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PubMed2006

Tolerance of local anesthetic for transrectal ultrasound-guided prostate biopsy: our experience and a literature review.

PURPOSE: To determine whether local anesthetic injection or gel reduced pain during transrectal ultrasound-guided prostate biopsies and whether there was significant difference between quadrant and apex-only anesthesia. METHODS: Between September 2001 and May 2002, 240 male patients with elevated prostate-specific antigen and (or) abnormal digital rectal examination were randomized into 1 of 4 groups: 1) transrectal lidocaine gel, 2) quadrant lidocaine injections, 3) apex-only lidocaine injections, or 4) no local anesthetic. Patients scored their pain on a numerical rating scale where 0 indicated no pain and 10 indicated worst pain. We analyzed mean and standard deviations of scores, using a 1-way analysis of variance (ANOVA) and post hoc multiple comparisons with Tukey's honestly significant difference (HSD) studentized range test to determine whether there were significant differences across the groups. RESULTS: There was no significant difference between local anesthetic gel (mean 3.1, SD 1.9) and no anesthetic (mean 3.5, SD 1.9) or between quadrant (mean 1.7, SD 1.7) and apex-only (mean 2.0, SD 1.8) local anesthetic injections. There was significant difference between quadrant injections (mean 1.7, SD 1.7) and no local anesthetic (mean 3.5, SD 1.9) and between apex-only injections (mean 2.0, SD 1.8) and no local anesthetic (mean 3.5, SD 1.9). CONCLUSION: There was significant pain reduction with local anesthetic injections but not with gel, and since there was no significant difference in efficacy between quadrant and apex-only injections, we recommend apex-only local anesthetic injections for transrectal ultrasound--guided prostate biopsies because it simplifies the injection procedure.

Administration, Topical↗
PubMed1984

Inhibition of binding of [3H]batrachotoxinin A 20-alpha-benzoate to sodium channels by local anesthetics.

The effects of several local anesthetics on the binding of ligands to receptors associated with voltage-sensitive sodium channels in rat brain synaptosomes have been examined. In the presence of 0.3 microM scorpion toxin, the 13 local anesthetics tested inhibited the specific binding of [3H]batrachotoxinin A 20 alpha-benzoate [( 3H]BTX-B), a ligand which binds to a receptor site responsible for the activation of sodium channel ion flux, in a dose-dependent fashion, with KD values ranging from 1.2 microM for tetracaine to 1.58 mM for benzocaine. A plot of log KD from these binding experiments against log K0.5 for inhibition of sodium currents by local anesthetics from electrophysiological experiments yielded a regression line with a slope of 0.84 and a correlation coefficient, r, of 0.86, demonstrating that the inhibition of [3H]BTX-B binding by local anesthetics occurs within a concentration range of physiological relevance. Tetracaine had little effect on basal 125I-labeled scorpion toxin binding to synaptosomes in the absence of batrachotoxin. However, in the presence of batrachotoxin, tetracaine inhibited the batrachotoxin-dependent increase in scorpion toxin binding (KD = 2.0 microM) in a dose-dependent manner, suggesting that inhibition of [3H]BTX-B binding by local anesthetics does not occur through binding at the scorpion toxin binding site. The inhibition of [3H]BTX-B binding by lidocaine was reversible within 30 min when samples were diluted from 10(-3)M to 10(-4) M lidocaine. Scatchard analysis of [3H]BTX-B binding to synaptosomes showed that bupivacaine and tetracaine reduced receptor affinity without decreasing maximal binding capacity. This reduction in receptor affinity in the presence of local anesthetics appears to be due, at least in part, to an increased rate of ligand dissociation from the receptor-ligand complex, suggesting an indirect allosteric mechanism for the inhibition of [3H]BTX-B binding by local anesthetics. Analysis of the effects of local anesthetics in terms of an allosteric model of drug action showed that they bind to inactive states of sodium channels with at least a 10-fold higher affinity than active states. A 7-fold difference in KD for inhibition of [3H]BTX-B binding between the local anesthetic stereoisomers RAC 109 I and RAC 109 II was observed. Similarly, the dissociation rate constant for the [3H]BTX-B/receptor complex was increased 9.3-fold in the presence of RAC 109 II and 4.3-fold in the presence of a comparable concentration of RAC 109 I.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗
PubMed1994

Alcohols and anesthetics enhance the function of 5-hydroxytryptamine3 receptors expressed in Xenopus laevis oocytes.

