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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of isoflurane 2.0 MAC on human atrioventricular conduction time was studied. A non-invasive recording system for the detection of His-Purkinje potentials based on signal averaging techniques was used. Recordings were made in 15 patients before and after induction with isoflurane. We were able to measure atrial (P-H) and His-Purkinje (HPS) conduction times in 11 patients. Mean (+/- SEM) P-H conduction time decreased from 101.8 +/- 5.3 to 89.3 +/- 3.3 ms (P less than 0.01). HPS conduction times did not change significantly. Heart rate increased significantly from 86.7 +/- 4.2 to 94.9 +/- 4.7 beats min-1 (P less than 0.05). Systolic blood pressure decreased from 117.3 +/- 4.6 to 94.1 +/- 4.7 mmHg (P less than 0.05). It is concluded that the effects of isoflurane on supraventricular conduction time in humans depend on interactions of several different mechanisms.
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PMID:Atrial and His-Purkinje conduction times during isoflurane anaesthesia in humans. 193 25

The effects of halothane, isoflurane, and enflurane on proximal (false tendon) and distal (apical) canine Purkinje fibers were measured in vitro to assess their comparative effects on fibers exhibiting characteristically long (proximal) and short (distal) action potential duration. High- and low-dose anesthetic effects were evaluated in three groups of six left ventricular preparations and were compared with the changes occurring at identical times in six control preparations using analysis of variance with repeated measures. Under control conditions in all groups, the action potential duration, measured at 90% repolarization (APD90, mean +/- SEM), of proximal fibers was longer than that of distal fibers (320 +/- 16 vs 252 +/- 11 ms, P less than or equal to 0.01). Halothane (0.3 and 0.7 mM), isoflurane (0.4 and 0.8 mM), and enflurane (0.6 and 1.0 mM) produced a dose-dependent decrease (P less than or equal to 0.01) of proximal fiber APD90 with less (P less than or equal to 0.01) change of distal fiber APD90 and reduced (P less than or equal to 0.05) regional differences of APD90 at the higher dose. The decreases of proximal fiber APD90 were greater (P less than or equal to 0.01) for 1.0 mM (1.7 MAC) enflurane (-66 +/- 7 ms) and 0.8 mM (3.0 MAC) isoflurane (-69 +/- 9 ms) than for 0.7 mM (2.9 MAC) halothane (-33 +/- 8 ms). We conclude that the regional actions of anesthetics on Purkinje fiber repolarization may influence conduction during the relative refractory period and the occurrence of arrhythmias associated with disparity of regional refractory characteristics in the ventricular conduction system.
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PMID:Actions of halothane, isoflurane, and enflurane on the regional action potential characteristics of canine Purkinje fibers. 195 42

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.
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PMID:Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver. 198 65

The cerebral pressure-flow relationship for halothane and isoflurance was studied at end-tidal concentrations which resulted in similar baseline mean arterial pressure (MAP). Two groups of New Zealand white rabbits (n = 8; each group) were studied with five regional blood flow determinations in each animal. Blood flow was determined by injecting radioactive microspheres during the following conditions: injection 1: after stable 2.05 per cent end-tidal isoflurane (1.0 MAC) Group I; or after stable 0.74 +/- 0.04 per cent end-tidal halothane (0.53 MAC) Group H. Injections 2-5: after MAP was increased 20, 40, 60, and 80 per cent respectively above baseline MAP by phenylephrine infusion. Baseline MAP was the same for both groups (64.3 +/- 3.1 vs 67.2 +/- 2.0 mmHg; mean +/- SEM; Group I and H respectively). Baseline total CBF (tCBF; 0.68 +/- 0.03 vs 0.86 +/- 0.05) and hemispheric CBF (hCBF; 0.64 +/- 0.03 vs 0.96 +/- 0.06) were significantly greater in Group H; no significant difference between groups was seen for baseline posterior fossa CBF (pCBF; 0.79 +/- 0.06 vs 0.75 +/- 0.04). For each experiment a pressure-flow curve was generated by curvilinear regression analysis. Significantly greater phenylephrine concentrations were required for injections 2-5 in Group H. Mean slopes and intercepts were derived for each group. Within each group comparison of the pressure-flow curves for hCBF vs MAP and pCBF vs MAP showed autoregulation was less impaired in posterior fossa structures (cerebellum and brain stem) for both anaesthetic agents (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the cerebral pressure-flow relationship for halothane and isoflurane at haemodynamically equivalent end-tidal concentrations in the rabbit. 231 Nov 50

