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PubMed1997

Baralyme dehydration increases and soda lime dehydration decreases the concentration of compound A resulting from sevoflurane degradation in a standard anesthetic circuit.

UNLABELLED: Soda lime and Baralyme brand carbon dioxide absorbents degrade sevoflurane to CF2 = C(CF3)OCH2F, a potentially nephrotoxic vinyl ether called Compound A. Dehydration of these absorbents increases both the degradation of sevoflurane to Compound A and the degradation of Compound A. The balance between sevoflurane degradation and Compound A degradation determines the concentration of Compound A issuing from the absorbent (the net production of Compound A). We studied the effect of dehydration on the net production of Compound A in a simulated anesthetic circuit. Mimicking continuing oxygen delivery for 1, 2, or 3 days after completion of an anesthetic, we directed a "conditioning" fresh gas flow of 5 L/min or 10 L/min retrograde through fresh absorbent in situ in a standard absorbent system for 16, 40, and/or 64 h. The conditioned absorbent was subsequently used (without mixing of the granules) in a standard anesthetic circuit in which a 3-L rebreathing bag substituted for the lung. Metabolism was mimicked by introducing 250 mL/min carbon dioxide into the "lung," and the lung was ventilated with a minute ventilation of 10 L/ min. At the same time, we introduced sevoflurane in a fresh gas inflow of 2 L/min at a concentration sufficient to produce an inspired concentration of 3.2%. Because of increased sevoflurane destruction by the absorbent, progressively longer periods of conditioning (dehydration) and/or higher inflow rates increased the delivered (vaporizer) concentration of sevoflurane required to sustain a 3.2% concentration. Dehydration of Baralyme increased the inspired concentration of Compound A by up to sevenfold, whereas dehydration of soda lime markedly decreased the inspired concentration of Compound A. IMPLICATIONS: Economical delivery of modern inhaled anesthetics requires rebreathing of exhaled gases after removal of carbon dioxide. However, carbon dioxide absorbents (Baralyme/soda lime) may degrade anesthetics to toxic substances. Baralyme dehydration increases, and soda lime dehydration decreases, degradation of the inhaled anesthetic sevoflurane to the toxic substance, Compound A.

Anesthetics, Inhalation↗

PubMed1998

Halogenated anesthetics inhibit Pseudomonas aeruginosa growth in culture conditions reproducing the alveolar environment.

UNLABELLED: We assessed the effects of halogenated anesthetics on Pseudomonas aeruginosa growth in a liquid nutrient broth. Sterile Petri dishes (3.5-cm diameter) were filled with a 1-mL suspension of a Pseudomonas aeruginosa strain and incubated at 37 degrees C. Exposure of bacterial plates to halothane, isoflurane, and enflurane administered at 1 and 2 minimum alveolar anesthetic concentration (MAC) were studied for different exposure times (1, 2, 3, and 4 h) using an airtight chamber. For each time, a control point was obtained. Serial dilutions and agar plates were made, and developed colonies were counted. A significant decrease in bacterial growth was observed from the second hour of exposure to every halogenated anesthetic. For long periods of exposure (3 and 4 h), bacterial growth was significantly reduced in the plates exposed to 2 MAC compared with 1 MAC. The maximal inhibition was observed after a 4-h exposure at 2 MAC and reached 60%, 49%, and 42% for halothane, isoflurane, and enflurane, respectively. We conclude that a decrease in Pseudomonas aeruginosa growth is observed after exposure to halogenated anesthetics, but whether this inhibition is clinically important remains to be demonstrated. IMPLICATIONS: Bacterial pneumonia is a major source of morbidity after general anesthesia. We measured the effects of volatile anesthetics on the growth of Pseudomonas aeruginosa, one of the pathogens most often isolated in hospital-acquired pneumonia. The experiments were performed in vitro in culture conditions reproducing those observed in the alveolar space. Volatile anesthetics inhibited the growth of these bacteria, but the clinical significance of this fact remains to be determined.

Anesthetics, Inhalation↗

PubMed1999

Evaluating T-wave amplitude as a guide for detecting intravascular injection of a test dose in anesthetized children.

