Minimum Alveolar Concentration (MAC) of Xenon with Sevoflurane in Humans

Background: Although more than 30 yr ago the minimum alveolar concentration (MAC) of xenon was determined to be 71%, that previous study had technological limitations, and no other studies have confirmed the MAC value of xenon since. The current study was designed to confirm the MAC value of xenon in adult surgical patients using more modern techniques.

Methods: Sixty patients were anesthetized with sevoflurane with or without xenon. They were randomly allocated to one of four groups; patients in group 1 received no xenon, whereas those in groups 2, 3, and 4 received end-tidal concentrations of 20, 40, and 60%, respectively (n = 15 each group). Target end-tidal sevoflurane concentrations were chosen using the "up-and-down" method in each group. After steady state sevoflurane and xenon concentrations were maintained for at least 15 min, each patient was monitored for a somatic response at surgical incision. Somatic response was defined as any purposeful bodily movement. The MAC of sevoflurane and its reduction by xenon was evaluated using the multiple independent variable logistic regression model.

Results: The interaction coefficient of the multiple variable logistic regression was not significantly different from zero (P = 0.143). The MAC of xenon calculated as xenon concentration that would reduce MAC of sevoflurane to 0% was 63.1%.     

Oral Clonidine Premedication Reduces Minimum Alveolar Concentration of Sevoflurane for Tracheal Intubation in Children

Background: Sevoflurane is a useful anesthetic for inhalational induction in children because of its low solubility in blood and relatively nonpungent odor. Clonidine has sedative and anxiolytic properties and reduces the requirement for inhalation agents. Nitrous oxide (N2 O) also decreases the requirement of inhaled anesthetics, but the effect is variable. The minimum alveolar concentration for tracheal intubation (MACTI) of sevoflurane was assessed with and without N2 O and clonidine premedication.

Methods: Seventy-two patients, aged 3-11 yr, were assigned to one of six groups (n = 12 each). They received one of three preanesthetic medications (two groups for each premedication): placebo (control), 2 micro gram/kg oral clonidine or 4 micro gram/kg oral clonidine. In one group of each premedication, anesthesia was induced with sevoflurane in oxygen; in the other group, anesthesia was induced with sevoflurane in the presence of 60% N2 O. Each concentration of sevoflurane at which tracheal intubation was attempted was predetermined according to Dixon's up-and-down method and held constant for at least 20 min before the trial.

Results: The MACTI of sevoflurane in the absence of N2 O (mean +/- SEM) was 3.2 +/- 0.2%, 2.5 +/- 0.1%, and 1.9 +/- 0.2% in the control, 2-micro gram/kg clonidine, and 4-micro gram/kg clonidine groups, respectively. Nitrous oxide (60%) decreased the MACTI of sevoflurane by 26%, 24%, and 27% in the control, 2-micro gram/kg clonidine, and 4-micro gram/kg clonidine groups.     

Additive Contribution of Nitrous Oxide to Sevoflurane Minimum Alveolar Concentration for Tracheal Intubation in Children

Background: To study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MACTI) with and without nitrous oxide in children.

Methods: Seventy-two children aged 1-7 yr were assigned randomly to receive one of three end-tidal concentrations of nitrous oxide and one of four end-tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane; 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end-tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight-blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation.

Results: Logistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P = 0.89) and was removed from the logistic model. The MACTI (+/- SE) of sevoflurane was 2.66 +/- 0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54 +/- 0.25%. Thirty-three percent and 66% nitrous oxide decreased the MACTI of sevoflurane by 18% and 40% (P < 0.001), respectively.     

Influence of Nitrous Oxide on Minimum Alveolar Concentration of Sevoflurane for Laryngeal Mask Insertion in Children

Background: Inhalational induction with sevoflurane and nitrous oxide is frequently used for Laryngeal Mask Airway (TM) (LMA (TM); Laryngeal Mask Company, Henley-on-Thames, United Kingdom) insertion in children. The authors determined the influence of nitrous oxide on the minimum alveolar concentration (MAC) of sevoflurane for LMA (TM) insertion.