The effects of propofol, nitrous oxide, and/or isoflurane on efferent activity of sympathetic muscle nerve fibers (MSA) were studied using percutaneous microneurographic recordings from the peroneal nerve. Eight ASA Physical Status 1 patients (30-70 yr of age) scheduled for otorhinolaryngeal surgery entered the study. The effects of propofol (2-2.5 mg.kg-1.min-1) induction, tracheal intubation, and maintenance of anesthesia with isoflurane (0.3%, 0.6%, and 1.2% end-tidal concentrations) and/or 70% nitrous oxide were studied with respect to MSA, arterial blood pressure, heart rate, and indices of skin blood flow (laser doppler photometry and finger pulse plethysmography). Induction of anesthesia with propofol decreased MSA to 34 +/- 2% (mean +/- SEM) (P less than 0.05), and subsequent tracheal intubation increased MSA rapidly to 151 +/- 23% (P less than 0.05) of the control level. Isoflurane administration both with and without nitrous oxide led to a decrease of MSA (P less than 0.05). However, during nitrous oxide/isoflurane anesthesia (1.0 MAC) MSA was 76 +/- 38% higher than when isoflurane was used alone, although this implied a decrease in anesthetic depth to 0.5 MAC. This indicates that nitrous oxide and isoflurane have opposite effects on sympathetic outflow. During undisturbed propofol, nitrous oxide, and/or isoflurane administration (up to 1.0 MAC), MSA retained its normal pulse synchronous pattern, indicating that modulation of sympathetic outflow from arterial baroreceptors was still present. Skin blood flow increased sevenfold to tenfold in association with propofol induction (P less than 0.05) and was maintained at an 11- to 19-fold increase during nitrous oxide and/or isoflurane anesthesia, without any difference between the two anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous recording of muscle nerve sympathetic activity during propofol, nitrous oxide, and isoflurane anesthesia in humans. 236 Jul 36

Epinephrine-induced dysrhythmias were studied in 19 dogs anesthetized with 1.25 MAC enflurane or isoflurane, or the same preceded by thiopental (20 mg/kg). In 11 (group 1) dogs, thiopental reduced the dose of epinephrine required for production of ventricular ectopy, bigeminy and tachycardia with enflurane, and only ventricular tachycardia with isoflurane (P less than 0.05). Thiopental potentiation of epinephrine-induced dysrhythmias with enflurane lasted 4 hr after induction. In eight (group 2) dogs, the arrhythmic dose (ADE in microgram/ml) and plasma level of epinephrine (PLE in ng/ml) for four or more ventricular extrasystoles in 15 sec were determined in the same animal under each of the four test conditions. ADE and PLE values (X +/- SEM) were, respectively, enflurane, 9.1 +/- 1.0 and 141 +/- 24 (8/8 dogs); enflurane-thiopental, 5.0 +/- 0.6 and 63 +/- 16 (8/8 dogs); isoflurane, 28.3 and 330 (1/7 dogs); and isoflurane-thiopental, 15.2 +/- 2.8 and 265 +/- 59 (5/7 dogs). In addition, thiopental had no effect on plasma epinephrine levels reached during epinephrine infusions with 1.0 (enflurane only), 2.0 (enflurane, isoflurane) and 4.0 micrograms X kg-1 X min-1 (isoflurane only). Nor were epinephrine levels reached during enflurane or enflurane-thiopental different from those reached during isoflurane or isoflurane-thiopental. It is concluded that thiopental potentiates several types of epinephrine-induced ventricular dysrhythmias with enflurane, but only ventricular tachycardia with isoflurane. Furthermore, isoflurane or isoflurane-thiopental were less sensitizing than enflurane or enflurane-thiopental. Finally, neither thiopental nor the anesthetic agents affected plasma epinephrine levels reached during epinephrine infusions lasting 3 min.
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PMID:Thiopental and epinephrine-induced dysrhythmias in dogs anesthetized with enflurane or isoflurane. 242 10

The effects of 2.0 MAC halothane on atrioventricular conduction times in humans were studied. A real-time recording system for the detection of surface His-Purkinje potentials based on signal averaging techniques was used. Recordings were made in 23 patients before and after the administration of halothane. In 18 patients we were able to measure atrial (P-H) and His-Purkinje (H-V) conduction times (78%). A small but statistically significant decrease in P-H conduction times from 115.3 +/- 3.9 (SEM) to 110.8 +/- 4.2 ms was found (P less than or equal to 0.01). H-V conduction times did not change significantly. Heart rates decreased significantly from 87.6 +/- 2.6 to 74.8 +/- 2.5 beats/min (P less than or equal to 0.01). Systolic blood pressures decreased from 118.9 +/- 3.7 to 103.6 +/- 4.2 mm Hg. It is concluded that the decrease in heart rate and the decrease in atrial conduction time caused by halothane can be explained by interactions of several different mechanisms. The specific combination of slowing heart rate and a decrease of atrial conduction time provides a possible explanation for atrial arrhythmias during the administration of halothane.
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PMID:Effects of halothane on the conduction system of the heart in humans. 258 51