UNLABELLED: Previous reports have suggested that accidental intravascular injection of an epinephrine-containing test dose increases T-wave amplitude in anesthetized children. We designed this study to prospectively determine whether changes in T-wave amplitude could be a reliable indicator for detecting intravascular injection. We studied 32 ASA physical status I infants and children (3.4 +/- 1.7 yr) undergoing elective minor surgeries during 1.0 minimum alveolar anesthetic concentration of sevoflurane and 67% nitrous oxide in oxygen. After the i.v. administration of atropine 0.01 mg/kg, the patients were randomly assigned to receive either saline (n = 16) or a test dose consisting of 1% lidocaine (0.1 mL/kg) with 1:200,000 epinephrine (0.5 microg/kg, n = 16) via a peripheral vein to simulate the intravascular injection of the test dose. Heart rate (HR) and systolic blood pressure (SBP) were recorded every 20 and 30 s, respectively, and the T-wave amplitude of lead II was continuously recorded for subsequent analysis. Of the 16 children receiving the test dose, 16, 13, and 16 developed increases in HR, SBP, and T-wave amplitude > or = 10 bpm, > or = 15 mm Hg, and > or = 25%, occurring at 30 +/- 7, 70 +/- 31, and 20 +/- 5 s, respectively. Because no patient receiving saline met these criteria, sensitivity, specificity, and positive and negative predictive values were all 100% based on the criteria using the T-wave amplitude and the peak HR. Our results suggest that changes in T-wave amplitude are as effective as HR for detecting the intravascular injection of an epinephrine-containing test dose in sevoflurane-anesthetized children. IMPLICATIONS: To determine whether an epidurally administered local anesthetic is unintentionally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that increases in T-wave amplitude by > or = 25% in lead II monitor electrocardiography are as effective as a heart rate increase > or = 10 bpm for detecting intravascular injection in sevoflurane-anesthetized children.

Anesthetics, Inhalation↗

PubMed1999

Prolongation of nerve and epidural anesthetic blockade by bupivacaine in a lipid emulsion.

UNLABELLED: We assessed the effect of a lipid emulsion of bupivacaine on prolonging peripheral nerve and epidural anesthetic blockade in the rat. The intensity and duration of motor and sensory blockade produced by a single injection of aqueous solution (BPV-as) and lipid emulsion (BPV-em) preparations of 0.5% bupivacaine were evaluated by electrophysiological methods. Both preparations induced complete, reversible motor and sensory blockade after injection. The latency time to the maximal blockade and the duration of anesthetic blockade were more prolonged for BPV-em than for BPV-as. The increase in duration of maximal blockade was 1.4 times for nerve and 1.3 times for epidural anesthesia. Histological evaluation of spinal roots and spinal cord sections did not show any abnormalities or differences between animals injected with BPV-as and those injected with BPV-em. Pharmacokinetic studies showed lower plasma peak concentration and a longer elimination half-life for BPV-em than for BPV-as. Thus, BPV-em prolongs the effects of local anesthetics, allows a similar degree of blockade, and reduces the systems toxic effects of anesthetics compared with BPV-as. IMPLICATIONS: We assessed a lipid emulsion containing bupivacaine for peripheral nerve and epidural anesthetic blockade in the rat. The emulsion allowed a complete blockade, while increasing the duration of the anesthetic effect (by 30%-40%), compared with the standard bupivacaine aqueous solution.

Anesthesia, Epidural↗

PubMed2000

Patch-clamp analysis of anesthetic interactions with recombinant SK2 subtype neuronal calcium-activated potassium channels.

UNLABELLED: Small conductance calcium-activated potassium channels (SK) mediate spike frequency adaptation and underlie the slow afterhyperpolarization in central neurons. We tested the actions of several anesthetics on the SK2 subtype of recombinant SK channels, cloned from rat brain and functionally expressed in a mammalian cell line. Butanol, ethanol, ketamine, lidocaine, and methohexital blocked recombinant SK2 channel currents, measured in the whole-cell patch clamp recording mode. The block was reversible, dose-dependent, and of variable efficacy. The inhaled anesthetics chloroform, desflurane, enflurane, halothane, isoflurane, and sevoflurane produced little or no block when applied at 1 minimum alveolar anesthetic concentration; varying degrees of modulation were observed at very large concentrations (10 minimum alveolar concentration). The extent of block by inhaled anesthetics did not appear to depend on concentration or membrane voltage. IMPLICATIONS: We describe differential effects of anesthetics on cloned small conductance calcium-activated potassium channels from brain that may play a role in generating the effects or side effects of anesthetics.

