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R B Weiskopf

Publications and source records attributed to R B Weiskopf.

At least 73 records · Page 4Linked to original sources
PubMed1991

Hemodynamic effects of desflurane/nitrous oxide anesthesia in volunteers.

We determined the cardiovascular effects of 0.91, 1.34, and 1.74 MAC of desflurane/nitrous oxide anesthesia (60% inspired nitrous oxide contributed 0.5 MAC at each level) in 12 healthy, normocapnic male volunteers. Desflurane/nitrous oxide anesthesia decreased systemic blood pressures, cardiac index, stroke volume index, systemic vascular resistance, and left ventricular stroke work index, and increased pulmonary arterial pressures and central venous pressure in a dose-dependent fashion, while heart rate was 10%-12% and mixed venous oxygen tension was 2-4 mm Hg higher at all MAC levels than at baseline (awake). Desflurane/nitrous oxide anesthesia modestly increased left ventricular end-diastolic cross-sectional area (preload) and decreased velocity of left ventricular circumferential fiber shortening, systolic wall stress (afterload), and area ejection fraction; this combination of changes indicates myocardial depression. At approximately comparable MAC levels, heart rate was lower and systemic blood pressures, central venous pressure, left ventricular stroke work index, and systemic vascular resistance usually were significantly higher during anesthesia with desflurane and nitrous oxide than during desflurane anesthesia alone (same volunteers, data collected in crossover design). After 7 h of anesthesia, regardless of the background gas, somewhat less cardiovascular depression and/or modest stimulation was apparent: cardiac index, area ejection fraction, and velocity of left ventricular circumferential fiber shortening recovered to or toward awake values, whereas heart rate was further increased. Evidence of circulatory insufficiency did not develop in any volunteers during the study. Segmental left ventricular function was normal at baseline, and no segmental wall-motion abnormalities, ST-segment change, or dysrhythmias developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1991

Does desflurane modify circulatory responses to stimulation in humans?

We asked if desflurane with or without nitrous oxide at 0.83, 1.24, and 1.66 MAC prevented cardiovascular responses to stimulation. We measured cardiac output, heart rate, systemic arterial blood pressure, central venous pressure, pulmonary arterial blood pressure, and systemic vascular resistance in six healthy male volunteers before (control) and at 0, 1, 2, 4, and 6 min after tetanic electrical stimulation (50, 100, and 200 Hz) of the ulnar nerve. At 0.83 and 1.24 MAC, cardiac output, mean systemic arterial blood pressure, heart rate, and pulmonary arterial blood pressure increased. Peak changes averaged 13%-20% and most frequently occurred 0-2 min after stimulation (P less than 0.05) with return to control values at 4-6 min (except for pulmonary arterial blood pressure). At 1.66 MAC, heart rate and systemic blood pressure responses were attenuated, but this level of anesthesia had equivocal effects on the cardiac output and pulmonary blood pressure responses. The addition of nitrous oxide attenuated the peak response of heart rate and cardiac output but not the peak response of mean systemic arterial blood pressure. In summary, 0.83 and 1.24 MAC desflurane did not abolish cardiovascular responses to stimulation, but 1.66 MAC attenuated the responses.

Administration, Inhalation↗
PubMed1991

Fluoride metabolites after prolonged exposure of volunteers and patients to desflurane.

We examined the metabolism of desflurane in 13 healthy volunteers given 7.35 +/- 0.81 MAC-hours (mean +/- SD) of desflurane and 26 surgical patients given 3.08 +/- 1.84 MAC-hours (mean +/- SD). Markers of desflurane metabolism included fluoride ion measured via an ion-specific electrode, nonvolatile organic fluoride measured after sodium fusion of urine samples, and trifluoroacetic acid determined by a gas chromatographic-mass spectrometric method. In both volunteer and patient groups, postanesthesia serum fluoride ion concentrations did not differ from background fluoride ion concentrations. Similarly, postanesthesia urinary excretion of fluoride ion and organic fluoride in volunteers was comparable to preanesthesia excretion rates. However, small but significant levels of trifluoroacetic acid were found in both serum and urine from volunteers after exposure to desflurane. A peak serum concentration of 0.38 +/- 0.17 mumol/L of trifluoroacetic acid and a peak urinary excretion rate of 0.169 +/- 0.107 mumol/h were detected in volunteers at 24 h after desflurane exposure. Although these increases in trifluoroacetic acid after exposure to desflurane were statistically significant, they are approximately 10-fold less than levels seen after exposure to isoflurane. Thus, desflurane strongly resists biodegradation, but a small amount is metabolized in humans.