One subunit of the 5-hydroxytryptamine3 (5-HT3) receptor has been cloned, and expression of cDNA coding for this protein in Xenopus oocytes results in the formation of homomeric ion channels. In the present study, this system was used to define the sensitivity of the 5-HT3 receptor to alcohols and anesthetics. Ethanol, in pharmacologically relevant concentrations, potentiated 5-HT-mediated currents, with the greatest potentiation observed at lower concentrations of 5-HT. Likewise, butanol stimulated the receptor but with greater efficacy and potency than ethanol. The volatile anesthetics isoflurane, halothane and 1,2,2-trifluorocyclobutane (F3) all enhanced 5-HT3 receptor function. Concentrations of these anesthetics below the minimal alveolar concentration for anesthesia (MAC) produced significant stimulation of 5-HT-mediated currents. Similar to the alcohols, the greatest enhancement of 5-HT3 receptor function by anesthetics was seen at lower concentrations of 5-HT. However, anesthetics were substantially more efficacious than ethanol in enhancing 5-HT3 receptor function. In the presence of 0.5 microM 5-HT, maximal stimulation by ethanol was approximately 50%, but anesthetic enhancement of 5-HT3 receptor-mediated currents did not reach a maximum. Over the concentrations tested, anesthetics potentiated 0.5 microM 5-HT-mediated currents by approximately 25% to 400%. The intravenous anesthetic propofol did not enhance 5-HT3 receptor function or change the potentiation of this receptor by halothane. These results suggest that alcohols and volatile anesthetics have similar actions on 5-HT3 receptor function, which is in agreement with results of studies with other members of the superfamily of ligandgated ion channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohols↗
PubMed1993

Effects of inhalational anesthetics on biochemical events in growing neuronal tips.

BACKGROUND: The influence of general anesthetics on developing organs has been a source of concern for many years. The central nervous system, which is developing rapidly at the time of birth, is of special interest in this regard. In this study, the biochemical characteristics of developing neural tips (growth cones) were examined after exposure to anesthetics to elucidate the molecular mechanism by which long-lasting alterations in the nervous system, including neuroteratogenicity, as previously described, were evoked. METHODS: Neonatal rats were exposed to an atmosphere containing inhalational anesthetics (1% halothane or 75% nitrous oxide) or a control atmosphere (25% O2 and 75% N2) for 6 h at postnatal day 1. After this exposure, growth cone particles were isolated from the forebrain using a recently devised cell fractionation method at postnatal days 2, 3, 4, and 5. Protein composition, phosphoprotein patterns, and protein kinase C (PKC) activities of the isolated growth cones were compared between each group exposed to anesthetics and the control group. The dose-response relationship of the action of anesthetics on PKC activity was also examined (at 0.5 and 0.75% halothane and 25 and 50% N2O). RESULTS: The increase in body weight and brain wet weight were not significantly affected by exposure to either anesthetic. No apparent influence on protein composition was observed by sodiumdodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE). However, calcium-dependent protein phosphorylation of the 46 kDa protein and of the 80 kDa protein, which is reported to be mediated by PKC, were significantly reduced after exposure to the anesthetics. A direct assay of PKC activity in growth cone particles indicated that PKC activity in the growth cone was 70.6 +/- 9.6% of the control value at 24 h after exposure to 1% halothane, and 63.2 +/- 4.9% after exposure to 75% nitrous oxide. Exposure to 0.75% halothane or 50% nitrous oxide had a similar, but lesser, effect on this parameter. In contrast, exposure to 0.5% halothane or 25% nitrous oxide evoked no apparent effect. Thus the PKC activity in growth cone particles, which is thought to play an important role in signal transduction in the developing brain, was shown to be affected by exposure to inhalational anesthetics over a range of concentrations. CONCLUSIONS: Considering the crucial role of growth cones in the establishment of the neuronal network, the interruption of signal transduction in the growth cone at a time that is critical in directing the neurite extension may evoke a long-lasting alteration in the neural network. Therefore, the effect of inhalational anesthetics on the growth cone enzyme observed in this study may have a major role in the mechanism that induces morphologic or behavioral neuroabnormalities in later life.