Anesthetics↗

PubMed2000

Evaluating hemodynamic and T wave criteria of simulated intravascular test doses using bupivacaine or isoproterenol in anesthetized children.

UNLABELLED: An increase in T wave amplitude > or =25% is a reliable indicator for detecting intravascular injection of lidocaine-epinephrine test dose in anesthetized children. We examined whether a simulated IV test dose containing bupivacaine instead of lidocaine, and isoproterenol instead of epinephrine, produces reliable changes in heart rate (HR) and T wave morphology. One hundred healthy infants and children (6-72 mo) were randomized to one of five groups (n = 20 each) during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen: atropine pretreatment (0.01 mg/kg IV) followed by 0.25% bupivacaine containing epinephrine 0.5 microg/kg IV, atropine followed by normal saline, atropine followed by 1% lidocaine containing isoproterenol 0.1 microg/kg, saline pretreatment followed by the lidocaine-isoproterenol test dose, and saline followed by saline. HR was recorded every 20 s and T wave amplitude of lead II was continuously recorded. All patients receiving the bupivacaine-epinephrine test dose and none receiving saline met the HR (positive if > or =10 bpm increase) and T wave criteria (positive if > or =25% increase in amplitude). The isoproterenol-containing test dose produced positive responses based only on the HR criterion with or without atropine pretreatment. Our results indicate that HR and T wave changes are useful if a bupivacaine-epinephrine test dose is used and that HR is the only useful indicator if an isoproterenol-containing test dose is used in sevoflurane-anesthetized children. IMPLICATIONS: To determine if an epidurally administered local anesthetic has been unintentionally injected into a blood vessel, a small dose of epinephrine or isoproterenol may be added to a local anesthetic. We found that an increase in heart rate > or =10 bpm and an increase in T wave amplitude of lead II >or =25% are useful indicators for detecting accidental intravascular injection of an epinephrine-containing test dose in sevoflurane-anesthetized children, whereas only a heart rate change is a reliable diagnostic tool if an isoproterenol-containing test dose is used.

Adrenergic beta-Agonists↗

PubMed2000

The anesthetic and recovery profile of two doses (60 and 80 mg) of plain mepivacaine for ambulatory spinal anesthesia.

UNLABELLED: Reports of transient neurological symptoms with the use of subarachnoid lidocaine has generated interest in alternate local anesthetics of intermediate duration, such as mepivacaine. This prospective randomized, double-blinded, dose-response study examined the anesthetic and recovery profiles of 60- and 80-mg doses of preservative-free plain mepivacaine for ambulatory spinal anesthesia. Sixty patients undergoing ambulatory anterior cruciate ligament repair of the knee under spinal anesthesia were randomized into two groups; Group 1 (29 patients) received 4 mL of 1.5% (60-mg dose) and Group 2 (31 patients) received 4 mL of 2% (80-mg dose) of plain mepivacaine. All patients received a combined spinal-epidural anesthetic technique. The epidural catheter was used only in the event the surgery outlasted the duration of surgical anesthesia with subarachnoid mepivacaine. Epidural supplementation was administered in three patients (12%) in Group 1 and one patient (3%) in Group 2 when the sensory block regressed to L-1 with surgery expected to last longer than 15 min. The cephalad dermatome level of the block and degree of motor block was comparable in the two groups. Times to two-segment and T-10 regression were comparable in the two groups (112 +/- 26 min in Group 1 versus 122 +/- 28 min in Group 2). Time to L-1 regression was significantly longer in Group 2 (146 +/- 28 min in Group 1 versus 159 +/- 19 min in Group 2). All of the ambulatory milestones were significantly faster in Group 1. Side effects, such as hypotension and emesis were negligible, severe bradycardia and urinary retention did not occur, and none of the patients in the two groups reported transient neurological symptoms over 24 h. In conclusion, plain mepivacaine in a 60- or 80-mg dose is a suitable local anesthetic choice for ambulatory spinal anesthesia with respect to anesthetic, as well as recovery profiles. IMPLICATIONS: We evaluated the anesthetic and recovery profiles of 60- and 80-mg doses of plain mepivacaine for ambulatory spinal anesthesia. Both doses produced comparable sensory and motor block. Sensory and motor regression and ambulatory milestones were 20-30 min longer with the 80-mg dose. Side effects were negligible and transient neurological symptoms were not reported during a 24-h follow-up.