Administration, Inhalation↗
PubMed1991

Cardiovascular actions of desflurane in normocarbic volunteers.

The cardiovascular actions of three concentrations of desflurane (formerly I-653), a new inhalation anesthetic, were examined in 12 unmedicated normocapnic, normothermic male volunteers. We compared the effects of 0.83, 1.24, and 1.66 MAC desflurane with measurements obtained while the same men were conscious. Desflurane caused a dose-dependent increase in right-heart filling pressure and a decrease in systemic vascular resistance and mean systemic arterial blood pressure. As measured by echocardiography, left ventricular end-diastolic area did not change except for a small increase at 1.66 MAC desflurane, and systolic wall stress was less at all concentrations of desflurane than during the conscious state. Desflurane did not change cardiac index or left ventricular ejection fraction. Heart rate did not change at 0.83 MAC, but progressively increased with deeper desflurane anesthesia. Stroke volume index was less at all concentrations of desflurane than while the men were conscious, but desflurane did not alter the velocity of ventricular circumferential fiber shortening. Mixed venous blood PO2 and oxyhemoglobin saturation were higher during all concentrations of desflurane anesthesia than during the conscious state. No volunteer developed a metabolic acidosis. We conclude that desflurane with controlled ventilation and constant PaCO2 causes cardiovascular depression, as indicated by the increased cardiac filling pressure and decreased stroke volume index and by no change in the velocity of circumferential fiber shortening in the presence of decreased systolic wall stress. However, cardiac output is well maintained, and heart rate does not increase at light levels of anesthesia. The cardiovascular actions of 0.83 and 1.66 MAC desflurane were also reexamined in 6 of the 12 men during the seventh hour of anesthesia. Prolonged desflurane anesthesia resulted in lesser cardiovascular depression than was evidenced during the first 90 min. The measures of cardiac filling (central venous pressure and left ventricular end-diastolic cross-sectional area) did not differ between the early and late periods of anesthesia. Systemic vascular resistance decreased further during the late period, but systolic wall stress did not differ between the two time periods. During the seventh hour of desflurane anesthesia, heart rate and cardiac index were higher at both anesthetic concentrations than during the first 90 min of anesthesia. Left ventricular ejection fraction and velocity of fiber shortening did not change with duration of desflurane anesthesia. Oxygen consumption, oxygen transport, the ratio of the two, mixed venous PO2, and mixed venous oxyhemoglobin saturation (SO2) increased late in the anesthetic in comparison with the first 90 min.

Adult↗
PubMed1991

Cardiovascular actions of desflurane with and without nitrous oxide during spontaneous ventilation in humans.

We investigated the cardiovascular actions of desflurane (formerly I-653) during spontaneous ventilation. We gave 0.8-0.9, 1.2-1.3, and 1.6-1.7 MAC desflurane in oxygen (n = 6) and in 60% nitrous oxide, balance oxygen (n = 6) to unmedicated healthy male volunteers. Both anesthetic regimens decreased ventilation, increased partial pressure of arterial carbon dioxide, and produced similar cardiovascular changes. In comparison with values obtained when the volunteers were conscious, desflurane anesthesia with spontaneous ventilation decreased systemic vascular resistance and mean arterial blood pressure. Cardiac index, heart rate, stroke volume index, and central venous blood pressure increased. Left ventricular ejection fraction increased at 0.83 MAC desflurane in oxygen, and otherwise did not differ from the conscious value. The velocity of ventricular circumferential fiber shortening, estimated by echocardiography, increased with desflurane in oxygen but did not change with desflurane in nitrous oxide. Oxygen consumption increased during desflurane and oxygen anesthesia, but not when nitrous oxide plus oxygen was the background gas. Desflurane increased oxygen transport, the ratio of oxygen transport to oxygen consumption, mixed venous partial pressure of oxygen, and oxyhemoglobin saturation. The cardiovascular changes with desflurane during spontaneous ventilation differ from those during controlled ventilation. With both background gases, spontaneous ventilation, in comparison with controlled ventilation, increased cardiac index, stroke volume, central venous pressure, left ventricular ejection fraction, velocity of circumferential fiber shortening, oxygen transport, and the ratio of oxygen transport to oxygen consumption but did not change mean arterial blood pressure except at 1.66 MAC desflurane in oxygen (when it was higher with spontaneous than with controlled ventilation).