Administration, Inhalation↗
PubMedDate not supplied

Progress in the development of ultra-long-acting local anesthetics.

BACKGROUND AND OBJECTIVES: Local anesthetic agents with a duration of action longer than the currently available local anesthetics could have widespread clinical application for the treatment of both chronic and acute pain. Over the last several decades, several different approaches have been used in the development of ultra-long-acting agents. There are currently promising preparations in development which may prove clinically useful in the near future. METHODS: A Medline search was conducted for relevant articles published in peer-reviewed journals between 1971 and 1996. Investigations related to prolongation of the effect of local anesthetics either by alterations in the local anesthetic molecule, use of new or novel agents, or use of new delivery systems were reviewed. In addition, bibliographies of relevant articles were searched to capture any articles that were missed by the Medline search. RESULTS: Over the last several decades, numerous attempts have been made to prolong the duration of action of local anesthetics. Initially, research focused on alterations in the local anesthetic molecule or the identification of new agents with local anesthetic action. Recently, the focus of much of the work has shifted to new drug-delivery systems such as polymers and liposomes. CONCLUSIONS: Although encouraging results have been reported in the literature, there is currently no agent or delivery system that has shown reliable and practical prolongation of local anesthetic effect in humans. There have been several encouraging reports in animals that have shown local anesthetic effects lasting up to several days, but these results must be validated and then performed in human studies before a clinically useful agent is found. Further research is warranted.

Anesthetics, Local↗
PubMed2003

Temperature and humidity of the Dräger Cato anesthetic machine circuit.

PURPOSE: The Dräger Cato anesthetic machine (Dräger, Lübeck, Germany) effectively humidifies and warms anesthetic gases, because it has a built-in hotplate to heat the breathing system, and expired gas passes through the CO2 absorbent three times during one breath. In the present study, we measured the temperature and absolute humidity (AH) of the anesthetic circuit in the Dräger Cato machine with and without heat moisture exchangers (HME), and compared them with those in another anesthetic machine, the Aestiva/5 (Datex-Ohmeda, Helsinki, Finland). METHODS: Forty-eight adult patients were randomly assigned to one of eight groups according to the anesthetic machine, fresh gas flow (FGF), and the use of HME (n = 6 each): Cato 0.51 x min(-1) without HME (group 1), Cato 1.01 x min(-1) without HME (group 2), Cato 0.51 x min(-1) with HME (group 3), Cato 1.01 x min(-1) with HME (group 4), Aestiva 0.51 x min(-1) without HME (group 5), Aestiva 1.01 x min(-1) without HME (group 6), Aestiva 0.51 x min(-1) with HME (group 7), and Aestiva 1.01 x min(-1) with HME (group 8). The temperature and AH of the anesthetic gases were measured with a Moiscope (S.K.I. Net, Tokyo, Japan), which was placed between the endotracheal tube and the Y-piece of the anesthetic circuit. The HME was placed between the Moiscope and the Y-piece of the anesthetic circuit. The temperature and AH of the anesthetic gases were measured at 5, 10, and 15 min and then every 15 min up to 150 min after tracheal intubation. RESULTS: Among the groups without HME (groups 1, 2, 5, and 6), the inspired temperatures and AH in groups 1 and 2 were significantly higher than those in groups 5 and 6 at all times during the study period (P < 0.01-0.001). The inspired temperatures and AH of the groups with HME (groups 3, 4, 7, and 8), were significantly higher than those in groups 2, 5, and 6 (P < 0.01-0.001). Among the groups with HME, the AH in group 3 was significantly higher than that in group 8 until the final study period. CONCLUSION: The present study indicates that the Dräger Cato machine was more effective in warming and humidifying respiratory gas than the Aestiva/5, and that Aestiva/5 without HME does not reach the optimal temperature and humidity ranges, even if minimal flow anesthesia (0.51 x min(-1)) is performed.