Adolescent↗

PubMed2000

The anesthetic potencies of alkanethiols for rats: relevance to theories of narcosis.

UNLABELLED: Meyer and Overton suggested that anesthetic potency correlates inversely with lipophilicity. Thus, MAC times the olive oil/gas partition coefficient equals an approximately constant value of 1.82 +/- 0.56 atm (mean +/- SD). MAC is the minimum alveolar concentration of anesthetic required to eliminate movement in response to a noxious stimulus in 50% of subjects. Although MAC times the olive oil/gas partition coefficient also equals an approximately constant value for normal alkanols from methanol through octanol, the value (0.156 +/- 0.072 atm) is 1/10th that found for conventional anesthetics. We hypothesized that substitution of sulfur for the oxygen in n-alkanols would decrease their saline/gas partition coefficients (i.e., decrease polarity) while sustaining lipid/gas partition coefficients. Further, we hypothesized that these changes would produce products of MAC times olive oil partition coefficients that approximate those of conventional anesthetics. To test these predictions, we measured MAC in rats, and saline and olive oil solubilities for the series H(CH(2))(n)SH, comparing the results with the series H(CH(2))(n)OH for compounds having three to six carbon atoms. As hypothesized, the alkanethiols had similar oil/gas partition coefficients, 1000-fold smaller saline gas partition coefficients, and MAC values 30 times greater than for comparable alkanols. Such findings are consistent with the notion that the greater potency of many alkanols (greater than would be predicted from conventional inhaled anesthetics and the Meyer-Overton hypothesis) results from their greater polarity. IMPLICATIONS: The in vivo anesthetic potency of alkanols and alkanethiols correlates with their lipophilicity and hydrophilicity.

Alcohols↗

PubMed2001

Local anesthetic actions on thromboxane-induced platelet aggregation.

UNLABELLED: Some local anesthetics (LA), in concentrations present in blood during IV or epidural infusion, inhibit thrombus formation in the postoperative period. Studies on thromboxane A2 (TXA2) signaling in a recombinant model suggest that interference with TXA2-induced platelet aggregation may explain, in part, the antithrombotic actions of epidural analgesia and IV LA infusion. In this study we investigated the effects of clinically used LAs (lidocaine, ropivacaine, and bupivacaine) on TXA2-induced early platelet aggregation (1-5 s) by using quenched-flow and optical aggregometry. Our findings demonstrate that the LAs tested seem to have only a limited ability to inhibit TXA2-induced platelet aggregation assessed at early times (1-5 s). Therefore, the clinical effects of LAs on thrombi formation are unlikely to be explained by this manner alone. At large LA concentrations, moderate effects were obtained. Prolonged incubation with LA did not significantly increase effectiveness, and the lack of an effect could not be explained by generation of secondary mediators. The results were independent of the anesthetic studied. Local anesthetic effects on TXA2-induced early platelet aggregation (1-5 s) are unlikely to play a major role in the clinically observed antithrombotic effects of local anesthetics. IMPLICATIONS: Local anesthetic effects on thromboxane A2-induced early platelet aggregation (1-5 s) are unlikely to play a major role in the clinically observed antithrombotic effects of local anesthetics. Thus, other potential targets need to be explored.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2002

The anesthetic mechanism of urethane: the effects on neurotransmitter-gated ion channels.