Administration, Inhalation↗
PubMed1991

[Solubility of desflurane (I-653), sevoflurane, isoflurane, and halothane in human blood].

The blood/gas partition coefficients for the new volatile anesthetic agent desflurane (I-653), sevoflurane, isoflurane, and halothane were determined, simultaneously, in 8 human volunteers to compare the solubilities of these agents in blood. The blood/gas partition coefficient for desflurane [0.49 +/- 0.03 (mean +/- SD)] was smallest, followed by sevoflurane (0.62 +/- 0.04), isoflurane (1.27 +/- 0.06), and halothane (2.46 +/- 0.09). Differences among the anesthetic agents were significant (P less than 0.001). The results of this study confirm that among these agents the solubility of desflurane in human blood is the smallest. The results suggest that the washin and washout of desflurane will be more rapid than that of sevoflurane, isoflurane, and halothane, and the washin and washout of sevoflurane will be more rapid than that of isoflurane and halothane.

Adult↗
PubMed1990

Cardiovascular actions of common anesthetic adjuvants during desflurane (I-653) and isoflurane anesthesia in swine.

To determine the cardiovascular actions of drugs commonly combined with inhalation anesthetics, we administered one drug from each of several classes of adjuvants to seven swine already anesthetized with equipotent concentrations (1.2 MAC) of desflurane, formerly I-653, a new inhaled anesthetic, or isoflurane. Succinylcholine (1 and 2 mg/kg), atracurium (0.6 mg/kg), and atropine (5 micrograms/kg) plus edrophonium (5 mg/kg) had no cardiovascular effects. Fentanyl was given in amounts that decreased MAC for the inhaled anesthetics by 25%-35%. A dose of 50 micrograms/kg IV had no cardiovascular effects during either anesthetic, whereas 100 micrograms/kg IV modestly increased systemic vascular resistance without changing other variables. Naloxone (100 micrograms/kg IV) during infusion of fentanyl decreased systemic vascular resistance and increased cardiac output during both desflurane and isoflurane anesthesia, increased heart rate during only isoflurane anesthesia, and did not affect mean arterial blood pressure during either anesthetic. Thiopental (2.5 and 5.0 mg/kg IV) decreased mean aortic blood pressure, cardiac output, stroke volume, and systemic vascular resistance during both anesthetics without altering heart rate or left- or right-sided cardiac filling pressures. The addition of 60% nitrous oxide caused no cardiovascular changes during desflurane anesthesia, but increased systemic vascular resistance and decreased cardiac output and stroke volume during isoflurane without altering heart rate or cardiac preload. We conclude that the usual clinical doses of adjuvants commonly administered during anesthesia have no untoward cardiovascular actions during 1.2 MAC desflurane or isoflurane anesthesia in swine.

Adjuvants, Anesthesia↗
PubMed1990

Hepatocellular integrity in swine after prolonged desflurane (I-653) and isoflurane anesthesia: evaluation of plasma alanine aminotransferase activity.

Desflurane, formerly known as I-653 (CF2H-O-CFH-CF3), is a new inhalation anesthetic derived by fluorine substitution for the alpha-ethyl chlorine of isoflurane (CF2H-O-CClH-CF3). The lower solubility and increased stability of desflurane provided by the C-F bond lessen biotransformation to potentially hepatotoxic metabolites. Repeated administration of desflurane to rats, with or without induced hepatic enzymes, does not result in evidence of hepatic injury. In the recent study we extended the tests for liver cell injury to another species, the pig. Our test included prolonged exposure to desflurane or isoflurane, both in the absence and presence of commonly used adjuvants. We measured plasma alanine aminotransferase activity in eight young female swine anesthetized in random order with desflurane (0.8-1.6 MAC) and isoflurane (0.7-1.4 MAC), for a total dose of about 5.5 MAC-hours of each anesthetic, 3-8 days apart. Plasma alanine aminotransferase activities remained in the normal range, and were not significantly greater over baseline values in samples drawn immediately after, 4 h after, or 3-8 days after (mean +/- SD, 6.1 +/- 2.1) the administration of either anesthetic was discontinued after the first study with either desflurane or isoflurane. Five additional pigs were given a mean total dose of 9.7 MAC-hours of desflurane or isoflurane in conjunction with succinylcholine, N2O, fentanyl, naloxone, atracurium, thiopental, edrophonium, and atropine. No changes in plasma alanine aminotransferase activity were detected in blood samples drawn at termination of the anesthesia, 24 h later, and 4-7 days later (mean +/- SD, 5.8 +/- 1.3).(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1990

Pharmacokinetics of desflurane, sevoflurane, isoflurane, and halothane in pigs.