Methods: One hundred twenty unpremedicated children (age, 1-9 yr; American Society of Anesthesiologists physical status I) were randomly assigned to receive 1 of 15 end-tidal concentrations of nitrous oxide and sevoflurane for inhalational induction via a facemask: 0% nitrous oxide with 1.2, 1.4, 1.6, 1.8, or 2.0% sevoflurane; 33% nitrous oxide with 0.8, 1.0, 1.2, 1.4, or 1.6% sevoflurane; or 67% nitrous oxide with 0.4, 0.6, 0.8, 1.0, or 1.2% sevoflurane. The LMA (TM) was inserted after steady state end-tidal anesthetic concentrations had been maintained for 15 min. The response to insertion was recorded by three independent blinded observers. The interaction between nitrous oxide and sevoflurane was determined using logistic regression analysis.

Results: The MAC of sevoflurane for LMA (TM) insertion (95% confidence limit) was 1.57% (1.42-1.72%), and the concentration of sevoflurane required to prevent movement in 95% of children was 1.99% (1.81-2.57%). The addition of 33% and 67% nitrous oxide linearly decreased the MAC of sevoflurane for LMA (TM) insertion by 22% and 49%, respectively (P < 0.001). The interaction coefficient between nitrous oxide and sevoflurane did not differ from zero (P = 0.7843), indicating that the relation was additive.     

Minimum Alveolar Concentration-Awake of Xenon Alone and in Combination with Isoflurane or Sevoflurane

Background: The minimum alveolar concentration (MAC)-awake is a traditional index of hypnotic potency of an inhalational anesthetic. The MAC-awake of xenon, an inert gas with anesthetic properties (MAC = 71%), has not been determined. It is also unknown how xenon interacts with isoflurane or sevoflurane on the MAC-awake.

Methods: In the first part of the study, 90 female patients received xenon, nitrous oxide (N2O), isoflurane, or sevoflurane supplemented with epidural anesthesia (n = 36 for xenon and n = 18 per group for other anesthetics). In the second part, 72 additional patients received either xenon or N2O combined with the 0.5 times MAC-awake concentration of isoflurane or sevoflurane (0.2% and 0.3%, respectively, based on the results of the first part; n = 18 per group). During emergence, the concentration of an assigned anesthetic (xenon or N2O only in the second part) was decreased in 0.1 MAC decrements every 15 min from 0.8 MAC or from 70% in the case of N2O until the patient followed the command to either open her eyes or to squeeze and release the investigator's hand. The concentration midway between the value permitting the first response to command and that just preventing it was defined as the MAC-awake.

Results: The MAC-awake were as follows: xenon, 32.6 +/- 6.1% (mean +/- SD) or 0.46 +/- 0.09 MAC; N2O, 63.3 +/- 7.1% (0.61 +/- 0.07 MAC); isoflurane, 0.40 +/- 0.07% (0.35 +/- 0.06 MAC); and sevoflurane, 0.59 +/- 0.10% (0.35 +/- 0.06 MAC). Addition of the 0.5 MAC-awake concentrations of isoflurane and sevoflurane reduced the MAC-awake of xenon to 0.50 +/- 0.15 and 0.51 +/- 0.16 times its MAC-awake as a sole agent, but that of N2O to the values significantly greater than 0.5 times its MAC-awake as a sole agent (0.68 +/- 0.12 and 0.66 +/- 0.14 times MAC-awake;P < 0.01, analysis of variance and Dunnett's test).     

Glibenclamide Effects on Renal Function and Histology after Acute Hemorrhage in Rats under Sevoflurane Anesthesia

Introduction. Hypovolemia from hemorrhage evokes protective compensatory reactions, such as the renin-angiotensin system, which interferes in the clearance function and can lead to ischemia. This study was designed to evaluate the effects of glibenclamide, a K⁺_ATP channel blocker, on renal function and histology in rats in a state of hemorrhagic shock under sevoflurane anesthesia. Material and Methods. Twenty Wistar rats were randomized into two groups of 10 animals each (G1 and G2), only one of which (G2) received intravenous glibenclamide (1 μg.g^?1), 60 min before bleeding was begun. Both groups were anesthetized with sevoflurane and kept on spontaneous respiration with oxygen-air, while being bled of 30% of volemia in three stages with 10 min intervals. There was an evaluation of renal function—sodium para-aminohippurate and iothalamate clearances, filtration fraction, renal blood flow, renal vascular resistance—and renal histology. Renal function attributes were evaluated at three moments: M1 and M2, coinciding with the first and third stages of bleeding; and M3, 30 min after M2, when the animals were subjected to bilateral nephrectomy before being sacrificed. Results. Significant differences were found in para-aminohippurate clearance, G1 < G2, and higher renal vascular resistance values were observed in G1. Histological examination showed the greater vulnerability of kidneys exposed to sevoflurane alone (G1) with higher scores of vascular and tubular dilatation. There were vascular congestion and tubular vacuolization only in G1. Necrosis and signs of tubular regeneration did not differ in both groups. Conclusion. Treatment with glibenclamide attenuated acutely the renal histological changes after hemorrhage in rats under sevoflurane anesthesia.     

