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Analysis of anesthetic action on the potassium channels of the Shaker mutant of Drosophila.

Recent evidence suggest that exposure to volatile anesthetic agents causes a change in conductance through an undelineated potassium channel. With recently developed genetic and molecular techniques the Drosophila melanogaster (D.m.) genome can be manipulated to study the role that potassium ion channel function plays in anesthetic action. The IA potassium channel is encoded by the Shaker (Sh) locus on the X chromosome of D.m. Because this channel may be one of those involved in volatile anesthetic action, we tested the sensitivity to isoflurane in three Shaker strains with different degrees of dysfunctional IA conductance (Shnull greater than ShKS133 greater than Sh5). Anesthetic sensitivity was also examined in mutant strains of D.m. which express abnormalities either in other potassium channel conductances (eag, slo) or other ion conductances (para). The normally conducting wild type served as the control. Two-day-old adult D.m. were stimulated with a heat source during exposure to the volatile anesthetic isoflurane, and the number moving in response to the noxious stimulus was noted. After testing the Shaker and control strains at no fewer than 13 concentrations, the IC50S (isoflurane concentration in percent vol/vol at which 50% of the flies did not respond to the heat stimulus) were derived. The IC50 values for Sh 5 (0.89), Sh133 (1.29), and Shnull (1.37) were significantly different from the wild type (0.56). The rank order of insensitivity of these Shaker mutants corresponded to the extent of the alteration in IA conductance as established by previous studies in these mutants. Neither eag (0.66), para (0.48), nor slo (0.63) differed significantly from the wild type. These data suggest that the IA potassium channel plays a role in volatile anesthetic action.

Animals↗

Triggering Glutamate Excretion in Corynebacterium glutamicum by Modulating the Membrane State with Local Anesthetics and Osmotic Gradients.

Corynebacterium glutamicum can be triggered to excrete glutamate by the addition of local anesthetics, particularly tetracaine. Glutamate efflux is a carrier-mediated process and not due to unspecific membrane permeabilization. The concentration of local anesthetics triggering optimum excretion depended on the type of anesthetic and varied, ranging from 0.1 (chlorpromazine), 1.3 (tetracaine), and 2.6 mM (butacaine) to 15 mM (benzocaine), in close resemblance to the order of efficiency in anesthetic effect. The onset of glutamate excretion was not correlated to a change in the viscosity or fluidity of the membrane, as measured by electron spin resonance spectroscopy, nor was it related to an action of the anesthetic as an uncoupler. Tetracaine-triggered glutamate excretion was sensitive to changes in the transmembrane osmotic gradient, although an osmotic gradient alone could not trigger glutamate excretion. Tetracaine-triggered glutamate efflux was inhibited by an external rise in osmolality and stimulated by a corresponding decrease. The effects of osmotic gradients and the addition of local anesthetics on glutamate excretion were mutually exchangeable, indicating similar modes of action. We suggest that this common principle is a change in the membrane strain. C. glutamicum cells which excrete glutamate without manipulation of the membrane, e.g., biotin-limited cells or glutamate production mutants, were not stimulated by the addition of tetracaine.

Journal Article↗

Role of the descending pressor pathway in the conscious and pentobarbital-anesthetized dog.

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.

Animals↗

Negative inotropy of halogenated anesthetics in ferret ventricular myocardium.

The effects of the volatile anesthetics halothane, enflurane, and isoflurane on amplitude and time variables of contraction and relaxation in isometric, isotonic, and zero-load clamped twitches of isolated right ventricular ferret papillary muscles (n = 24) were compared with those of changing extracellular Ca2+ concentration [( Ca2+]o). Contraction and relaxation variables were compared at equal contraction amplitudes to determine whether the studied anesthetics exert specific effects on contraction and relaxation other than those that may exist as a consequence of their negative inotropic effect. Both changes in [Ca2+]o and anesthetic concentrations had quantitatively and qualitatively similar effects on the following variables of contraction amplitude: peak isometric developed force (DF), maximal extent of shortening (DL), and maximal unloaded velocity of shortening (MUVS). Analysis of anesthetic concentration-effect curves normalized for effects to changes in [Ca2+]o demonstrated that anesthetic effects relative to those of changes in [Ca2+]o were greater on DF greater than DL greater than MUVS. When compared with twitches of equal amplitude in low [Ca2+]o, halothane, enflurane, and isoflurane accelerated isometric and isotonic relaxation. These data are consistent with the hypothesis that the negative inotropic effects of halothane, enflurane, and isoflurane are mostly a consequence of a reduction of intracellular Ca2+ availability and that anesthetic-induced decreases in myofibrillar Ca2+ responsiveness play only a minor role.

