic release of dopamine from rat striatal slices.
Using in vitro superfusion techniques and electrical field stimulation, a volatile anesthetic, halothane, decreased impulse-dependent vesicular release, but did not affect amphetamine-induced cytoplasmic release of dopamine (DA) from the rat striatal slice preparations loaded with [3H]-DA. Contrary to previous in vivo studies, halothane at concentrations applied (1% to 4%) did not enhance the release of DA from slice preparation in which the cell bodies were absent, and therefore, the possible site of action was located on the axon terminals. In this in vitro experiment, halothane decreased the fractional release of DA in a concentration-dependent manner and attenuated the increase of impulse-dependent DA release when amphetamine or nomifensine administration was combined with electrical stimulation. D2-receptor agonists (quinpirole and apomorphine) reduced the release, and antagonists (sulpiride and haloperidol) enhanced the release of DA. In the presence of halothane, D2-receptor antagonists had no effect on DA release. It is concluded that halothane may have some modulatory effect on D2-receptor mediated presynaptic control of DA release.
Action Potentials↗
A small dose of midazolam decreases the time to achieve hypnosis without delaying emergence during short-term propofol anesthesia.
STUDY OBJECTIVE: To evaluate the effect of a small dose of midazolam (10 microg kg(-1)) on induction and emergence during short-term propofol anesthesia and to investigate the effects of subsequent administration of flumazenil. DESIGN: Double-blinded, prospective, randomized study. SETTING: Operating room of a medical college hospital. PATIENTS: 30 male ASA physical status I and II patients (ages 51 to 75) scheduled for minor surgery under spinal anesthesia. INTERVENTIONS: Patients were randomly allocated to one of three groups: the placebo-propofol-placebo (PP) group, the midazolam-propofol-placebo (MP) group, or the midazolam-propofol-flumazenil (MF) group. After administering placebo or midazolam (10 microg kg(-1)), propofol 250 microg kg(-1) min(-1) was infused. Immediately after confirming that the patient was hypnotized, we terminated the propofol infusion and administered placebo or flumazenil (5 microg kg(-1)). MEASUREMENTS: The dose and the times required to achieve hypnosis (the first endpoint) and to emerge from anesthesia (the second endpoint). The plasma concentration at each endpoint was determined. MAIN RESULTS: Midazolam significantly decreased the dose and time needed to achieve hypnosis [PP vs. MP, 66 +/- 14 vs. 48 +/- 15 mg, 260 +/- 55 vs. 179 +/- 44 sec, respectively (mean +/- SD)]. Thus, the plasma concentration of propofol at hypnosis was significantly lower (PP vs. MP, 3.31 +/- 0.78 vs. 2.41 +/- 0.57 microg mL(-1)). The time to emerge from anesthesia was not prolonged by midazolam, and was further shortened by administration of flumazenil (PP, MP vs. MF, 237 +/- 77, 207 +/- 71 s vs. 126 +/- 56 sec, respectively). Flumazenil also reversed the reduction in propofol concentration induced by midazolam at emergence (PP, MP, and MF, 0.54 +/- 0.17, 0.37 +/- 0.15, and 0.59 +/- 0.22 microg mL(-1), respectively). CONCLUSIONS: Coadministration of 10 microg kg(-1)midazolam decreases the dose and time required to achieve hypnosis with propofol induction without delaying emergence from anesthesia. Additional administration of flumazenil further shortens the time to emerge from midazolam-propofol anesthesia.
Adjuvants, Anesthesia↗
Loading of mechanical pressure activates mitogen-activated protein kinase and early immediate gene in intestinal epithelial cells.
Intestinal mucosa is continuously exposed to mechanical forces. We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process.
Animals↗
High-dose flumazenil potentiates the hypnotic activity of propofol, but not that of thiopental, in ddY mice.