Adult↗
PubMed1980

Surface activities of tertiary amine local anesthetics at air/water interface in the presence and absence of phospholipid monolayers.

Adsorption of procaine and tetracaine to the dipalmitoyl phosphatidylcholine monolayers at the air/water interface is analyzed in terms of two types of interaction: (1) between the phospholipid molecules and the ligand molecules, and (2) among the ligand molecules themselves. The presence of the phospholipid monolayer increases the surface concentration of the anesthetics. The interaction energy, omega AB, between the phospholipid molecules and the anesthetic molecules at the interface accounts for this excess adsorption. The values were --2.95 kT for procaine and --2.99 kT for tetracaine where k is the Boltzmann constant and T = 298 K. The adsorption of the local anesthetics to the interface was cooperative. The interaction energy, omega AA, between the anesthetics molecules on the surface determines the cooperativity. The values were --0.056 kT for procaine and --0.397 kT for tetracaine, where T = 298 K. This parameter determines the slope of the curve plotted relating the surface concentration (gamma) and the logarithm of the bulk concentration (log C). When (omega AA/kT) greater than or equal to 1, the adsorption follows the phase-transition. A parameter KA, which is related to the difference of the free energy of anesthetics between the surface and the bulk molecules, locates the take-off point of the adsorption curve at the log C axis. The values were 2.15 x 10(3) for procaine and 7.00 x 10(3) for tetracaine. In spite of the general assumption that the difference in the clinical potency among local anesthetics are attributable to their lipid solubility, the present results showed that the phospholipid-anesthetic interaction energies for procaine and tetracaine were similar. The larger surface concentration of tetracaine than procaine at the same bulk concentration was due to the combined effect of KA and omega AA. KA represents the tendency of the anesthetic molecules to escape from the hydrogen-bonded water phase, and omega AA determines the cooperativity factor causing these molecules to aggregate at the interface. It was also observed that the charged forms of the anesthetics have non-zero surface activities.

Adsorption↗
PubMedDate not supplied

Decreasing frequency of anesthetic cardiac arrests.

STUDY OBJECTIVE: To determine whether the anesthetic cardiac arrest rate decreased following the introduction of enhanced respiratory monitoring and increased safety awareness during the past decade. DESIGN: Epidemiologic study of surgical anesthetic morbidity as represented by intraoperative cardiac arrests. SETTING: Operating room suite of a large university hospital. PATIENTS: 241,934 patients undergoing surgery over a period of 20 years. INTERVENTIONS: Anesthetic cardiac arrest rates from two decades were compared. The first decade (1969 to 1978) predated safety initiatives, while the second (1979 to 1988) included them. MEASUREMENTS AND MAIN RESULTS: Anesthetic cardiac arrests were identified, and their causes (respiratory vs nonrespiratory) and preventability (identifiable error) were determined shortly after their occurrence, as part of an ongoing study initiated in 1969. They provided numerators for rate calculations; total surgical anesthetics provided the denominators. The anesthetic cardiac arrest rate decreased by one-half from the first decade (2.1 arrests/10,000 anesthetics) to the second (1.0/10,000), a significant difference (p = 0.032, Fisher's Exact Test). The rate for preventable arrests due to respiratory causes declined significantly from 0.8/10,000 to 0.1/10,000 (p = 0.013) and accounted for most of the observed decrease in the overall anesthetic cardiac arrest rate. The rates for preventable nonrespiratory arrests and nonpreventable arrests did not change significantly. CONCLUSIONS: The results support the hypothesis that improved respiratory monitoring was effective in decreasing anesthetic morbidity.

Anesthesia↗
PubMed1985

Different relations between infarct size and occluded bed size in barbiturate-anesthetized versus conscious dogs.