Animals↗

Blood pressure responses to cyclic blood volume changes in awake and anesthetized dogs.

A dynamic analysis of blood pressure regulation was performed in conscious and anesthetized dogs. The mean arterial pressure (MAP) responses to 5 and 10% sinusoidal changes in total blood volume with cycle lengths of 1, 4, and 8 min were measured in anesthetized 1) control dogs, 2) carotid and vagal baroreflex (CVB)-denervated animals, and 3) spinal-ablated dogs; in addition, the MAP responses to 10% sinusoidal blood volume changes with cycle lengths ranging from 0.25 to 8 min were measured in conscious control and CVB-denervated dogs. The presence of the baroreflexes in both the conscious and anesthetized control dogs essentially eliminated MAP excursions during the cyclic volume changes. The MAP changes in both the conscious and anesthetized denervated dogs were large. However, the responses in the anesthetized denervated dogs were linear, stationary, and cycle-length insensitive with respect to the sinusoidal forcing function, whereas the responses in the conscious CVB-denervated dogs were nonlinear, nonstationary, and cycle-length dependent. These results indicate that the cardiovascular system in the anesthetized CVB-denervated and spinal-ablated dogs is passive or "hydraulic" in nature; conversely, factors other than the carotid and vagal baroreflexes appear to exist that alter the arterial pressure responses to cyclic blood volume perturbations in the conscious CVB-denervated dogs.

Anesthesia, General↗

Comparison of carotid baroreflex control of plasma AVP concentration in conscious and anesthetized dogs.

We compared carotid sinus baroreflex control of endogenous plasma arginine vasopressin (AVP) in chronically prepared conscious and acutely prepared anesthetized dogs. The carotid sinuses of both conscious and pentobarbital-anesthetized dogs were isolated bilaterally and perfused at constant pressures. Carotid sinus pressure (CSP) was changed between 200 and 50 mmHg in 25-mmHg steps in intact conscious and anesthetized dogs. Similar runs were repeated after vagotomy. Mean arterial pressure (MAP) and heart rate (HR) were monitored. At each interval of CSP, blood was withdrawn for AVP analysis by radioimmunoassay. MAP responses to changes in CSP were not different in the four experimental groups. Both anesthesia and vagotomy increased the HR responses to changes in CSP. With vagi intact, AVP increased at high CSP in conscious but not in anesthetized dogs. After vagotomy, low CSP led to an increase in plasma AVP that did not differ between conscious and anesthetized dogs. The results suggest that the release of AVP is modulated by the action of the carotid baroreflex as a normal component of an integrated efferent response. The response is similar in conscious and pentobarbital-anesthetized dogs and is normally buffered by reflexes with vagal afferents.

Analysis of Variance↗

Ventilatory responses to lung inflation and arterial CO2 in halothane-anesthetized dogs.

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration (TE) in chloralose-urethan-anesthetized dogs. Surgical removal of the carotid bodies abolishes this interaction. Since halothane anesthesia in hyperoxia greatly impairs peripheral chemoreflexes, experiments were conducted to determine whether hypercapnia would attenuate the effects of Paw on f and TE in halothane-anesthetized dogs (approximately 1.5 minimum alveolar concentration). Integrated activity of the phrenic nerve was monitored as a function of Paw (2-12 cmH2O) in a vascularly isolated left lung at varied levels of arterial PCO2 (PaCO2; 38-80 Torr) controlled by inspired gas concentrations ventilating the denervated but perfused right lung. Halothane was administered only to the right lung. The results were as follows: 1) integrated phrenic amplitude increased with PaCO2 but was unaffected by Paw; 2) f decreased as Paw increased but was not affected by PaCO2; 3) the inspiratory duration (TI) increased as PaCO2 increased but was unaffected by Paw; 4) TE increased as Paw increased but was unaffected by PaCO2; and 5) there was no phrenic response to intravenous sodium cyanide (50-100 micrograms/kg). Thus, unlike chloralose-urethan-anesthetized dogs, hypercapnia does not attenuate the effect of lung inflation on f or TE in halothane-anesthetized dogs. Furthermore, hypercapnia increases TI during halothane anesthesia, an effect found after carotid denervation but not found in intact chloralose-urethan-anesthetized dogs. It is suggested that these differences between chloralose-urethan- and halothane-anesthetized dogs may be due to functional carotid chemoreceptor denervation by halothane.