Some investigators believe that the dog is less sensitive than are humans to the anesthetic/analgesic actions of opioids. The alfentanil plasma concentration [ALF] vs anesthetic effect relationship has been determined for humans undergoing surgery. This study was designed to determine the [ALF] vs anesthetic relationship for alfentanil in the enflurane-anesthetized dog and thereby to provide data by which the [ALF] vs anesthetic effect relationships in the dog and in humans could be compared. Mongrel dogs (n = 10) were anesthetized with enflurane, and enflurane MAC (EMAC) was determined in each dog. After this, each dog received at least three incremental infusions of alfentanil using infusion rates of 0.625, 1.6, 8, 32, or 80 micrograms.kg-1.min-1. EMAC and [ALF] were determined during each infusion rate. There was a linear increase in [ALF] produced by incremental infusions of alfentanil (r = 0.999). Administration of alfentanil produced a dose-dependent reduction of EMAC up to a maximum of 72.5 +/- 3.7% (mean +/- SEM) at 32 micrograms.kg-1.min-1 ([ALF] = 960 +/- 86 ng/ml); a ceiling effect was evident. The degree of EMAC reduction (69%) produced by an infusion rate of 8 micrograms.kg-1.min-1 ([ALF] = 223 +/- 13 ng/ml) was not statistically different from the EMAC reductions produced by infusion rates of 32 (73% reduction at [ALF] = 960 +/- 86 ng/ml) or 80 micrograms.kg-1.min-1 (70% reduction at [ALF] = 2613 +/- 247 ng/ml) (P greater than 0.05). The relative potency of alfentanil was one-seventh to one-tenth that of fentanyl studied under identical conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The enflurane-sparing effect of alfentanil in dogs. 289 24

Using the radioactive microsphere technique regional cerebral blood flow (rCBF) and total CBF (tCBF) were examined in rats at three time periods: baseline (CBF1) during 1.5 MAC inspired isoflurane-oxygen anesthesia, CBF2; during 1.5 MAC inspired isoflurane anesthesia combined with hypotension induced by hemorrhage and CBF3; during isoflurane and hemorrhage plus phenylephrine infused to restore mean arterial pressure (MAP) to baseline. For CBF1 MAP was 89 +/- 3 mmHg (mean +/- SEM, n = 9) with PaCO2 44 +/- 1 mmHg. For CBF2 following graded hemorrhage MAP was 48 +/- 2 mmHg and PaCO2 43 +/- 1 mmHg. For CBF3 MAP was 93 +/- 2 and PaCO2 45 +/- 1 mmHg, following infusion of phenylephrine (PE) at 13.9 +/- 4.0 micrograms.kg-1.min-1. Total CBF1 was 1.84 +/- 0.18 ml.g-1.min-1, tCBF2 1.32 +/- 0.09 ml.g-1.min-1 (P less than 0.05 vs. tCBF1) and tCBF3 2.60 +/- 0.18 (P less than 0.05 vs. tCBF1 and 2). For tCBF3 hemoglobin concentration had decreased 23% from 14.2 +/- 0.2 g.100 ml-1 to 11.0 +/- 0.5 g.100 ml-1 (P less than 0.05). Regional CBF decreased significantly in seven of 12 regions examined from CBF1 to CBF2 and was significantly higher in all regions for CBF3. For CBF1-3 infratentorial blood flows (cerebellar and brain stem) were significantly higher than flows to the supratentorial structures (cerebral cortical and basal ganglia). During isoflurane anesthesia, phenylephrine infused to support MAP following hemorrhagic hypotension effectively maintains rCBF and tCBF. There is no indication that phenylephrine infused to increase MAP following hemorrhage results in cerebral vasoconstriction in rats anesthetized with isoflurane.
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PMID:Phenylephrine increases regional cerebral blood flow following hemorrhage during isoflurane-oxygen anesthesia. 291 62

Inspiratory mechanical loads were applied to the airway continuously for 5 min in healthy young adult volunteers maintained in a near steady-state of halothane anesthesia 1.1 MAC. The loads, both flow resistive and elastic in nature, had been selected to reduce the first loaded tidal volume approximately 10, 30 or 50%--these being designated "small," "medium," and "large" loads, respectively. The actual magnitudes of resistive load were 8 +/- 1, 21 +/- 3, and 48 +/- 6 cmH2O X l-1 X s, and of elastic load 6 +/- 1, 18 +/- 1, and 41 +/- 5 cmH2O X l-1 (mean +/- SEM). All loads caused an immediate reduction of ventilation proportional to the size of the load. This was followed by a gradual recovery of ventilation toward control values over approximately 2 min and then nearly stable ventilation for the rest of the loading period. Respiratory frequency was unchanged throughout. At 5 min of loading, ventilation and PaCO2 had been nearly steady for 3 min and O2 uptake and CO2 output at the airway were unchanged from control, suggesting the establishment of a near steady respiratory state. With the small and medium loads of both types, ventilation and PaCO2 in this near steady-state were not detectably different from control. With the large loads, however, ventilation was significantly reduced and PaCO2 slightly increased. The end-expiratory position of the chest wall and the relative contributions of the rib cage and abdomen-diaphragm to ventilation, as estimated by anteroposterior chest wall magnetometers, were not consistently altered by any load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory compensation for continuous inspiratory resistive and elastic loads during halothane anesthesia in humans. 293 23


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