BACKGROUND: Flumazenil is a specific benzodiazepine agonist, which is reported to have a partial benzodiazepine agonist-like effect at a high dose. This study investigated the effects of flumazenil and midazolam on the hypnotic dose of propofol and thiopental in ddY mice, using a behavioral model. METHODS: Mice were given either propofol or thiopental intravenously to induce hypnosis, which was defined as a loss of the righting reflex. The mice were pre-treated with flumazenil (0.05, 0.1, or 0.2 mg kg(-1)) or midazolam (0.1 or 0.2 mg kg(-1)), and given propofol or thiopental after a 30-s delay. RESULTS: Pre-treatment with flumazenil (0.1 or 0.2 mg kg(-1)) significantly decreased the hypnotic dose of propofol compared to the control group (9.3+/-0.39 [8.5-10.0] or 9.0+/-0.28 [8.5-9.6] vs. 10.8+/-0.42 [9.9-11.6] mg kg(-1) (ED50+/-SEM and [95% confidence interval]) P<0.05), but not that of thiopental (9.1+/-0.30 [8.5-9.7] with 0.2 mg kg(-1) flumazenil vs. 9.3+/-0.42 [8.4-10.1] mg kg(-1) with saline). Midazolam reduced the hypnotic dose of both propofol and thiopental. Flumazenil antagonized the potentiating effect of midazolam (0.2 mg kg(-1)) on the hypnotic activity of propofol. CONCLUSIONS: These results suggest that the hypnotic activity of propofol is potentiated by the partial agonist activity of flumazenil in ddY mice.
Anesthetics, Intravenous↗
Comparison of plasma alpha glutathione S-transferase concentrations during and after low-flow sevoflurane or isoflurane anaesthesia.
BACKGROUND: We evaluated the effect of low-flow sevoflurane anaesthesia, in which compound A is generated, and isoflurane anaesthesia, in which compound A is not generated (n=13 in each group), on hepatocellular integrity using alpha glutathione S-transferase (GST). Alpha GST is a more sensitive and specific marker of hepatocellular damage than is aminotransferase activity and correlates better with hepatic histology. METHODS: Sevoflurane or isoflurane were delivered without nitrous oxide with a fresh gas flow of 1 l/min. Concentrations of compound A in the circuit were measured hourly, and plasma alpha GST concentrations were measured perioperatively. RESULTS: Mean duration of anaesthesia was 338+/-92 min in the sevoflurane group and 320+/-63 min in the isoflurane group. Mean compound A concentration in the sevoflurane group was 28.6+/-9.0 ppm. There was no significant difference in alpha GST concentrations between the sevoflurane and isoflurane groups during or after anaesthesia. CONCLUSION: These results indicate that low-flow sevoflurane and isoflurane anaesthesia have the same effect on hepatic function, as assessed by plasma alpha GST concentrations.
Adult↗
Substeps within the 8-nm step of the ATPase cycle of single kinesin molecules.
Kinesin is a molecular motor that moves processively by regular 8-nm steps along microtubules. The processivity of this movement is explained by a hand-over-hand model in which the two heads of kinesin work in a coordinated manner. One head remains bound to the microtubule while the other steps from the alphabeta-tubulin dimer behind the attached head to the dimer in front. The overall movement is 8 nm per ATPase cycle. To investigate elementary processes within the 8-nm step, we have developed a new assay that resolves nanometre displacements of single kinesin molecules with microsecond accuracy. Our data show that the 8-nm step can be resolved into fast and slow substeps, each corresponding to a displacement of approximately 4 nm. The substeps are most probably generated by structural changes in one head of kinesin, leading to rectified forward thermal motions of the partner head. It is also possible that the kinesin steps along the 4-nm repeat of tubulin monomers.
Animals↗
The mitochondrial permeability transition contributes to acute ethanol-induced apoptosis in rat hepatocytes.
Acute ethanol intoxication induces oxidative stress and apoptosis in primary cultured hepatocytes. Oxidative stress can trigger mitochondrial cytochrome c release initiating the mitochondrial pathway of apoptosis. Based on this information, we formulated the hypothesis that ethanol induced oxidative stress causes mitochondrial dysfunction resulting in apoptosis. In the present study, we found that the mitochondrial membrane permeability transition (MPT) is essential for induction of mitochondrial cytochrome c release and caspase activation of ethanol. The short-term incubation with ethanol (50 mmol/L) induced the MPT, cytochrome c release, caspase activation, and apoptosis of cultured rat hepatocytes. Hepatocyte apoptosis was prevented by caspase inhibitors (i.e., Z-VAD-fmk, DEVD-cho, and DMQD-cho). An MPT inhibitor, cyclosporin A, also prevented ethanol-induced cytochrome c release, caspase activation, and apoptosis, suggesting that acute ethanol-induced apoptosis is MPT dependent. Ethanol-induced MPT was also attenuated by N'N'-dimethylthiourea (DMTU, a scavenger of hydrogen peroxide, 10 mmol/L) and N-acetyl-cysteine (NAC, an antioxidant, 5 mmol/L). Preventing hepatocyte MPT by DMTU or NAC attenuated cytochrome c release as well as caspase activation, suggesting that ethanol-induced oxidative stress mediates the MPT. Thus, acute ethanol induces MPT via oxidative stress, and the MPT mediates mitochondrial pathway of apoptosis in hepatocytes exposed to acute ethanol.