We tested the prediction that the alveolar washin and washout, tissue time constants, and pulmonary recovery (volume of agent recovered during washout relative to the volume taken up during washin) of desflurane, sevoflurane, isoflurane, and halothane would be defined primarily by their respective solubilities in blood, by their solubilities in tissues, and by their metabolism. We concurrently administered approximately one-third the MAC of each of these anesthetics to five young female swine and determined (separately) their solubilities in pig blood and tissues. The blood/gas partition coefficient of desflurane (0.35 +/- 0.02) was significantly smaller (P less than 0.01) than that of sevoflurane (0.45 +/- 0.02), isoflurane (0.94 +/- 0.05), and halothane (2.54 +/- 0.21). Tissue/blood partition coefficients of desflurane and halothane were smaller than those for the other two anesthetics (P less than 0.05) for all tissue groups. As predicted from their blood solubilities, the order of washin and washout was desflurane, sevoflurane, isoflurane, and halothane (most to least rapid). As predicted from tissue solubilities, the tissue time constants for desflurane were smaller than those for sevoflurane, isoflurane, and halothane. Recovery (normalized to that of isoflurane) of the volume of anesthetic taken up was significantly greater (P less than 0.05) for desflurane (93% +/- 7% [mean +/- SD]) than for halothane (77% +/- 6%), was not different from that of isoflurane (100%), but was less than that for sevoflurane (111% +/- 17%). The lower value for halothane is consistent with its known metabolism, but the lower (than sevoflurane) value for desflurane is at variance with other presently available data for their respective biodegradations.

Anesthetics↗
PubMed1989

Epinephrine-induced premature ventricular contractions and changes in arterial blood pressure and heart rate during I-653, isoflurane, and halothane anesthesia in swine.

I653 is a new inhalation anesthetic having especially desirable recovery characteristics because of its very low blood and tissue solubility. Investigations of its cardiovascular and electroencephalographic effects have revealed actions similar to those of isoflurane. However, these studies did not evaluate the potential of I653 to predispose the heart to epinephrine-induced arrhythmias. In this investigation, we studied eight domestic swine to compare the effects of I653 with those of other anesthetics on the cardiac arrhythmogenic actions of intravenously infused epinephrine. I653, isoflurane, and halothane each were given, on separate days, at 0.7-0.8 and at 1.1-1.2 MAC. The rate of infusion of epinephrine needed to produce premature ventricular contractions (PVCs) when the animals were anesthetized with I653 (6.9 +/- 0.7 and 6.6 +/- 0.9 micrograms.kg-1.min-1 at 0.8 and 1.2 MAC) did not differ from that during isoflurane anesthesia (5.7 +/- 1.1 and 6.0 +/- 1.0 micrograms.kg-1.min-1 at 0.7 and 1.1 MAC), but was greater than that required during halothane anesthesia (1.3 +/- 0.2 and 1.1 +/- 0.3 micrograms.kg-1.min-1 at 0.7 and 1.1 MAC). Similar mean arterial blood pressures and heart rates resulted from like infusions of epinephrine during I653 and isoflurane anesthesia. PVCs occurred at lesser infusion rates of epinephrine and at lower mean arterial blood pressures and heart rates with halothane than with I653 or isoflurane. Anesthetic concentration, over the range studied, did not alter the infusion rate of epinephrine required to produce arrhythmias with any anesthetic. The authors conclude that I-653 and isoflurane have similar properties with respect to epinephrine-induced arrhythmias and increases in heart rate and arterial blood pressure.

Anesthetics↗
PubMed1989

Cardiovascular safety and actions of high concentrations of I-653 and isoflurane in swine.