The relation between infarct size and occluded bed size in barbiturate-anesthetized (n = 32) and conscious (n = 34) dogs was compared using models of the left anterior descending (n = 43) and circumflex (n = 23) coronary arteries with 2 day old infarcts. Infarct and occluded bed (postmortem coronary arteriography) masses were measured by computerized planimetry of weighed left ventricular rings. For either type of occlusion, infarcts were larger in anesthetized than in conscious dogs (56 versus 33% occluded bed, p less than 0.001), with greater slopes of the linear regressions between infarct size and occluded bed size (p less than 0.001) and less epicardial sparing (p less than 0.05) on topographic mapping. Although arterial and left atrial pressures were similar in the two groups, heart rates were higher in the anesthetized dogs, both before (127 versus 88 beats/min, p less than 0.001) and after (151 versus 109 beats/min, p less than 0.001) occlusion. Myocardial blood flow distribution (radioactive microspheres, n = 33) favored the epicardium in anesthetized dogs, with lower endocardial-epicardial flow ratios pre- and postocclusion. Also, the level of total plasma catecholamines (radioenzymatic assay) was higher in barbiturate-anesthetized (n = 5) than in conscious (n = 5) dogs. Increasing the heart rate in conscious dogs (n = 18) to that of the anesthetized group (139 beats/min) by pacing produced larger infarcts and greater linear regression slopes, as seen in anesthetized dogs. Decreasing the heart rate in anesthetized dogs (n = 7) to that of the conscious group (98 beats/min) by sinoatrial node destruction and pacing resulted in smaller infarcts and lower linear regression slope, as seen in conscious dogs. Thus, the larger infarcts in barbiturate-anesthetized dogs appeared to be related mainly to the tachycardia, although transmural maldistribution of flow and increased circulating catecholamines might have contributed.

Analysis of Variance↗
PubMed1994

Use of Drosophila mutants to distinguish among volatile general anesthetics.

The way general anesthetics cause their clinically useful effects on the nervous system is not known. Since the principal determinant of the potency of these agents is their solubility in oil, the role of chemical structure in affecting anesthetic targets has been obscured. In this work, we use an intense beam of light (Tinklenberg, J. A., Segal, I. S., Tianzhi, G. & Maze, M. (1991) Ann. N.Y. Acad. Sci. 625, 532-539) to assess the effect of general anesthetics on the capacity of fruit flies to sense a noxious stimulus and respond to it. By examining the effect of halothane-resistant (har) mutations on the potency of various volatile anesthetics in this assay, we establish similarities and differences between these agents that highlight the was chemical structure influences anesthetic action. In general, the potencies of anesthetics with different chemical structure are affected to different extents by one or more har mutations. However, three anesthetics of related structure (enflurane, isoflurane, and desflurane) show quantitatively indistinguishable alterations in potency in each of four genetic tests. These results not only identify important structural features of anesthetics but also place limits on the classical view that all anesthetics act at a common target.

Animals↗
PubMed1988

Conscious state comparisons of the effects of the inhalation anesthetics and diltiazem, nifedipine, or verapamil on specialized atrioventricular conduction times in spontaneously beating dog hearts.

The effects of enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were contrasted to awake (control) in 22 chronically instrumented dogs. Dogs were studied with and without diltiazem (DIL), nifedipine (NIF), vehicle for NIF (VEH), or verapamil (VER). These calcium channel blockers (CCB) were administered iv to achieve clinically effective steady-state plasma levels in awake dogs. CCB plasma levels in awake dogs, subsequently anesthetized with ENF (N = 10), HAL (N = 10), or ISO (N = 11), were: DIL = 94 +/- 13 to 124 +/- 9 ng/ml, NIF = 4 +/- 1 to 7 +/- 2 ng/ml, VER 108 +/- 23 to 147 +/- 9 ng/ml. Anesthetized dogs had approximate two-fold increases in plasma levels of DIL or VER. There was no anesthetic effect on plasma levels for NIF. In the absence of CCBs, HAL increased AV nodal conduction time (AVN) compared to awake. There was a 4-10% increase in His-Purkinje (HP) and ventricular (VENT) conduction time with each anesthetic. The CCBs did not alter HP or VENT in awake dogs, but AVN was increased 15-23% by DIL and 28-38% by VER. Three of ten dogs with VER developed complete heart block or AV junctional escape rhythm at each level of ENF. One dog with VER developed type I, 2 degrees (Wenckebach) AV block at each level of HAL and ISO. No dogs with DIL had heart block or escape rhythms during anesthesia. In anesthetized dogs without heart block or escape rhythms, the increase in AVN with VER ranged from 46 to 69%, and with DIL from 36 to 55%. The CCB had no added effects on HP or VENT with any anesthetic. Finally, there were no effects of NIF alone or with the anesthetics on specialized conduction that could not be attributed to VEH. The authors conclude that with the inhalation anesthetics, antiarrhythmic plasma levels of DIL or VER prolong AV nodal most compared to infranodal conduction time. Additionally, heart block or escape rhythms appear more likely with VER and any of the potent inhalation anesthetics.