Animals↗
The effects of low-flow sevoflurane and isoflurane anesthesia on renal function in patients with stable moderate renal insufficiency.
UNLABELLED: Sevoflurane degrades to Compound A, which is nephrotoxic in rats. Therefore, the renal effects of Compound A is an area of intense debate. We investigated the effects of low-flow sevoflurane and isoflurane anesthesia on renal function in patients with stable renal insufficiency. Seventeen patients with a serum creatinine level of more than 1.5 mg/dL were anesthetized with sevoflurane or isoflurane at a total flow of 1 L/min. Serum creatinine and blood urea nitrogen were measured before anesthesia and again 1, 2, 3, 5, 7, and 14 days after anesthesia. The 24-h creatinine clearance was measured before anesthesia and 7 days after anesthesia. There were no significant differences in the blood urea nitrogen levels, serum creatinine concentrations, or creatinine clearance before and after anesthesia within each group. These results suggest that sevoflurane and isoflurane have similar effects on renal function in patients with moderately impaired renal function. Further study of the effects of low-flow sevoflurane anesthesia on impaired renal function with a larger sample size than ours is required to resolve the issue of sevoflurane safety in patients with renal insufficiency. IMPLICATIONS: The serum creatinine and blood urea nitrogen data indicate that, for exposures of <130 ppm/h in Compound A inspired area under the curve, renal effects of low-flow sevoflurane are similar to those of isoflurane in patients with stable renal insufficiency.
Aged↗
The determinants of propofol induction of anesthesia dose.
UNLABELLED: Recently it was reported that the pharmacokinetics of propofol are modified by changes in cardiac output. The objective of this study was to evaluate the effects of cardiac output and other factors on the hypnotic dose of propofol. One-hundred surgical patients were administered indocyanine green immediately before the induction of anesthesia to measure their cardiac outputs and blood volumes. Propofol (250 microg. kg(-1). min(-1)) was infused IV for 8 min, and the hypnotic dose of propofol and the time to hypnosis were recorded. The plasma concentration of propofol immediately after 2 mg/kg infusion was measured. Multiple regression analysis showed that, in addition to age and weight, cardiac output was a small but significant factor for predicting the hypnotic dose of propofol (R(2) = 0.468, P < 0.001), the time to hypnosis (R(2) = 0.454, P < 0.001), and the plasma concentration of propofol (R(2) = 0.248, P < 0.01). Cardiac output, age, and weight showed similar partial coefficients for the hypnotic dose (0.128, 0.137, and 0.140, respectively). IMPLICATIONS: This study demonstrates a significant relationship between cardiac output and the hypnotic dose of propofol. We suggest that anesthesiologists should include cardiac output, as well as age and weight, in calculating the induction dose of propofol.
Adolescent↗
Continuous infusion of prostaglandin E(1) and epidural analgesia for a patient with paroxysmal nocturnal hemoglobinuria.
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Alprostadil↗
The carbon dioxide absorption capacity of Amsorb is half that of soda lime.
UNLABELLED: A new CO(2) absorbent, Amsorb (A), which does not contain monovalent bases, is ideal because it does not degrade volatile anesthetics to either Compound A (from sevoflurane) or carbon monoxide (from desflurane, enflurane, or isoflurane). The CO(2) absorption capacity of A, however, has not been investigated under clinical conditions. In this study, we compared the longevity (time to exhaustion) and CO(2) absorption capacity (the volume of CO(2) absorbed before CO(2) rebreathing occurs) of A under low-flow anesthesia (1 L/min) with those of two soda lime absorbents-Medisorb (M) and Sodasorb (S)-by using a 750-mL ADU canister and a 1350-mL Aestiva 3000 canister. In the study with the ADU canister, the longevity of A was 213 +/- 71 min, significantly less than those of M (445 +/- 125; P < 0.01) and S (503 +/- 89; P < 0.001). The CO(2) absorption capacity (L/100 g absorbent) of A was 5.5 +/- 1.2, significantly less than those of M (10.7 +/- 1.7) and S (12.1 +/- 1.8; P < 0.001). In the study with the Aestiva 3000 canister, the longevity of A was 218 +/- 61 min, significantly less than those of M (538 +/- 136) and S (528 +/- 103; P < 0.001). The CO(2) absorption capacity (L/100 g absorbent) of A was 7.6 +/- 1.6, significantly less than those of M (14.4 +/- 1.8) and S (14.8 +/- 2.3; P < 0.001). These results indicate that the CO(2) absorption capacity of A is half that of M or S and that the difference in the CO(2) absorption capacity between A and M or S is almost constant, regardless of the canister design. IMPLICATIONS: The CO(2) absorption capacity of Amsorb is half that of Medisorb and Sodasorb under clinical low-flow (1 L/min) anesthesia with either a 750-mL Ohmeda ADU compact or a 1350-mL Ohmeda Aestiva 3000 canister.