Anesthesia, General↗

Effect of anesthetic and convulsant barbiturates on N-methyl-D-aspartate receptor-mediated calcium flux in brain membrane vesicles.

The effects of anesthetic and convulsant barbiturates on brain N-methyl-D-aspartate (NMDA) receptor function were examined in a cell-free membrane vesicle preparation from mouse hippocampus. Increases in intracellular free calcium concentrations (Cai) were determined using a fluorescent dye, Indo-1, after stimulation with the NMDA receptor agonist, L-glutamate. Anesthetic barbiturates inhibited NMDA responses in a concentration-dependent manner with a rank order of potency of secobarbital > amobarbital > pentobarbital > mephobarbital = phenobarbital >> barbital. However, the IC50 values for these barbiturates were larger than probable blood anesthetic concentrations. Barbiturates with both anesthetic and convulsant effects in mice [optical isomers of pentobarbital and secobarbital, 5-(2-cyclohexylideneethyl)-5-ethylbarbituric acid and (+/-)-dimethylbutylbarbituric acid] also reduced NMDA responses. Inhibition of NMDA responses by racemic pentobarbital or isomers of pentobarbital was noncompetitive. Resting Cai was altered by all barbiturates tested except secobarbital and barbital, but not in a consistent manner, suggesting that the effect of barbiturates on resting Cai is not related either to their effects on NMDA receptor responses or to their behavioral effects. These results show that anesthetic and convulsant barbiturates inhibit NMDA responses, but their anesthetic and convulsant activities may be primarily due to their effects on other brain targets.

Animals↗

Reflex cardiovascular and respiratory effects of serotonin in conscious and anesthetized dogs.

Cardiovascular and respiratory effects of intra-left atrial or intra-left ventricular injection of serotonin were studied in conscious dogs (n = 8), anesthetized closed-chest dogs (n = 13) and anesthetized open-chest dogs (n = 9). Serotonin (50-200 microgram), injected as a bolus, resulted in an initial bradycardia and hypotension followed by a delayed tachycardia and hypertension in the conscious dogs. The hypertension was seen as an increase of 21.5 +/- 2.7 (mean +/ SE) mm Hg from a control pressure of 102.5 +/- 1.9 mm Hg, whereas the initial decrease in pressure was 22.6 +/- 1.9 mm Hg. The tachycardia was 23.3 +/- 3.9 beats/min above a control heart rate of 104.9 +/- 3.9 beats/min whereas the bradycardia was 58.5 +/- 3.7 beats/min below control. There was a significant attenuation of the hypotension in both groups of anesthetized dogs. In fact, no hypotension was elicited in the open-chest anesthetized dogs. Open-chest anesthetized dogs showed only a hypertensive response (mean increase 67.2 +/- 5.5 mm Hg). Stimulation of respiration was seen in all groups of dogs. In conscious dogs there was a 214.8 +/- 15.4% increase in respiratory depth and a 20.8 +/- 3.1 breaths/min increase in respiratory rate. Atropine significantly reduced the bradycardia and abolished the hypotension in conscious dogs. Bilateral cervical vagotomy did not abolish the response in open-chest anesthetized dogs. We conclude that the so-called "hypertensive coronary chemoreflex" is altered dramatically by the state of the preparation and by anesthesia.

Anesthesia↗

High throughput modular chambers for rapid evaluation of anesthetic sensitivity.