Anesthesia, Inhalation↗
PubMed1994

Local anesthetics depress the calcium current of rat sensory neurons in culture.

BACKGROUND: Local anesthetics are known to inhibit the voltage-gated sodium current (INa) of the nerve membrane, but it has not been fully studied whether anesthetic concentrations of local anesthetics depress the voltage-gated calcium current (ICa) of mammalian neurons. The effects of local anesthetics on ICa evoked in cultured rat dorsal root ganglion cells were studied. METHODS: Whole cell patch clamp recordings were made from rat dorsal root ganglion cells cultured for 1-3 weeks. ICa was recorded using patch electrodes filled with Cs-aspartate in Na(+)-free external solution containing 5 mM-Ba2+. All drugs, including local anesthetics, were applied by miniperfusion from micropipettes by pressure ejection. RESULTS: Tetracaine (300 microM) depressed the peak amplitudes of high voltage-activated (HVA)-ICa to 22.6 +/- 8.8% of control values (n = 14) without affecting the current-voltage relation. A tetracaine dose-response curve for HVA-ICa indicated an apparent dissociation constant of 79.5 microM. Tetracaine (30 microM) depressed nicardipine-sensitive HVA-I(Ca) (L-type) to 14.3 +/- 6.7% (n = 6), omega-conotoxin-sensitive HVA-ICa (N-type) to 81.6 +/- 9.6% (n = 7), and low voltage-activated (LVA)-ICa (T-type) to 65.1 +/- 11.1% (n = 6) of their respective controls. Local anesthetics other than tetracaine also depressed HVA-ICa but were of different potency; the rank sequence was dibucaine > tetracaine > bupivacaine >> procaine = lidocaine. CONCLUSIONS: These results suggest that both HVA-ICa and LVA-ICa are depressed by tetracaine used at the concentrations required for spinal anesthesia and that the L-type Ca2+ channel among Ca2+ channel subtypes is the most susceptible to tetracaine. A good correlation between local anesthetic potencies to inhibit HVA-ICa and their anesthetic potencies implies that the inhibition of calcium influx through voltage-gated channels may contribute to spinal anesthetic mechanisms.

Animals↗
PubMed2004

Anesthetics and cerebral metabolism.

PURPOSE OF REVIEW: This review focuses on the utilization of the effects of general anesthetics on cerebral metabolism as revealed by imaging for therapeutic and preventive purposes, for understanding mechanisms of anesthetic action, and for elucidating mechanisms of cerebral processing in humans. RECENT FINDINGS: General anesthetics suppress cerebral metabolism significantly. This effect has been used for neuroprotection during inadequate cerebral blood flow. With the advent of noninvasive imaging techniques, this suppression has also been used to image and map the sites of anesthetic action in the living human brain. Volatile agents, intravenous anesthetics, and analgesics have all begun to be explored using mostly positron emission tomography. The ability of anesthetics to change global baseline brain metabolism has created the opportunity to examine the relevance of global baseline (resting) brain activity in terms of region-specific cerebral processing. SUMMARY: Anesthetics experimentally appear to be useful for neuroprotection, at least during the early post-ischemic period. Identification of the cerebral sites of anesthetic action by in vivo human brain imaging provides new insights into the mechanism of action of these agents. Anesthetic-related manipulation of baseline brain metabolism demonstrates the significant contribution of this global activity to regional cerebral processing.

Journal Article↗
PubMed2001

Recovery from carotid artery catheterization performed under various anesthetics in male, Sprague-Dawley rats.