Minimum Alveolar Concentration of Halothane and Enflurane Are Decreased in Early Pregnancy

Background: Minimum alveolar concentration (MAC) of isoflurane is decreased in early pregnancy but it is not known whether this occurs to the same extent with other inhalational anesthetics. The MAC of halothane and enflurane were compared in pregnant women undergoing elective termination of pregnancy and in nonpregnant women.

Methods: We studied 16 pregnant women scheduled for termination of pregnancy at 8 to 13 weeks gestation and 16 nonpregnant patients undergoing laparoscopic sterilization. Eight patients in each group received halothane and the others received enflurane. After inhalational induction of anesthesia and tracheal intubation, MAC was determined in each patient by observing the motor response to a 10-s, 50-Hz, 80-mA transcutaneous electric tetanic stimulus to the ulnar nerve at varying concentrations of either halothane or enflurane. The end-tidal concentration of inhalational anesthetic was kept constant for at least 15 min before each stimulus and the concentration was varied ultimately in steps of 0.05 vol% (halothane) or 0.10 vol% (enflurane) until a sequence of three alternate responses (move, not move, move) or (not move, move, not move) was obtained. Minimum alveolar concentration for each person was taken as the mean of the two concentrations just permitting and just preventing movement, and MAC for the group was the median of individual MAC values. Confidence intervals were calculated for the percentage decrease in MAC for pregnant women compared with nonpregnant women.

Results: The median (range) MAC of halothane, 0.58 vol% (0.53 to 0.58), and enflurane, 1.15 vol% (0.95-1.25), in the pregnant women were less than those in the nonpregnant women, 0.75 vol% (0.70 to 0.78), P = 0.0005 and 1.65 vol% (1.45 to 1.75), P = 0.0007, respectively. The percentage decrease (95% CI) in MAC for pregnant women was 27% (20 to 27%) for halothane and 30% (24 to 36%) for enflurane.     

Effects of Concentration and Volume of 2-Chloroprocaine on Epidural Anesthesia in Volunteers

Background: Effect of local anesthetic concentration and volume on the spread and density of epidural anesthesia is unclear. This study was performed to delineate effects of a threefold difference in concentration and volume of 2-chloroprocaine on epidural anesthesia.

Methods: Twelve healthy volunteers underwent lumbar epidural anesthesia with 300 mg of 2-chloroprocaine as a 3% (10 ml) and a 1% (30 ml) solution in a randomized, double-blind, balanced, crossover fashion. Sensory block was assessed with pinprick, touch (calibrated plastic filament), cold, and electrical stimulation. Motor block was assessed at the quadriceps and gastrocnemius muscles with isometric force dynamometry. Differences between solutions were assessed with repeated measures analysis of variance followed by post hoc testing.

Results: The number of dermatomes blocked to pinprick, touch, and cold was significantly greater with the 1% concentration (2 dermatomes greater than the 3% concentration on average, P < 0.05). Similar intensity of sensory block to electrical stimulation developed at the hip and knee and was unaffected by concentration of 2-chloroprocaine. Similar intensity of motor block developed at the quadriceps with both concentrations.     

Recovery and Kinetic Characteristics of Desflurane and Sevoflurane in Volunteers after 8-h Exposure, including Kinetics of Degradation Products

Background: Desflurane and sevoflurane permit speedier changes in anesthetic partial pressures than do older halogenated anesthetics. The authors determined the kinetic characteristics of desflurane and sevoflurane and those of compound A [CH2 F-O-C(= CF2)(CF3)], a nephrotoxic degradation product of sevoflurane.

Methods: Volunteers received 1.25 minimum alveolar concentration of desflurane or sevoflurane, each administered for 8 h in a fresh gas inflow of 2 l/min. Inspired (FI) and end-tidal (FA) concentrations of anesthetic and compound A were measured during administration, and FA relative to FAO (the last end-tidal concentration during administration) during elimination. The indices of recovery were also measured.