The ratio of lethal-to-anesthetic concentration can be used to define the margin of safety of an inhaled anesthetic. In mechanically ventilated swine the fatal concentration of I-653, a new inhaled anesthetic, was 23.9 +/- 0.06% (mean +/- SE), and of isoflurane, 6.22 +/- 0.23%. The ratio of fatal anesthetic concentration-to-MAC for I-653 (2.45 +/- 0.11) was less than that determined for isoflurane (3.02 +/- 0.13; P less than 0.01) but relatively greater than that reported previously for other inhaled anesthetics. As with other inhaled anesthetics, the concentration of I-653 causing cardiovascular collapse exceeds that producing apnea, making cardiovascular collapse during spontaneous ventilation unlikely. Mean aortic blood pressure and cardiac output decreased as linear functions of anesthetic concentration. Values for these variables for isoflurane were greater than those for I-653 at concentrations exceeding 1.5 MAC. Heart rate, blood lactate concentration, and base-deficit did not change with anesthetic depth. Mixed venous PO2, mixed venous oxyhemoglobin saturation, and the ratio of oxygen transport to oxygen consumption remained at or above values in conscious swine but decreased similarly with both anesthetics when anesthetic concentration increased to within 0.5 MAC of the fatal concentration. Thus, the latter three variables, reflecting the fraction of delivered oxygen that is consumed, and "mean" tissue PO2 appear to be useful indices of anesthetic concentrations approaching those producing cardiovascular collapse.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1989

Washin and washout of isoflurane administered via bubble oxygenators during hypothermic cardiopulmonary bypass.

Washin and washout of a volatile anesthetic given through the oxygenator during hypothermic (23.4 +/- 2.1 degrees C) cardiopulmonary bypass were studied in nine patients. The authors administered isoflurane and measured its partial pressure in arterial (Pa) and venous (Pv) blood and the gas exhausted from the oxygenator (PE) at 1, 2, 4, 8, 16, 32, and 48 min during washin. These measurements were repeated during washout, which coincided with rewarming. During washin, PE, Pa, and Pv progressively rose toward inlet gas partial pressure (PI). Equilibration of Pa with PI was 41% after 16 min, 51% after 32 min, and 57% after 48 min of washin. During washout, Pa declined to 24% of its peak after 16 min and to 13% after 32 min. Washin and washout were considerably slower in mixed venous blood. Washin of isoflurane appeared to occur more slowly during cardiopulmonary bypass than during administration via the lungs in normothermic patients, presumably because hypothermia increases tissue capacity, compensating for the effect of hemodilution that otherwise would decrease the blood/gas partition coefficient. During rewarming, washout appeared to occur as rapidly as from the lungs of normothermic patients. This may have resulted from the declining blood/gas partition coefficient (due to rewarming) and relatively limited tissue stores of isoflurane. The relationship between exhaust and arterial partial pressures was reasonably consistent; for clinical purposes, measurement of PE can be used to estimate Pa.

Cardiopulmonary Bypass↗
PubMed1989

Metabolism of I-653 and isoflurane in swine.

Fluoride ion concentrations were measured in plasma samples taken from chronically instrumented domestic swine before, immediately after, and 4 hours after exposure to either I-653 or isoflurane. Each anesthetic was administered at concentrations between 0.7 and 1.6 MAC and the total dose of anesthetic given was approximately 5.5 MAC hours for each agent. Plasma fluoride ion concentrations immediately after and 4 hours after exposure to isoflurane were approximately three times greater than values obtained in awake swine before anesthesia. In contrast, swine given I-653 had no detectable elevation in plasma fluoride concentration immediately after anesthesia, but a 17% (P less than 0.05) increase in plasma fluoride ion concentration 4 hours after anesthesia. These results imply that I-653 is metabolized less than is isoflurane in swine.

Anesthetics↗
PubMed1988

I653 and isoflurane produce similar dose-related changes in the electroencephalogram of pigs.

I653 is a new volatile anesthetic structurally similar to enflurane and isoflurane. Since enflurane can induce convulsions, whereas isoflurane progressively depresses cortical electrical activity, the authors believed it important to assess the effect of I653 on the EEG (in both the "time" and "frequency" domain). The EEG was assessed visually and quantitatively, and a new EEG parameter was introduced. The burst-suppression ratio (percentage of time the EEG was isoelectric) quantified the extent of burst suppression phenomena. Eight swine were anesthetized with I653 or isoflurane in oxygen and in random sequence, exposed to approximately 0.8, 1.2, or 1.6 MAC with normocapnea and to 1.2 MAC with hypocapnea (PETCO2 of 25 mmHg). Four animals were also anesthetized with 3.2% (1.2 MAC) enflurane in oxygen. Both I653 and isoflurane produced a dose-related depression of cortical electrical activity. At 0.8 and 1.2 MAC of either agent, occasional sharp waves occurred singly, were apparently not related to external (auditory) stimuli, and probably represented normal variation in the EEG. No electrographic or gross motor seizures occurred with either I653 or isoflurane. In contrast, all pigs given enflurane developed seizures during hypocapnea. At equipotent concentrations, I653 and isoflurane had the same effect on EEG parameters. Increasing doses of either I653 or isoflurane caused decreasing amplitude and frequency and increasing suppression. Hypocapnea during either agent slightly increased high-frequency activity, and slightly decreased burst suppression.