This study was designed to determine the time to recovery from carotid artery catheterization using multiple criteria and to compare recovery times between three common anesthetics. Male Sprague-Dawley rats, chronically instrumented with radio-telemetry transmitters, were anesthetized with sodium pentobarbital, halothane or a mixture of ketamine, xylazine and acepromazine before an indwelling catheter was placed in the carotid artery. The procedure was completed in less than 15 min. Changes in body weight, food and water consumption, blood pressure, heart rate and activity were used to determine recovery. As judged by recovery of body weight, animals anesthetized with each of the anesthetics recovered by the 4th day after catheterization. Food and water consumption normalized by 1-2 days after surgery. Heart rates and blood pressures during the light phase of the photoperiod were significantly increased for 2 days by all anesthetics. During the dark phase of the photoperiod, heart rates and blood pressures were not significantly affected by pentobarbital or halothane anesthesia, but were significantly decreased and increased respectively on the night immediately following surgery in the ketamine / xylazine / acepromazine-anesthetized rats. Delayed elevations of heart rate were observed in pentobarbital and halothane anesthetized rats on days and/or nights 5 and 6 post surgery. Animal activity patterns during the light phase of the photoperiod were not affected by pentobarbital or halothane, but were increased by ketamine 2 days after surgery. During the dark phase, halothane transiently reduced activity whereas ketamine-anesthetized rats showed reduced activity for 4 nights post surgery. These studies show that recovery depends on the criteria selected and the anesthetic used, but, in general, 2-4 days were required for recovery from this relatively simple procedure.

Anesthesia↗
PubMed1999

Comparison of Cardiovascular Parameters and/or Serum Chemistry and Hematology Profiles in Conscious and Anesthetized Rhesus Monkeys (Macaca mulatta).

The rhesus monkey is often used in pre-clinical research, and such studies frequently involve a variety of anesthetic conditions. Therefore, it is important to determine baseline physiologic blood chemistry and cardiovascular parameters in anesthetized animals to facilitate appropriate comparisons. The present study compares the cardiovascular parameters, hematology, serum chemistry, and blood gas levels of rhesus monkeys anesthetized with pentobarbital, isoflurane, ketamine, and propofol. Hematology, serum chemistry, and blood gas levels were unaffected by the four anesthetic regimens. However, because of its formulation, propofol is inappropriate for use in animals in which changes in tryglycerides will be evaluated. Compared to those in conscious, unrestrained monkeys, heart rates were higher in anesthetized animals, but the rates of anesthetized animals were similar regardless of anesthetic agent used. In contrast, mean arterial blood pressure was lower in animals anesthetized with pentobarbital, propofol, or isoflurane than in the conscious monkeys. However, mean arterial pressure of ketamine-anesthetized monkeys was similar to that of the conscious monkeys.

Journal Article↗
PubMed1992

[An unusual cause of anesthetic ventilator malfunction].

We report a case of malfunction of an anesthetic ventilator by an unusual cause. A 48-year-old male with gastric cancer was scheduled for gastrectomy. Anesthesia was maintained with enflurane, N2O, O2 and epidural blockade using a semiclosed circuit system. The patient was ventilated using AV1 anesthetic machine (Dräger Co.). Forty minutes after induction of anesthesia, chest movement of the patient suddenly stopped. There was no gas flow to the patient during inspiratory phase. Air leak was not found in anesthetic respiratory circuit and at the bellows of the ventilator. The supply of oxygen and air to the anesthetic machine was sufficient. Since we could not find any cause of the ventilator failure, anesthesia was maintained with manual ventilation by using another anesthetic machine until completion of the surgery. After the surgery, we recognized that the controller unit of expiratory valve of the ventilator was obstructed by a Tamper Proof Film, which seals the outlet of a commercial bag of lactated Ringer's solution (Solulact, Terumo Co.). It seems that the film dropped accidentally between the main part and the ventilator system of anesthetic machine when the bellows was exchanged before the surgery, and moved on to the controller unit of the expiratory valve of the ventilatory system during surgery. In conclusion, it is necessary for anesthetists to understand the inner structure and system of the anesthetic machine and to check the anesthetic machine to avoid the troubles and accidents related to anesthetic machine.

Anesthesia, Closed-Circuit↗
PubMed1989

Isoflurane anesthesia in sandhill cranes (Grus canadensis): minimal anesthetic concentration and cardiopulmonary dose-response during spontaneous and controlled breathing.