Results: The ratio FI /FA rapidly approached 1.0, with values greater for sevoflurane (desflurane 1.06 +/- 0.01 vs. sevoflurane 1.11 +/- 0.02, mean +/- SD). The ratio FA /FI for compound A was approximately 0.8. The FA /FAO ratio decreased slightly more rapidly with desflurane than with sevoflurane, and objective measures indicated faster recovery with desflurane: The initial response to command (14 +/- 4 min vs. 28 +/- 8 min [means +/- SD]) and orientation (19 +/- 4 vs. 33 +/- 9 min) was quicker, and recovery was faster as defined by results of the Digit Symbol Substitution, P-deletion, and Trieger tests. Desflurane produced less vomiting (1 [0.5, 3]; median [quartiles] episodes) than did sevoflurane (5 [2.5, 7.5] episodes). The FA /FAO ratio for compound A decreased within 5 min to a constant value of 0.1.     

Preconditioning by Sevoflurane Decreases Biochemical Markers for Myocardial and Renal Dysfunction in Coronary Artery Bypass Graft Surgery: A Double-blinded, Placebo-controlled, Multicenter Study

Background: Preconditioning by volatile anesthetics is a promising therapeutic strategy to render myocardial tissue resistant to perioperative ischemia. It was hypothesized that sevoflurane preconditioning would decrease postoperative release of brain natriuretic peptide, a biochemical marker for myocardial dysfunction. In addition, several variables associated with the protective effects of preconditioning were evaluated.

Methods: Seventy-two patients scheduled for coronary artery bypass graft surgery under cardioplegic arrest were randomly assigned to preconditioning during the first 10 min of complete cardiopulmonary bypass with either placebo (oxygen-air mixture only) or sevoflurane 4 vol% (2 minimum alveolar concentration). No other volatile anesthetics were administered at any time during the study. Treatment was strictly blinded to anesthesiologists, perfusionists, and surgeons. Biochemical markers of myocardial dysfunction and injury (brain natriuretic peptide, creatine kinase-MB activity, and cardiac troponin T), and renal dysfunction (cystatin C) were determined. Results of Holter electrocardiography were recorded perioperatively. Translocation of protein kinase C was assessed by immunohistochemical analysis of atrial samples.

Results: Sevoflurane preconditioning significantly decreased postoperative release of brain natriuretic peptide, a sensitive biochemical marker of myocardial contractile dysfunction. Pronounced protein kinase C [delta] and [epsilon] translocation was observed in sevoflurane-preconditioned myocardium. In addition, postoperative plasma cystatin C concentrations increased significantly less in sevoflurane-preconditioned patients. No differences between groups were found for perioperative ST-segment changes, arrhythmias, or creatine kinase-MB and cardiac troponin T release.     

Antiemetic Activity of Propofol after Sevoflurane and Desflurane Anesthesia for Outpatient Laparoscopic Cholecystectomy

Background: Controversy exists regarding the effectiveness of propofol to prevent postoperative nausea and vomiting. This prospective, randomized, single-blinded study was designed to evaluate the antiemetic effectiveness of 0.5 mg/kg propofol when administered intravenously after sevoflurane- compared with desflurane-based anesthesia.

Methods: Two hundred fifty female outpatients undergoing laparoscopic cholecystectomy were assigned randomly to one of four treatment groups. All patients were induced with intravenous doses of 2 mg midazolam, 2 [micro sign]g/kg fentanyl, and 2 mg/kg propofol and maintained with either 1-4% sevoflurane (groups 1 and 2) or 2-8% desflurane (groups 3 and 4) in combination with 65% nitrous oxide in oxygen. At skin closure, patients in groups 1 and 3 were administered 5 ml intravenous saline, and patients in groups 2 and 4 were administered 0.5 mg/kg propofol intravenously. Recovery times were recorded from discontinuation of anesthesia to awakening, orientation, and readiness to be released home. Postoperative nausea and vomiting and requests for antiemetic rescue medication were evaluated during the first 24 h after surgery.

Results: Propofol, in an intravenous dose of 0.5 mg/kg, administered at the end of a sevoflurane-nitrous oxide or desflurane-nitrous oxide anesthetic prolonged the times to awakening and orientation by 40-80% and 25-30%, respectively. In group 2 (compared with groups 1, 3, and 4), the incidences of emesis (22% compared with 47%, 53%, and 47%) and requests for antiemetic rescue medication (19% compared with 42%, 50%, and 47%) within the first 6 h after surgery were significantly lower, and the time to home-readiness was significantly shorter in duration (216 +/- 50 min vs. 249 +/- 49 min, 260 +/- 88 min, and 254 +/- 72 min, respectively).     