BACKGROUND: Anesthetic sensitivity is determined by the interaction of multiple genes. Hence, a dissection of genetic contributors would be aided by precise and high throughput behavioral screens. Traditionally, anesthetic phenotyping has addressed only induction of anesthesia, evaluated with dose-response curves, while ignoring potentially important data on emergence from anesthesia. METHODS: We designed and built a controlled environment apparatus to permit rapid phenotyping of twenty-four mice simultaneously. We used the loss of righting reflex to indicate anesthetic-induced unconsciousness. After fitting the data to a sigmoidal dose-response curve with variable slope, we calculated the MAC(LORR) (EC50), the Hill coefficient, and the 95% confidence intervals bracketing these values. Upon termination of the anesthetic, Emergence timeRR was determined and expressed as the mean +/- standard error for each inhaled anesthetic. RESULTS: In agreement with several previously published reports we find that the MAC(LORR) of halothane, isoflurane, and sevoflurane in 8-12 week old C57BL/6J mice is 0.79% (95% confidence interval = 0.78-0.79%), 0.91% (95% confidence interval = 0.90-0.93%), and 1.96% (95% confidence interval = 1.94-1.97%), respectively. Hill coefficients for halothane, isoflurane, and sevoflurane are 24.7 (95% confidence interval = 19.8-29.7%), 19.2 (95% confidence interval = 14.0-24.3%), and 33.1 (95% confidence interval = 27.3-38.8%), respectively. After roughly 2.5 MAC(LORR) x hr exposures, mice take 16.00 +/- 1.07, 6.19 +/- 0.32, and 2.15 +/- 0.12 minutes to emerge from halothane, isoflurane, and sevoflurane, respectively. CONCLUSION: This system enabled assessment of inhaled anesthetic responsiveness with a higher precision than that previously reported. It is broadly adaptable for delivering an inhaled therapeutic (or toxin) to a population while monitoring its vital signs, motor reflexes, and providing precise control over environmental conditions. This system is also amenable to full automation. Data presented in this manuscript prove the utility of the controlled environment chambers and should allow for subsequent phenotyping of mice with targeted mutations that are expected to alter sensitivity to induction or emergence from anesthesia.

Journal Article↗

Influence of inhaled anesthetics on the pharmacokinetics and pharmacodynamics of morphine.

We determined the magnitude and duration of the effect of morphine (1.0 mg/kg intravenous bolus) on isoflurane and halothane minimum alveolar concentration (MAC) in six dogs anesthetized on two occasions in cross-over fashion. Plasma morphine concentration-time profiles and changes in PaCO2 were determined after morphine injection. After morphine injection, the end-tidal anesthetic dose was manipulated over the course of a 4-h observation period to account for the decline in plasma morphine concentration and to maintain an anesthetic level equivalent to 1.0 MAC isoflurane or halothane alone. Morphine decreased the MAC of halothane and isoflurane. The magnitude of MAC decrease was related to time after morphine injection and was similar for a given time with both halothane and isoflurane. For example, at 28.8 +/- 3.6 (mean +/- SE) and 34.8 +/- 6.3 min after morphine injection, the MAC for halothane and isoflurane were reduced by 35.7% +/- 4.5% and 39.3% +/- 3.4%, respectively. By 4 h after morphine injection, the MAC reduction for both anesthetics was less than 10% in most of the animals. Except for systemic clearance of morphine during halothane and isoflurane (40.1 +/- 6.1 and 53.7 +/- 5.6 mL.min-1.kg-1, respectively), there were no differences in disposition kinetics of free morphine associated with the two inhaled anesthetics. Morphine increased PaCO2 to a similar degree with both halothane (from 42.2 +/- 2.1 mm Hg to 55.6 +/- 2.3 mm Hg) and isoflurane (46.2 +/- 2.4 mm Hg to 55.3 +/- 2.1 mm Hg). Respiratory depression was abolished by noxious stimulation (tail clamp) and naloxone in all animals with both anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

A cholinergic agonist induces cerebral hyperemia in isoflurane- but not pentobarbital-anesthetized dogs.

We tested whether the cerebral blood flow (CBF) response to the cholinergic agonist oxotremorine (OXO) is affected by the choice of anesthetics in dogs. We studied two anesthetics, pentobarbital and isoflurane, which produce similar levels of cerebral metabolic depression but have opposing effects on CBF. We also tested the contribution of nitric oxide (NO, or a NO-containing compound) in mediating the CBF response to OXO by determining whether NO synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) would attenuate OXO-induced hyperemia in both anesthetic groups. CBF (microspheres) was measured before and after OXO administration (50 micrograms.kg-1.min-1 intravenously [i.v.] for 10 min). Animals were divided randomly to receive OXO alone (n = 10) or L-NAME (40 mg/kg i.v.) followed by OXO (n = 10). Within each group, half of the animals received pentobarbital anesthesia (30 mg/kg i.v.) and half received isoflurane (1.4% end-tidal). In pentobarbital-anesthetized animals OXO produced no change in blood flow to cerebrum, caudate, diencephalon, neurohypophysis, or cerebellum in the absence (e.g., cerebrum 37 +/- 2 vs 42 +/- 5 mL/min/100 g) or presence of L-NAME (e.g., cerebrum, 29 +/- 4 vs 30 +/- 3 mL.min-1 x 100 g-1). In isoflurane-anesthetized animals, however, blood flow to forebrain regions increased after OXO (e.g., cerebrum 108 +/- 10 vs 232 +/- 15 mL.min-1 x 100 g-1; P < 0.05) without alteration in oxygen consumption in cerebrum (CMRO2) or blood flow to hindbrain regions. In isoflurane-anesthetized animals, L-NAME decreased baseline blood flow to cerebrum, caudate, diencephalon, cerebellum, and neurohypophysis (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

Optical imaging of SI topography in anesthetized and awake squirrel monkeys.

