Ultrasound-guided interscalene blocks: understanding where to inject the local anaesthetic.

Although ultrasound-guided regional anaesthesia has gained in popularity, few data exist describing the optimal location(s) to inject local anaesthetic. Our objective was to compare, for interscalene blocks, the effectiveness of an injection between the middle scalene muscle and brachial plexus sheath (peri-plexus) with an injection within the brachial plexus sheath (intra-plexus). We enrolled 170 patients undergoing shoulder surgery with general anaesthesia and interscalene block in this randomised, controlled trial. Our primary outcome variable was loss of shoulder abduction. Block quality was also measured and defined by an evaluation of onset time, sensory and motor loss and duration. There was no difference between the two groups in block onset times or block quality. After adjusting for sex, age and volume injected, intra-plexus blocks lasted a mean of 2.6 h (16%) longer (95% CI 0.25-5.01, p=0.03) than peri-plexus blocks.

Mercury suppression of a potassium current in human B lymphocytes.

Mercury is a recognized environmental toxin. Several organ systems are targeted by this substance and impairment of immune function is known to result from exposure to mercury. Using the patch clamp technique in the whole cell configuration on resting human B lymphocytes we have identified an outward potassium current and studied the effects of mercury on this current. We present data that demonstrate: (i) the absence of inward currents; (ii) a time and voltage dependent outward current with a threshold of -40 mV and reversal potential near EK+; (iii) blocking of this current by TEA (tetraethylammonium chloride) in a dose dependent manner; (iv) a slow time course for recovery from inactivation of this outwardly rectifying K+ current and, (v) the diminution and final block of this potassium current by mercury. These data supplement the findings from our laboratories that demonstrate inhibitory effects on B cell activation by mercury. We propose that the movement of potassium ions across the B cell membrane, an event presumed to be one of the first signals in the mitogenic process, is a target of mercury toxicity.

Ionic signals in T47D human breast cancer cells.

Increasing evidence that ion channels play a key role in the modulation of cellular mitogenesis led us to investigate the membranes of T47D human breast cancer cells to identify the ion currents present. We report here the results of voltage-clamp studies in the whole-cell configuration on isolated, non-synchronized single cells obtained from a ductal breast carcinoma. In these studies we identified an outward rectifying potassium current and a chloride current. The potassium current activated at potentials more positive than -40 mV, reached an average value of 1.4 nA, and did not inactivate with time. This current was sensitive to block by extracellular tetraethylammonium chloride (TEA, IC50 = 1 micro M), was insensitive to charybdotoxin (CTX, IC50 = 7.8 micro M), and was not diminished by repetitive pulses separated by 1 s. Rapid voltage-dependent inactivation of the current was demonstrated by tail current analysis. The current appeared calcium-insensitive. Application of hyperpolarizing pulses did not elicit an inward potassium rectifier current. Treatment with tetrodotoxin did not reveal the presence of an inward sodium current. The potassium current was increased by the presence of aspartate in place of chloride and in the presence of the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). We conclude that currents present in T47D breast cancer cells include a chloride current and a voltage-gated potassium outward rectifier. We suggest that the potassium current, either alone or in conjunction with potassium currents reported in different human breast cancer cell lines by others, may play a role in the modulation of the cell cycle.

Effects of cadmium on potassium currents in activated B lymphocytes.

We have applied the patch clamp technique in the whole-cell configuration to study whole-cell currents in B lymphocytes under three conditions: (i) resting; (ii) interleukin-4 (IL-4)-treated; and (iii) IL-4 plus cadmium-treated murine B lymphocytes. Through these experiments we have: (i) confirmed our earlier findings and the observation of others that resting B cells express only outward currents; (ii) confirmed the presence of an inwardly rectifying K+ current elicited by treatment with the lymphokine IL-4 that was revealed in our previous study on single channel currents; (iii) demonstrated that both inward and outward rectifying K+ currents in IL-4-treated B cells are dramatically reduced by exposure to 20 microM cadmium; and (iv) determined that the activation curve of the IL-4-induced inward rectifier is shifted to more negative voltages by cadmium. We propose that one of the mechanisms by which cadmium can mediate toxicity in activated B lymphocytes is through the suppression and modulation of potassium currents, effects that may alter the timing of entry into the cell cycle.