Comparison of Minimum Alveolar Concentration between Intravenous Isoflurane Lipid Emulsion and Inhaled Isoflurane in Dogs

Background: As in inhaled isoflurane anesthesia, when isoflurane lipid emulsion (ILE; 8%, vol/vol) is intravenously administered, the primary elimination route is through the lungs. This study was designed to determine the minimum alveolar concentration (MAC) and the time course of washout of isoflurane for intravenously infused ILE by monitoring end-tidal isoflurane concentration.

Methods: Twelve healthy adult mongrel dogs were assigned randomly to an intravenous anesthesia group with 8% ILE or to an inhalation anesthesia group with isoflurane vapor. An up-and-down method and stimulation of tail clamping were used to determine MAC of 8% ILE by intravenous injection in the intravenous anesthesia group and MAC by the inhaled approach in the inhalation anesthesia group, respectively. Isoflurane concentration and partial pressure in end-tidal gas, femoral arterial blood, and jugular venous blood were measured simultaneously just before each tail clamping and during washout.

Results: The induction time in the intravenous anesthesia group (105 +/- 24 s) was shorter than that in the inhalation anesthesia group (378 +/- 102 s; P < 0.01). MAC of 8% ILE by intravenous injection (1.12 +/- 0.18%) was significantly less than MAC by the inhaled approach (1.38 +/- 0.16%; P < 0.05). No significant difference was found between the two groups in the time course of washout of isoflurane.     

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

Background: Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury.

Methods: The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra.

Results: A large decrease in MAC (to <= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >= 90%) in both chronic and acute cold-block spinal animals.     

Glycine Receptor Antagonism: Effects of ACEA-1021 on the Minimum Alveolar Concentration for Halothane in the Rat

Background: Glycine and glutamate binding sites are allosterically coupled at the N-methyl-n-aspartate (NMDA) receptor complex. Previous studies have shown that antagonism of glutamate at the NMDA receptor reduces the minimum alveolar concentration (MAC) for volatile anesthetics. 5-Nitro-6, 7-dichloro-2, 3-quinoxalinedione (ACEA-1021) is a competitive antagonist at the glycine recognition site of the NMDA receptor. The purpose of this study was to determine whether glycine receptor antagonism also reduces volatile anesthetic requirements in the rat.

Methods: In experiment 1, Sprague-Dawley rats were anesthetized with halothane in 50% Oxygen2 -balance Nitrogen2 and their lungs mechanically ventilated. They were randomly assigned to one of three groups according to the dose of ACEA-1021 administered (0, 20, or 40 mg/kg intravenously; n = 6). The bolus dose of ACEA-1021 was followed by a continuous intravenous infusion of vehicle or ACEA-1021 at 14 mg *symbol* kg sup -1 *symbol* h sup -1. Halothane MAC was then determined by the tail-clamp method. In experiment 2, awake rats were randomly assigned to groups according to the same dosages of ACEA-1021 as in experiment 1. Arterial CO2 tension and mean arterial pressure were recorded before and 5 and 30 min after the start of the infusion. The infusion was then stopped, and the time to recovery of the righting reflex was recorded.

Results: In experiment 1, ACEA-1021 decreased halothane MAC (mean + SD) in a dose-dependent manner (control, 0.95 plus/minus 0.15 vol%; ACEA-1021 20 mg/kg, 0.50 plus/minus 0.14 vol%; ACEA-1021 40 mg/kg, 0.14 plus/minus 0.16 vol%; P < 0.01). In experiment 2, arterial CO2 tension was increased by ACEA-1021 (control, 38 plus/minus 3 mmHg; ACEA-1021 20 mg/kg, 43 plus/minus 3 mmHg; ACEA-1021 40 mg/kg, 48 plus/minus 2 mmHg; P < 0.01). Mean arterial pressure was not affected by any dose of ACEA-1021. The righting reflex was abolished in rats receiving ACEA-1021 40 mg/kg only and recovered 30 plus/minus 7 min after discontinuation of the infusion.     