Orderly topographic maps in the primary somatosensory cortex (SI) serve as an anchor for our understanding of somatosensory cortical organization. However, this view is mostly based on data collected in the anesthetized animal. Less is known about these topographies in the awake primate. Even less is known about the relative activations of different subdivisions of SI (areas 3a, 3b, 1, and 2). Toward the goal of understanding the functional activation of SI, we conducted intrinsic signal optical imaging of areas 3b and 1 in awake squirrel monkeys. Monkeys were imaged repeatedly for a period of >2 years in awake and anesthetized states in response to vibrotactile and electrocutaneous stimuli presented to individual fingerpads. During this period, we found stable somatotopic maps in both the anesthetized and awake states, consistent with electrophysiologically recorded maps in areas 3b and 1 in the anesthetized state. In the awake animal, signal sizes were larger, but variability was greater, leading to decreased signal-to-noise ratios. Topographic activations were larger (in both area and amplitude) in the awake animal, suggesting either a less precise topography and/or more complex integration. This brings into question the role of a precise topographic map during behavior. In addition, whereas in the anesthetized animal strongest imaging signals were obtained from area 3b, in the awake animal, area 1 activation dominated over that in area 3b. Differences in relative dominance of area 3b versus area 1 suggest that inter-areal interactions in the alert animal differ substantially from that in the anesthetized animal.

Anesthesia↗

Blood anesthetic levels during surface-induced deep hypothermia under halothane-diethyl ether azeotrope anesthesia.

Blood anesthetic concentration and clinical indicators related to anesthetic management during surface-induced deep hypothermia were determined in seven adult mongrel dogs. The azeotrope of halothane and diethyl ether was assayed by gas chromatography. Blood concentration of halothane ranged from a pre-cooling control of 0.74 vol % to 0.11 vol % at 20 degrees C rewarming; ether ranged from 0.06 vol % at 20 degrees C rewarming to 0.22 vol % at 35 degrees C rewarming. Administration of anesthetic was reduced during cooling because of the spontaneous decrease in mean arterial pressure and heart rate. After elective circulatory arrest was induced, anesthetic was not required until after cardiac resuscitation at about 22 degrees C rewarming. Initial clinical signs indicating a need to increase administration of anesthetic included spontaneous respiration and an increase in mean arterial pressure. Blood azeotrope concentration was significantly lower during rewarming than at comparable temperatures during cooling. We conclude that blood concentration of halothane and ether changes as a function of body temperature and that anesthetic demand may be diminished following total circulatory arrest.

Anesthesia, Inhalation↗

Relationships between a proprietary index, bispectral index, and hemodynamic variables as a means for evaluating depth of anesthesia in dogs anesthetized with sevoflurane.

OBJECTIVE: To evaluate relationships among various techniques for monitoring anesthetic depth in sevoflurane-anesthetized dogs undergoing orthopedic surgery. ANIMALS: 10 dogs. PROCEDURE: Dogs were medicated with acepromazine (0.05 mg/kg, IM), buprenorphine (0.01 mg/kg, IM), and atropine (0.04 mg/kg, IM). Anesthesia was induced and maintained with sevoflurane. Cardiovascular and respiratory responses were monitored. Anesthetic depth was monitored by use of the bispectral index (BIS), and a proprietary index was used to monitor activity of the autonomic nervous system. RESULTS: A significant decrease in BIS was seen after induction but concurrent changes were not observed for the other techniques. The proprietary index increased significantly after intubation, but no changes were seen for the other techniques. No significant changes were detected during incision or when higher nociceptive stimuli were applied. We did not identify a correlation between BIS and the proprietary index, the proprietary index and hemodynamic variables, or the BIS and hemodynamic variables during induction and maintenance. A significant increase in the proprietary index and BIS was detected at the time of resumption of reflexes. During anesthetic recovery, a correlation was found between the proprietary index and BIS but not between hemodynamic variables and the other techniques. CONCLUSIONS AND CLINICAL RELEVANCE: A significant increase in the proprietary index, but not the BIS or hemodynamic variables, was detected during intubation. Anesthetic induction with sevoflurane did not prevent the sympathetic stimulus attributable to tracheal intubation. Monitoring of hemodynamic variables does not provide sufficient information to allow clinicians to evaluate stress during anesthetic recovery.