Anesthesia, Inhalation↗
PubMed1988

Cardiovascular effects of I653 in swine.

I653 (difluoromethyl 1-fluoro 2,2,2-trifluoroethyl ether) is a new inhalation anesthetic with a low blood-gas partition coefficient and no demonstrable toxicity. The authors examined its cardiovascular effects at 0.8, 1.2, and 1.6 MAC in eight chronically instrumented domestic swine mechanically ventilated to maintain normocarbia. These data were compared with those obtained while the animals were conscious and while anesthetized with isoflurane at approximately equal MAC multiples. I653 caused dose-related decreases in mean arterial blood pressure (95 +/- 2 mmHg, mean +/- SE, conscious; 65 +/- 3 mmHg, 0.8 MAC; 55 +/- 3 mmHg, 1.2 MAC; and 48 +/- 2 mmHg, 1.6 MAC). At 0.8 MAC, systemic vascular resistance decreased 35% from the conscious condition value. Despite the decreases in blood pressure and systemic vascular resistance, and dose-dependent increases in right- and left-heart filling pressures, stroke volume fell in a dose-related fashion (2.11 +/- 0.10, 1.57 +/- 0.08, 1.37 +/- 0.06, and 1.10 +/- 0.06 ml/kg; conscious, 0.8, 1.2, and 1.6 MAC). At 0.8 MAC, cardiac output was unchanged (220 +/- 12 ml.min-1.kg-1) from the conscious condition (210 +/- 8 ml.min-1.kg-1), as heart rate increased (142 +/- 7 beats/min, at 0.8 MAC vs. 100 +/- 3 beats/min, conscious) and systemic vascular resistance decreased. At concentrations greater than 0.8 MAC, heart rate decreased towards but did not reach the conscious value (127 +/- 4 at 1.2 MAC, 120 +/- 4 at 1.6 MAC). Systemic vascular resistance increased slightly at 1.6 MAC compared to the values at 0.8 and 1.2 MAC, but was always less than in the conscious condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1988

In vitro anesthetic washin and washout via bubble oxygenators: influence of anesthetic solubility and rates of carrier gas inflow and pump blood flow.

The uptake and elimination of volatile anesthetic agents administered to patients under conditions of hemodilution and hypothermia during cardiopulmonary bypass have not been determined. To define the limitations imposed by oxygenators, we defined washin and washout curves for volatile anesthetic agents administered to bubble oxygenators primed with diluted blood (without connection to a patient). There was rapid equilibration of anesthetic partial pressure between delivered gas and blood (85-90% within 16 minutes). Increasing the gas inflow to the oxygenator from 3 to 12 L/min hastened washin and washout slightly, while increasing the pump blood flow from 3 to 5 L/min had no effect. Rates of washin and washout of anesthetics differed as a function of their blood/gas solubilities: enflurane greater than isoflurane greater than halothane during washin; isoflurane greater than enflurane greater than halothane during washout. However, these differences were small. Oxygenator exhaust partial pressures of anesthetic correlated with simultaneously obtained blood partial pressures, suggesting that monitoring exhaust gas may be useful clinically.

Anesthetics↗
PubMed1988

Minimum alveolar concentration of I-653 and isoflurane in pigs: definition of a supramaximal stimulus.

We determined the anesthetic potencies of a new fluorinated anesthetic, I-653, and isoflurane in pigs as a preliminary to a study of the relative cardiovascular and electroencephalographic effects of these agents. Clamps were sequentially applied to the dew claw and/or tail of each animal to determine the minimum alveolar concentration (MAC) that suppressed movement in response to each of these stimuli. MAC obtained by clamping the tail (8.28 +/- 1.34% [mean +/- standard deviation] for I-653 and 1.65 +/- 0.36% for isoflurane) was more variable and lower than MAC obtained by clamping the dew claw (10.00 +/- 0.94% for I-653 and 2.04 +/- 0.19% for isoflurane). We conclude that the type of stimulus applied affects the MAC value obtained for I-653 and isoflurane. Clamping the tail is not a supramaximal stimulus in pigs; a greater stimulus is provided by clamping the dew claw.

Anesthetics↗