UNLABELLED: Urethane is widely used as an anesthetic for animal studies because of its minimal effects on cardiovascular and respiratory systems and maintenance of spinal reflexes. Despite its usefulness in animal research, there are no reports concerning its molecular actions. We designed this study to determine whether urethane affects neurotransmitter-gated ion channels. We examined the effects of urethane on recombinant gamma-aminobutyric acid(A), glycine, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, and neuronal nicotinic acetylcholine receptors expressed in Xenopus oocytes. Urethane potentiated the functions of neuronal nicotinic acetylcholine, gamma-aminobutyric acid(A), and glycine receptors, and it inhibited N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors in a concentration-dependent manner. At concentrations close to anesthetic 50% effective concentration, urethane had modest effects on all channels tested, suggesting the lack of a single predominant target for its action. This may account for its usefulness as a veterinary anesthetic. However, a large concentration of urethane exerts marked effects on all channels. These findings not only give insight into the molecular mechanism of anesthetics but also caution that neurophysiologic measurements from animals anesthetized with urethane may be complicated by the effects of urethane on multiple neurotransmitter systems. Our results also suggest that small changes in multiple receptor systems can produce anesthesia. IMPLICATIONS: Urethane modestly affects multiple neurotransmitter systems at an anesthetic concentration. Our findings suggest that these degenerate effects of urethane can produce anesthesia and that urethane has a potential to influence neuronal measurements made in in vivo preparations.

Anesthetics, Intravenous↗

PubMed2002

The neurotoxicity of local anesthetics on growing neurons: a comparative study of lidocaine, bupivacaine, mepivacaine, and ropivacaine.

UNLABELLED: Local anesthetics can be neurotoxic. To test the hypothesis that exposure to local anesthetics produces morphological changes in growing neurons and to compare this neurotoxic potential between different local anesthetics, we performed in vitro cell biological experiments with isolated dorsal root ganglion neurons from chick embryos. The effects of lidocaine, bupivacaine, mepivacaine, and ropivacaine were examined microscopically and quantitatively assessed using the growth cone collapse assay. We observed that all local anesthetics produced growth cone collapse and neurite degeneration. However, they showed significant differences in the dose response. The IC(50) values were approximately, 10(-2.8) M for lidocaine, 10(-2.6) M for bupivacaine, 10(-1.6) M for mepivacaine, and 10(-2.5) M for ropivacaine at 15 min exposure. Some reversibility was observed after replacement of the media. At 20 h after washout, bupivacaine and ropivacaine showed insignificant percentage growth cone collapse in comparison to their control values whereas those for lidocaine and mepivacaine were significantly higher than the control values. Larger concentrations of the nerve growth factor (NGF) did not improve this reversibility. In conclusion, local anesthetics produced morphological changes in growing neurons with significantly different IC(50). The reversibility of these changes differed among the four drugs and was not influenced by the NGF concentration. IMPLICATIONS: Local anesthetics induce growth cone collapse and neurite degeneration in the growing neurons. Mepivacaine was safer than lidocaine, bupivacaine, and ropivacaine for the primary cultured chick neurons.

Amides↗

PubMed2002

A second-generation blood substitute (perflubron emulsion) increases the blood solubility of modern volatile anesthetics in vitro.

UNLABELLED: Perfluorocarbon-based emulsions increase the blood solubility of isoflurane, enflurane, and halothane, with a maximal effect reported for the less soluble isoflurane. Current volatile anesthetics are less soluble and may be more affected by this phenomenon. Perflubron (Oxygent(TM)) is a perfluorocarbon-based emulsion in late-stage clinical testing in surgical patients for use as a temporary oxygen carrier. We tested the hypothesis that perflubron increases the solubility of isoflurane, sevoflurane, and desflurane, as reflected by their blood/gas partition coefficient (lambda(Bl:g)). Fresh whole-blood samples were drawn from eight volunteers and mixed with perflubron to obtain concentrations of 1.2%, 1.8%, and 3.6% by volume (equivalent to in vivo doses of 1.8 to 5.4 g/kg, which represent up to twice the intended clinical dose range). By using the double-extraction method, we demonstrated increased lambda(Bl:g) for isoflurane, sevoflurane, and desflurane. However, the solubility in blood does not really change, because volatile anesthetics are actually partitioning into perflubron. Increasing the amount of emulsion in the blood consequently increases the amount of gas carried, as reflected by the measured linear correlation between the lambda(Bl:g) values of all three volatile anesthetics and perflubron doses. Even though the increase ranges from 0.9 (desflurane) to 2.6 (sevoflurane) times the normal value, the apparent lack of clinical implications in current trials with perflubron may trigger further in vivo experiments. IMPLICATIONS: Perflubron increases the in vitro solubility of volatile anesthetics when present in the blood at clinically relevant concentrations. Volatile anesthetics actually partition into the emulsion, but the solubility in the blood does not change. Further studies are needed to assess whether perflubron will affect the pharmacokinetics of volatile anesthetics in vivo.