Acepromazine↗

Effects of tail docking using a rubber ring with or without anesthetic on behavior and production of lactating cows.

Production and behavioral measures were recorded to determine the level of stress and pain associated with tail docking adult dairy cows with a rubber ring. The possible advantages of using an epidural anesthetic were also examined. Sixty-four lactating, mixed-parity, Holstein cows were randomly assigned to one of four treatment groups. The treatments were rubber ring docking with epidural anesthetic (RRA), rubber ring docking without anesthetic (RR), control with epidural anesthetic (CA), and control without anesthetic (C). Behavior was examined on d 0, +1, +2, and +6. Milk production and feed intake were monitored. Cows exhibited subtle behavioral changes following application of rubber rings, as well as after epidural administration on d 0 and tail amputation on d +6. After treatment on d 0, the RR, RRA, and CA groups displayed less tail shaking than the C group. The RR and RRA cows continued to exhibit less tail shaking on d +1, +2, and +6. Also on d 0, the RR and RRA groups held their tails in the raised position less than the C and CA groups. After amputation on d +6, the RR and RRA groups spent longer with their tails pressed to their bodies than the C and CA groups. No significant differences in milk production or feed intake were found. Results suggest that tail-docking adult dairy cattle with rubber rings causes, at most, mild discomfort and that there is no benefit in using an epidural anesthetic. However, long-term effects need to be investigated.

Amputation, Surgical↗

Arteriovenous fistula in chronic renal failure patients: comparison between three different anesthetic techniques.

The creation of arteriovenous fistula is an established form of therapy for patients with chronic renal failure. Anesthetic management in such patients is governed by the presence of risk factors such as hypertension, ischemic heart disease, diabetes, chronic pulmonary disease, anemia, coagulopathy, metabolic acidosis and/or hyperkalemia. In an attempt to improve the quality of anesthetic care and outcome we designed the present study to compare the different anesthetic techniques which are used for creation of arteriovenous fistula. Retrospectively we reviewed 164 patients who underwent creation of arteriovenous fistula. We retrieved the data concerning the age, sex, ASA class, and coexisting diseases. The patients were classified into three groups depending on the anesthetic technique received. Group A (n = 48) patients received general anesthesia; group B (n = 39), patients received brachial plexus block and group C (n = 77), patients received local infiltration anesthesia. Chi-square test was used to compare between the percentages among the different groups. The percentages of cardiac patients showed significant differences between groups A and B and also between groups A and C. There was a significant difference between the groups A and B also between the groups A and C but not between groups B and C concerning age. ASA classes were not significantly different among the groups. Among the total number of patients, 34 were diabetics and 75 patients were cardiac. Axillary brachial plexus block was complete in 70% of patients and incomplete in 27% and failed in 3% of patients. We conclude that chronic renal failure patients are at increased risk during anesthesia. We conclude that brachial plexus blockade or local anesthetic infiltration are good alternatives to general anesthesia in these patients undergoing creation of arteriovenous fistula. Age, ASA class and cardiac status were the three determining factors for the choice of the anesthetic technique. Further multivariate prospective study are needed to confirm these results.

Adult↗

[Batching of low-concentration anesthetics with evaporators used in apparatuses for inhalation anesthesia].

The accuracy of the anesthetic vaporizers with modern vaporizing devices is complicated by necessity of providing small anesthetic vapor concentration for a wide range of gas flows, especially at small flows, and at use of a combination of inhalation anesthesia with intravenous one. Compliance with the requirements of the international standards concerning the accuracy of low-concentration anesthetic vapor batching also does not provide management of anesthesia depth at various stages of surgical operations. The problem is solved well by replacement traditional vaporizers with so-called barbotage ones equipped by adjustment of vapor concentration by modem electronic methods. It is even more promising to use direct injection of the liquid anesthetics into the respiratory contour of infusion pump. However, because individual sensitivity of patients to anesthetics is rather variable, these devices do not provide regulation of the depth of anesthesia. Therefore, stability rather than accuracy of batching of low-concentration anesthetics with evaporators used in apparatuses for inhalation anesthesia is of cardinal importance, Methods of objective instrumental evaluation of the depth of anesthesia require further research and implementation.

Anesthesia, Inhalation↗