Information on species differences in responses to inhalation anesthetics has been established in a variety of mammalian and non-mammalian species, but comparable studies have not been reported in birds. The purpose of this study was to determine minimal anesthetic concentration and cardiopulmonary concentration-response effects of isoflurane in Sandhill cranes. Six cranes were anesthetized with isoflurane in oxygen. Gases sampled through a polyethylene tube inserted to the distal end of an endotracheal tube were used for measurements of isoflurane concentrations using an infrared gas analyzer. Body temperature was maintained at 40 +/- 0.5 degrees C. The minimal anesthetic concentration for isoflurane was determined during spontaneous ventilation, and concentration-response data were collected at 1, 1.5, and 2.0 times the minimal anesthetic concentration. Concentration-response data were repeated during mechanically controlled breathing with PaCO2 maintained between 27 and 35 mm Hg. The minimal anesthetic concentration for isoflurane was 1.34 +/- 0.14 vol% (mean +/- SD). Concentration-dependent respiratory depression during spontaneous breathing was evidenced in all cranes by an increase in PaCO2. Isoflurane induced apnea in two of the cranes during spontaneous ventilation at 2 times the minimal anesthetic concentration. As the concentration of isoflurane was increased, mean arterial blood pressure decreased during both spontaneous and controlled ventilation. Mean arterial blood pressure was higher during controlled ventilation than during spontaneous ventilation. The minimal anesthetic concentration for isoflurane in Sandhill cranes is similar to values for isoflurane minimal anesthetic concentration in mammals. Isoflurane has dose-dependent effects on cardiopulmonary function qualitatively similar to those observed in mammals.

Anesthesia↗
PubMed1988

Combined depressant effects of diltiazem and volatile anesthetics on contractility in isolated ventricular myocardium.

Because the volatile anesthetics depress the entry of calcium (Ca) into myocardial cells and also alter release of intracellular Ca stores, additional pharmacologic blockade of Ca entry could potentially enhance anesthetic-induced depression. The depressant effects of the calcium entry blocker diltiazem combined with the volatile anesthetics halothane, enflurane, or isoflurane were investigated in isolated guinea pig papillary muscle. Muscle contractions were studied in normal Tyrode solution after rest and at stimulation rates of 0.1, 0.25, 0.5, 1, 2, and 3 Hz. Anesthetics were studied in the presence of 0.1 and 1 microM diltiazem, which depressed tension to approximately 85 and 55% of control at 2-3 Hz, respectively; depression at the higher concentration was frequency-dependent. Depressant effects of enflurane were determined as previously done for equianesthetic concentrations (approximately 1 and 2 MAC) of halothane and isoflurane. At all stimulation rates, 1.7 and 3.5% enflurane depressed peak tension and dT/dt-max to approximately 73 and 50% of the mean control-recovery value, respectively. After control measurements of contractile characteristics, effects of 0.1 microM diltiazem were determined alone and then with the addition of halothane (0.75 or 1.5%), isoflurane (1.3 or 2.5%), or enflurane (1.7 or 3.5%), respectively. Recovery from anesthetic was then determined in the continued presence of diltiazem. After rest and at rates less than or equal to 0.5 Hz, equianesthetic concentrations of these volatile agents caused similar depression in the presence of diltiazem. At 3 Hz stimulation rate, 1.3% isoflurane caused significantly less contractile depression than did 1.7% enflurane or than 0.75% halothane. At 2-MAC concentrations, differences among the anesthetics were more apparent: 2.5% isoflurane depressed peak tension and dT/dt-max less than did halothane at 1-3 Hz stimulation rates, and depressed dT/dt-max less than 3.5% enflurane at 2-3 Hz. Similar frequency-dependent differences in depression by approximately 2 MAC anesthetics were observed in the presence of 1 microM diltiazem. The patterns of depressant action by the volatile anesthetics were similar to those previously observed in the absence of diltiazem. Furthermore, when the volatile anesthetic depression of contractions was combined with the depression due to diltiazem-induced blockade of Ca entry, the resulting contractile depression did not differ significantly from a prediction that assumed simply additive effects.

Animals↗