Algorithms↗

PubMed2003

Volatile anesthetics reduce agonist affinity at nicotinic acetylcholine receptors in the brain.

UNLABELLED: In previous studies we and others have demonstrated that the activation of nicotinic acetylcholine receptors (nAChRs) is inhibited by subanesthetic concentrations of volatile anesthetics. The mechanism by which activation is inhibited is unknown. Studies of the evolutionarily related nAChRs from the electric fish Torpedo have suggested that volatile anesthetics alter the affinity of the agonist for the receptor. We studied the effect of two volatile anesthetics, isoflurane and sevoflurane, on equilibrium binding of the high-affinity nicotinic agonist epibatidine to nicotinic receptors from mouse brain. We studied binding to male and female brain separately, because sex differences in nicotine responses have been reported. Male and female brains have equal epibatidine binding without anesthetic. Isoflurane and sevoflurane reduce the binding of [(3)H]epibatidine to male and female nicotinic receptors, but only at concentrations at and above those required for anesthesia. The 50% inhibitory concentration for isoflurane inhibition of [(3)H]epibatidine binding to male brain was 0.58 +/- 0.07 mM and to female brain was 1.62 +/- 0.30 mM. The 50% inhibitory concentration for sevoflurane inhibition of [(3)H]epibatidine binding to male brain was 0.77 +/- 0.05 mM and to female brain was 0.77 +/- 0.04 mM. There was no statistically significant difference in the effect of either drug between sexes (P > 0.05). Although there is a slight decrease in agonist affinity at anesthetic concentrations, the marked reductions in nAChR function at subanesthetic concentrations cannot be attributed to changes in agonist affinity. IMPLICATIONS: Volatile anesthetics reduce the activation of nicotinic acetylcholine receptors by an unknown mechanism. We have demonstrated that although isoflurane and sevoflurane inhibit agonist affinity, the concentrations required are too large to be responsible for the dynamic changes observed.

Acetylcholine↗

PubMed1975

Local effects of anesthetics on regional hypoxic pulmonary vasoconstriction.

The hypothesis that halogenated anesthetics and N2O locally inhibit hypoxic pulmonary vasoconstriction (HPV) was tested. Selective ventilation of the left lower lobe of the lung with N2 in dogs anesthetized with pentobarbital caused blood flow to the lobe to decrease 55.5 +/- 2.0 per cent and lobar vascular resistance to increase 148 +/- 8 per cent. Responses to hypoxia were remeasured during administration of various MAC multiples of inhalation anesthetics to the left lower lobe and following systemic administration of intravenous anesthetics. Isoflurane and fluorexene progressively inhibited and finally almost extinguished the vasoconstriction response as anesthetic concentration increased to 3 MAC. N2O moderately diminished HPV. Halothane had little, and intravenous anesthetics had no, significant effect on HPV. It is concluded that N2O, isoflurane, and fluroxene locally inhibit regional HPV and via this mechanism may increase total venous admixture.

Anesthesia, Inhalation↗

PubMed1975

Hypocapnic bronchoconstriction and inhalation anesthetics.

The effects of halothane, enflurane, and methoxyflurane on hypocapnic bronchoconstriction (increased airway resistance and decreased compliance of the lung) were studied in vivo in the isolated left lower lobe of the canine lung. Hypocapnic bronchoconstriction, induced by altering the concentration of CO2 in gas ventilating the lobe, was repeated in the presence and absence of various concentrations of anesthetic gases (halothane: 0.5, 1.0, and 3.0 per cent; enflurane: 1.0, 3.0, and 5.0 per cent; methoxyflurane: 0.25, 0.50, and 1.0 per cent). In the higher concentrations, all three drugs blocked the bronchoconstrictor effect produced when the inspired CO2 was decreased from 5 to 0 per cent. In lower concentrations, halothane was the most effective blocking drug. Propranolol did not affect the ability of the three anesthetics to block hypocapnic bronchoconstriction, nor did the beta-receptor blocking drug sotalol affect the blocking effects of halothane. The ability of these anesthetics to block hypocapnic bronchoconstriction probably is mediated not through an adrenergic mechanism but by one that is nonspecific. (Key words: Lung, bronchoconstriction; Carbon dioxide, hypocarbia; Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Anesthetics, volatile, methoxyflurane.)