Absorption↗
Early pregnancy does not reduce the C(50) of propofol for loss of consciousness.
UNLABELLED: Requirements for inhaled anesthetics decrease during pregnancy. There are no published data, however, regarding propofol requirements in these patients. Because propofol is often used for induction of general anesthesia when surgery is necessary in early pregnancy, we investigated whether early pregnancy reduces the requirement of propofol for loss of consciousness using a computer-assisted target-controlled infusion (TCI). Propofol was administered using TCI to provide stable concentrations and to allow equilibration between blood and effect-site (central compartment) concentrations. Randomly selected target concentrations of propofol (1.5-4.5 microg/mL) were administered to both pregnant women (n = 36) who were scheduled for pregnancy termination and nonpregnant women (n = 36) who were scheduled for elective orthopedic or otorhinolaryngologic surgery. The median gestation of the pregnant women was 8 wk (range, 6-12 wk). Venous blood samples for analysis of the serum propofol concentration were taken at 3 min and 8 min after equilibration of the propofol concentration. After a 10-min equilibration period of the predetermined propofol blood concentration, a verbal command to open their eyes was given to the patients twice, accompanied by rubbing of their shoulders. Serum propofol concentrations at which 50% of the patients did not respond to verbal commands (C(50) for loss of consciousness) were determined by logistic regression. There was no significant difference in C(50) +/- SE of propofol for loss of consciousness between the Nonpregnant (2.1 +/- 0.2 microg/mL) and Pregnant (2.0 +/- 0.2 microg/mL) groups. These results indicate that early pregnancy does not decrease the concentration of propofol required for loss of consciousness. IMPLICATIONS: The C(50) of propofol for loss of consciousness in early pregnancy did not differ from that in nonpregnant women, indicating that there is no need to decrease the propofol concentration for loss of consciousness when inducing general anesthesia for termination of pregnancy.
Abortion, Induced↗
Effects of probenecid on renal function in surgical patients anesthetized with low-flow sevoflurane.
BACKGROUND: Dehydrofluorination of sevoflurane by carbon dioxide absorbents in anesthesia machines produces compound A, which is nephrotoxic in rats. Several clinical studies indicate that prolonged low-flow sevoflurane anesthesia is associated with an increased urinary excretion of biochemical markers, such as protein. Probenecid, a competitive inhibitor of organic anion transport, diminishes compound A nephrotoxicity in rats. The purpose of the present study was to examine the effects of low- and high-flow sevoflurane anesthesia on urinary excretion of biochemical markers in humans and to examine the effects of probenecid on urinary excretion of these markers. METHODS: Elective surgical patients (n = 64) were assigned to four groups (n = 16 each): low-flow sevoflurane plus probenecid (LSP), low-flow sevoflurane (LS), high-flow sevoflurane plus probenecid (HSP), and high-flow sevoflurane (HS). Probenecid (2.0 g) was administered orally 2 h before the induction of anesthesia in both the LSP and HSP groups. Nothing was administered orally 2 h before the induction of anesthesia in either the LS or HS groups. All patients underwent prolonged low-flow (1 l/min) or high-flow (6 l/min) sevoflurane anesthesia. Urinary excretion of protein, albumin, beta(2)-microglobulin, glucose, and N-acetyl-beta-d-glucosaminidase was measured for up to 7 days postoperatively. RESULTS: Sevoflurane doses were similar in all four groups. There were no differences in blood urea nitrogen, creatinine, or creatinine clearance among the four groups after anesthesia. Average values for urinary excretion of protein, beta(2)-microglobulin, and N-acetyl-beta-d-glucosaminidase in the LS group were significantly higher than those in the other groups (LSP, HSP, HS; P < 0.05). There was no significant difference between the LS and LSP groups in average values for urinary excretion of albumin and glucose, although there were significant differences between the LS and both high-flow sevoflurane groups (HSP, HS). CONCLUSIONS: Low-flow sevoflurane, which produces a sevenfold higher compound A exposure than high-flow sevoflurane, resulted in significant increases of several biochemical markers in half of the patients. Probenecid appears to provide protection against these renal effects.