Reduced Renal Calcium Excretion in the Absence of Sclerostin Expression: Evidence for a Novel Calcium-Regulating Bone Kidney Axis

The kidneys contribute to calcium homeostasis by adjusting the reabsorption and excretion of filtered calcium through processes that are regulated by parathyroid hormone (PTH) and 1α,25-dihydroxyvitamin D₃ (1α,25[OH]₂D₃). Most of the filtered calcium is reabsorbed in the proximal tubule, primarily by paracellular mechanisms that are not sensitive to calcium-regulating hormones in physiologically relevant ways. In the distal tubule, however, calcium is reabsorbed by channels and transporters, the activity or expression of which is highly regulated and increased by PTH and 1α,25(OH)₂D₃. Recent research suggests that other, heretofore unrecognized factors, such as the osteocyte-specific protein sclerostin, also regulate renal calcium excretion. Clues in this regard have come from the study of humans and mice with inactivating mutations of the sclerostin gene that both have increased skeletal density, which would necessitate an increase in intestinal absorption and/or renal reabsorption of calcium. Deletion of the sclerostin gene in mice significantly diminishes urinary calcium excretion and increases fractional renal calcium reabsorption. This is associated with increased circulating 1α,25(OH)₂D₃ levels, whereas sclerostin directly suppresses 1α-hydroxylase in immortalized proximal tubular cells. Thus, evidence is accumulating that sclerostin directly or indirectly reduces renal calcium reabsorption, suggesting the presence of a novel calcium-excreting bone-kidney axis.     

Management of Ascites after Radical Surgery in Gastric Cancer Patients With Liver Cirrhosis and Minimal Hepatic Dysfunction

A radical lymph node dissection is important for the cure of gastric cancer. However, such a procedure in patients with liver cirrhosis (LC) could develop serious complications such as massive ascites. To determine the management of postoperative ascites, 26 gastric cancer patients with LC were reviewed retrospectively. Child-Pugh status was grade A in all 26 patients. Thirteen (50%) patients had advanced gastric cancer, and a D2 lymph nodes dissection was performed in 25 (96.2%) patients. The mean number of dissected lymph nodes was 33 ± 11 (range: 11–54). An abdominal closed suction drain was placed in 12 (46.2%) patients, and the average amount of fluid drainage was 463 ml/day. The drainage tube was removed on about the eleventh postoperative day (range: day 6 to day 13), and diuretics were used in 8 (30.8%) patients. A paracentesis was needed in one patient but no postoperative surgical morbidity or mortality was observed. Therefore, an extended lymph node dissection is safe in gastric cancer patients with mild hepatic dysfunction. Liver cirrhosis and postoperative ascites can be managed conservatively without any complications.     

Use of the Splenic and Hepatic Artery for Renal Revascularization in Patients with Atherosclerotic Renal Artery Disease

p = 0.17) and the average number of antihypertensive medications decreased to 1.9 (p= 0.001). During the median follow-up of 33 months, 10 patients died, mainly from cardiac causes. Our experience indicates that the splenic and hepatic arteries provide useful alternatives to renal revascularization in selected circumstances with an acceptable rate of perioperative mortality and morbidity. The expected long-term survival in this group of patients is low.     

Blockade of AMPA Receptors and Volatile Anesthetics: Reduced Anesthetic Requirements in GluR2 Null Mutant Mice for Loss of the Righting Reflex and Antinociception but Not Minimum Alveolar Concentration

Background: The [alpha]-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of glutamate receptor mediates fast excitatory neurotransmission in the central nervous system. Many general anesthetics inhibit AMPA receptors in vitro; however, it is not certain if this inhibition contributes to the behavioral properties of these drugs. AMPA receptors lacking the GluR2 subunit are resistant to blockade by barbiturates in vitro. Paradoxically, GluR2 null mutant (-/-) mice are more sensitive to barbiturate-induced loss of the righting reflex (LORR) compared with wild-type (+/+) littermates. To determine if interactions between anesthetics and AMPA receptors account for the increased sensitivity of (-/-) mice, the effects of volatile anesthetics that do not directly inhibit AMPA receptors were examined.

Methods: Isoflurane, halothane, desflurane, or sevoflurane were administered to (-/-) and (+/+) littermate controls. Anesthetic requirements for LORR, movement to tail clamp (minimum alveolar concentration [MAC]), and hind-paw withdrawal latency (HPWL) were determined. Electrophysiologic methods examined the inhibition of AMPA receptors by isoflurane and halothane.

Results: Anesthetic requirements for LORR and HPWL were decreased, whereas MAC values were unchanged in (-/-) mice. Isoflurane and halothane caused minimal inhibition of AMPA receptors at clinically relevant concentrations.