Effect of hypothermic cardiopulmonary bypass on nitroprusside metabolism.

At a rectal temperature of 25 degrees C, six patients undergoing hypothermic cardiopulmonary bypass received intravenous infusions of sodium nitroprusside (SNP) at a rate of 7.3 +/- 1.7 micrograms/kg/min for 20 minutes. Total SNP dose per patient was 11.0 +/- 1.1 mg. Blood samples for serum cyanide (CN-), red blood cell cyanide (RBC CN-), and thiocyanate (SCN-) determinations were drawn immediately before SNP infusion. These determinations were repeated at the end of the infusion, at the start of rewarming, and at a rectal temperature greater than 34 degrees C and 1, 4 (five subjects), and 24 hours (three subjects) thereafter. Extracorporeal blood flow was held constant at 2.4 L/min/m2 and mean arterial pressure was maintained between 50 to 100 mm Hg with phenylephrine (3.62 +/- 0.75 mg) during SNP infusion and trimethaphan (37.8 +/- 15.6 mg) after the end of the infusion. There was a significant increase in RBC CN- after the SNP infusion that lasted until the subjects were rewarmed. One subject developed a peak RBC CN- level of 0.8 microgram/ml. Plasma CN- levels changed little throughout and SCN- levels were elevated only after rewarming. The nonenzymatic release of free CN- from SNP was not inhibited by hypothermia, while the enzymatic detoxification of CN- to SCN- may have been delayed.

The effect of ventilation on systemic blood gases in the presence of left ventricular ejection during cardiopulmonary bypass.

The effect of pulmonary ventilation upon systemic arterial blood gases during cardiopulmonary bypass in the presence of left ventricular ejection was evaluated in 20 adult male patients undergoing coronary artery bypass grafting. Following rewarming, establishment of a sinus rhythm, and production of a pulse pressure of at least 20 mm Hg on the arterial pressure trace caused by left ventricular ejection, arterial blood gases were obtained from the arterial and venous extracorporeal circuits and the radial arterial cannula. Patients were then randomly assigned to a nonventilation (n = 10) or a ventilation (n = 10) group. The ventilation group was given 10 breaths/min with 100% oxygen at a tidal volume of 10 ml/kg. Whereas the nonventilation group received apneic oxygenation at zero end-expiratory pressure. After 5 minutes the arterial blood gas data were again obtained. Significant findings (p less than 0.05) included decreases in systemic carbon dioxide tension and increases in systemic pH in the ventilation group and decreases in systemic oxygen tension in the nonventilation group. Although the changes in the arterial blood gases were significant, these changes occurred well within the limits of clinical acceptability. It is concluded that left ventricular ejection for short periods during full cardiopulmonary bypass does not necessitate pulmonary ventilation.

OMNI scale perceived exertion at ventilatory breakpoint in children: response normalized.

PURPOSE: The Children's OMNI Scale of Perceived Exertion was used to identify a response normalized rating of perceived exertion (RPE)-Overall, RPE-Legs, and RPE-Chest that corresponds to the ventilatory breakpoint (Vpt) in 8- to 12-yr-old female and male children. METHODS: Subjects were a priori stratified into two fitness groups on the basis of peak oxygen uptake (VO2 peak): average (A) (41.0-49.0 mL x kg(-1) x min(-1); N = 24) and above average (AA) (50.0-58.0 mL x kg(-1) x min(-1); N = 24). Vpt was determined by a progressive cycle ergometer protocol to VO2 peak. RESULTS: A gender effect was not observed for any descriptive or dependent variable. Mean VO2peak for the A group was 1.72 L x min(-1) and for the AA group 2.04 L x min(-1). Vpt corresponded to 64.0% VO2 peak for A and 74.0% VO2peak for AA. RPE-Overall (mean A and AA, 6.1), RPE-Legs (mean A and AA, 7.2), and RPE-Chest (mean A and AA, 4.5) did not differ between the fitness groups. CONCLUSION: Findings indicated that undifferentiated and differentiated RPE-Vpt were similar between female and male children who varied in VO2peak and Vpt. A comparatively stable RPE-Vpt for 8- to 12-yr-old children that vary in VO2peak and Vpt indicates a group normalized perceptual response.

Children's OMNI scale of perceived exertion: mixed gender and race validation.