Adrenergic beta-Antagonists↗

PubMed1979

Decrease in dose requirement of d-tubocurarine by volatile anesthetics.

Volatile anesthetics are known to decrease the requirements for neuromuscular blocking agents. To obtain a quantitative measure of the extent of this drug interaction, studies were performed on isolated guinea pig nerve--lumbrical muscle preparations exposed to methoxyflurane, halothane, isoflurane, diethyl ether, fluroxene, and enflurane in concentrations equal to MAC. From the relationship between indirect twitch height and d-tubocurarine concentration, the concentration depressing the twitch height by 50 per cent was determined. In the presence of MAC levels of anesthetic, the ED50 was decreased by the following fractional amounts: methoxyflurane, 0.311; halothane, 0.334; isoflurane, 0.335; diethyl ether, 0.462; fluroxene, 0.580; enflurane, 0.697. Comparison of the fractional decrease of d-tubocurarine dose requirement by an anesthetic at MAC and previously obtained values for the fractional depression of end-plate depolarization by an anesthetic at MAC showed that the more the anesthetic depresses depolarization, the smaller the d-tubocurarine dose requirement. Thus, clinically observed decreases in dose requirements may be explained by the effects of the anesthetics on chemosensitivity of the end-plate region.

Anesthetics↗

PubMed1983

Effects of halogenated hydrocarbon anesthetics on responses to ligation of a coronary artery in chronically prepared rats.

Responses to ligation of the left anterior descending coronary artery (blood pressure, heart rate, ECG, arrhythmias, myocardial tissue loss, and mortality) were investigated in chronically prepared rats anesthetized with one of various halogenated hydrocarbon anesthetics. Halothane (inhaled concentrations of 0, 0.25, 0.5, 1.0, and 2.0%) reduced arrhythmias, mortality, and "S-T" segment changes in the ECG in a dose-related manner. The most effective antiarrhythmic concentrations were 0.5 and 1.0%. Other halogenated hydrocarbon anesthetics (chloroform, enflurane, isoflurane, methoxyflurane, and trichlorethylene) were investigated at minimal anesthetic concentrations. Of these, only chloroform and enflurane reduced arrhythmias. However, both increased mortality as a result of nonarrhythmic causes. At one-half anesthetic concentrations, chloroform (0.25%) and enflurane (0.75%) were not antiarrhythmic and mortality resulting from nonarrhythmic causes was not increased. In the chronically prepared rat, halothane at anesthetic and subanesthetic concentrations has antiarrhythmic actions against ligation-induced arrhythmias, reducing mortality. Of the other halogenated hydrocarbons tested, only enflurane and chloroform had antiarrhythmic actions, however, mortality was high with both agents because of accompanying cardiovascular depression.

Anesthesia↗

PubMed1983

Selective actions of intravenous anesthetics on nicotinic- and muscarinic-receptor-mediated responses of the dog adrenal medulla.

The selective actions of intravenous anesthetics on the cholinergic nicotinic and muscarinic responses of adrenal medullary cells were studied using isolated dog adrenals perfused with modified Locke's solution. Log-probit dose-response curves of the inhibitory effects of the anesthetics on the catecholamine releases induced by acetylcholine, nicotine, and muscarine were determined. Percentage inhibition by the anesthetics at clinically relevant concentrations were 98% of nicotine- and 31% of muscarine-induced releases by alphaxalone 2.6 microM, 76% of nicotine and 13% of muscarine by thiopental 23.9 microM, 86% of nicotine and no inhibition of muscarine by ketamine 17.0 microM, and no inhibition of either response by diazepam 5.0 microM. The ratio of IC50 (concentration for 50% inhibition), which was calculated by dividing IC50 for muscarine by IC50 for nicotine, showed a variety of values ranging from 3.9 for diazepam to 38.0 for ketamine. The results suggest that each anesthetic has characteristic selective inhibitory effects on nicotinic and muscarinic cholinergic responses. The differing effects on the muscarinic responses might be one of the factors contributing to the characteristic properties of each anesthetic, whereas the inhibition of nicotinic responses might reflect a common property for many anesthetics.

Adrenal Medulla↗