Adult↗
Chronic ethanol consumption exacerbates microcirculatory damage in rat mesentery after reperfusion.
Although the negative effect of excessive alcohol consumption on later stressful events has long been recognized, pathophysiological mechanisms are incompletely understood. We examined possible roles of oxygen radicals and glutathione content in mesenteric venules of chronically ethanol-fed rats exposed to ischemia-reperfusion. Changes in microvascular hemodynamics, such as red blood cell (RBC) velocity, leukocyte adherence, and albumin extravasation, were monitored in postcapillary venules by intravital fluorescence microscopy. Chronic ethanol feeding significantly exaggerated the magnitude of the decrease in RBC velocity, the increased number of adherent leukocytes, and increased albumin leakage elicited by 10 min of ischemia followed by 30 min of reperfusion. Oxidative stress in the endothelium of venules monitored by dihydrorhodamine 123 (DHR) fluorescence was more severe in rats fed ethanol chronically. Both superoxide dismutase and N-acetyl-L-cysteine, which is known to increase glutathione content, reduced the ischemia-reperfusion-induced decrease in RBC velocity, the number of adherent leukocytes, and the increase in albumin leakage, as well as oxidative activation of DHR. This suggests that the increased reperfusion-induced microvascular disturbances in the mesenteric venules of rats fed ethanol chronically are significantly correlated with excessive production of oxygen-derived free radicals and decreased glutathione synthesis.
Alcoholism↗
Validity of NIR spectroscopy for quantitatively measuring muscle oxidative metabolic rate in exercise.
The purpose of this study was to examine the validity of the quantitative measurement of muscle oxidative metabolism in exercise by near-infrared continuous-wave spectroscopy (NIRcws). Twelve male subjects performed two bouts of dynamic handgrip exercise, once for the NIRcws measurement and once for the (31)P-magnetic resonance spectroscopy (MRS) measurement as a standard measure. The resting muscle metabolic rate (RMRmus) was independently measured by (31)P-MRS during 15 min of arterial occlusion at rest. During the first exercise bout, the quantitative value of muscle oxidative metabolic rate at 30 s postexercise was evaluated from the ratio of the rate of oxyhemoglobin/myoglobin decline measured by NIRcws during arterial occlusion 30 s after exercise and the rate at rest. Therefore, the absolute values of muscle oxidative metabolic rate at 30 s after exercise [VO(2NIR(30))] was calculated from this ratio multiplied by RMRmus. During the second exercise bout, creatine phosphate (PCr) resynthesis rate was measured by (31)P-MRS at 30 s postexercise [Q((30))] under the same conditions but without arterial occlusion postexercise. To determine the validity of NIRcws, VO(2NIR(30)) was compared with Q((30)). There was a significant correlation between VO(2NIR(30)), which ranged between 0.018 and 0. 187 mM ATP/s, and Q((30)), which ranged between 0.041 and 0.209 mM ATP/s (r = 0.965, P < 0.001). This result supports the application of NIRcws to quantitatively evaluate muscle oxidative metabolic rate in exercise.
Adenosine Triphosphate↗
Full remission of panic attacks in a schizophrenic patient after switching from haloperidol to risperidone.
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Adult↗
Knee stability after repair of isolated midsubstance tears of the posterior cruciate ligament.
This study was made to compare the results after operative versus non-operative management for tears in the substance of posterior cruciate ligament. The subjects were 40 patients, half of whom were managed operatively and the other half non-operatively. End-to-end suture was performed on the operated group. The procedure was followed by cast immobilization for 4 weeks. Non-operative management consisted of immobilization in a cast for 4 weeks after arthroscopy. The average follow-up periods were 6 years 7 months and 4 years 3 months. The operated knees were significantly more stable than those of the non-operated group on stress radiographs (p<0.0001), but not to the extent of an age-matched control group (p<0.0001). The knee rating scores did not indicate any improvement of the functional outcome in the operated group. Surgery resulted in better posterior laxity than non-operative management; the achieved stability, however, was clearly less than in controls.
Journal Article↗