PURPOSE: The newly developed Children's OMNI Scale of Perceived Exertion (category range: 0 to 10) was validated using separate cohorts of female and male, African American and white subjects. Each of the four cohorts contained 20 clinically normal, nonobese children, 8-12 yr of age. METHODS: A cross-sectional, perceptual estimation paradigm using a single multi-stage cycle ergometer test protocol was used. Oxygen uptake (VO2; mL x min(-1)), heart rate (HR; beats x min(-1)) and ratings of perceived exertion for the overall body (RPE-Overall), legs (RPE-Legs), and chest (RPE-Chest) were determined at the end of each continuously administered 3-min power output (PO) (i.e., 25, 50, 75, and 100 W) test stage. RESULTS: The range of responses over the four POs for all cohorts was VO2: 290.8 to 1204.0 mL x min(-1); HR: 89.2 to 164.4 beats x min(-1); and RPE-Overall, RPE-Legs, and RPE-Chest: 0.85 to 9.1. First-order correlation and linear regression analyses were performed for each cohort separately and the total sample using a repeated measures paradigm over the four POs. For all correlation/regression paradigms RPE-Overall, RPE-Legs, and RPE-Chest distributed as a positive linear function of both VO2 and HR; r = 0.85 to 0.94; P < 0.01. Differences between RPE-Overall, RPE-Legs, and RPE-Chest were examined with ANOVA for the repeated measures paradigm. RPE-Legs was higher (P < 0.01) than RPE-Chest and RPE-Overall at 25, 50, 75, and 100 W. RPE-Chest did not differ from RPE-Overall at 25 and 50 W but was lower (P < 0.01) than RPE-Overall at 75 and 100 W. CONCLUSION: The psycho-physiological responses provide validity evidence for use of the Children's OMNI Scale over a wide range of dynamic exercise intensities.

Effects of varying post-KR intervals upon children' motor performance.

An experiment using post-KR interval methodology was designed to investigate the developmental relationship of age and processing speed regarding performance on a ballistic linear slide task. The hypothesis drawn from the developmental literature was that, given a short time for processing information, younger children should perform less efficiently than older children and adults. However, an increase in processing time should result in performances being more similar. Subjects in the experiment were 90 female children equally divided among 7 and 11-yr-olds and adults. Within age, subjects were randomly assigned to one of three post-KR interval groups: 3, 6, and 12 sec. Conclusions support the processing deficits hypotheses of Chi (1976): given enough time to process KR, the children's performance was not significantly different from the performance of adults.

Voluntary movement strategies of individuals with unilateral peripheral vestibular hypofunction.

This study compared voluntary movement strategies of patients with unilateral peripheral vestibular hypofunction with those of age-matched healthy control subjects. All subjects performed three voluntary movement tasks with their dominant upper extremity: a forward flexion arm movement through 90 degrees, a reach to an overhead target, and a reach to a side target. Subjects performed the movement tasks sitting and standing (Body Position), and under precued and choice reaction time (RT) conditions (Task Certainty). Measures of motor planning and movement execution included RT and movement time (MT), respectively. Statistical analysis included separate Group x Task Certainty x Body Position ANOVA calculations for each task. Across tasks, results suggested no between group differences for RT. A Task Certainty main effect for the side and overhead tasks indicated that the choice RT situation resulted in longer RTs as compared to the precued RT condition. Movement time differed between the two groups. Across all three voluntary movement tasks, vestibular impaired subjects moved more slowly than control subjects. Providing vestibular subjects with a precue did not bring MT performance to the level of controls. Body position influenced MT for the side task only. Across both groups of subjects, MT for the side task was longer when performed in the standing position. The results of this study suggest that individuals with unilateral peripheral vestibular hypofunction initiate voluntary movement responses with similar timing as control subjects, but require more time to complete the movement. Vestibular rehabilitation should include goal-directed movement and should address issues of movement speed.

Ultrasound guidance improves the success rate of a perivascular axillary plexus block.

BACKGROUND: Traditional approaches to performing brachial plexus blocks via the axillary approach have varying success rates. The main objective of this study was to evaluate if a specific technique of ultrasound guidance could improve the success of axillary blocks in comparison to a two injection transarterial technique. METHODS: Fifty-six ASA physical status I-III patients presenting for elective hand surgery were prospectively randomized to receive an axillary block performed by either a transarterial technique (Group TA) or an ultrasound-guided perivascular approach (Group US). Both groups received a total of 30 ml of 1.5% lidocaine (225 mg) with 5 microg/ml epinephrine. Patients were then evaluated for block onset in specific nerve distributions and whether or not the block acted as a surgical anesthetic. RESULTS: Group TA sustained more failures defined as conversion to general anesthesia or the inability to localize the artery [Group TA eight patients (29%) vs. Group US in which 0 patients required conversion to general anesthesia (0%) P < 0.01]. Group US demonstrated a reduction in performance times vs. Group TA (7.9 +/- 3.9 min vs. 11.1 +/- 5.7 min, P < 0.05). By 30 min post-injection, there were no significant differences between groups TA and US in terms of the proportion of patients demonstrating a complete motor or sensory loss. CONCLUSION: Ultrasonographic guidance improves the overall success rate of axillary blocks in comparison to a transarterial technique.

The effects of halothane on abnormal automaticity in canine cardiac Purkinje fibers.

UNLABELLED: Abnormal automaticity is the spontaneous beating of cardiac cells with abnormally depolarized resting membrane potentials. The effects of halothane on cardiac arrhythmias caused by abnormal automaticity are controversial, with either antiarrhythmic effects or enhancement of abnormal automaticity reported by different authors. The goal of the present investigation was to clarify the effects of halothane on abnormal automaticity induced by superfusing excised canine Purkinje fibers (PF) with barium chloride. Intracellular microelectrodes recorded action potentials from fibers superfused with buffer solution in a tissue bath. Barium chloride 0.25 mM reduced maximal diastolic potential from -82.1 +/- 5.6 mV to -67.4 +/- 9.4 mV (mean +/- SD, P < 0.05). Fibers developed abnormal automatic rhythms at a rate of 47.1 +/- 5.9 bpm. Halothane, 0.5%-4%, was added to the superfusate. Halothane reduced the rate of firing in a dose-dependent manner, so that abnormal automaticity was abolished by 4% halothane and reduced by lesser concentrations. Serendipitously, during barium superfusion, two additional fibers developed early afterdepolarizations, a cause of triggered arrhythmias in patients with long Q-T syndrome. Halothane abolished early afterdepolarizations in each. In this model of barium toxicity in excised canine PF, halothane antagonized both abnormal automaticity and early afterdepolarizations. IMPLICATIONS: Life-threatening cardiac arrhythmias may occur during anesthesia. An arrhythmia called abnormal automaticity occurs after heart attacks and can be mimicked by adding barium to small segments of heart tissue. Halothane abolished abnormal automaticity in these tissues, which suggests that it or similar agents may benefit patients prone to developing such abnormal rhythms during surgery.

Effects of halothane and quinidine on intracardiac conduction and QTc interval in pentobarbital-anesthetized dogs.

To confirm in vitro data that halothane and quinidine depressed cardiac conduction and prolonged action potential (AP) duration, the electrocardiogram and His bundle electrogram were recorded in dogs during basal pentobarbital anesthesia, after 1% halothane or quinidine (2.38 +/- 0.22 micrograms/mL serum concentration [mean +/- SEM]), or both. Purkinje fibers from a second dog were superfused with blood from the intact (support) dog, and APs were recorded. In the intact dogs, 1% halothane caused no changes in the electrocardiogram or His bundle electrogram. Quinidine prolonged QRS duration, QT interval, and rate-corrected QT (P < 0.05). Ventricular conduction (HS interval) slowed, and atrial effective refractory period increased (P < 0.05). Quinidine combined with halothane widened QRS, QT, and rate-corrected QT, prolonged the HS interval, and increased the vulnerability of the atrioventricular node to conduction block. Three of 20 dogs developed torsades de pointes-type ventricular tachycardia during simultaneous quinidine and halothane administration. In cross-superfused Purkinje fibers, the AP duration to 50% repolarization was shortened, and conduction time was prolonged by 1% halothane (both P < 0.05). Quinidine decreased AP amplitude, prolonged AP duration to 90% repolarization, and slowed conduction (P < 0.05). Quinidine combined with halothane decreased AP amplitude, and prolonged both AP duration to 90% repolarization and conduction (P < 0.05). When 1% halothane and therapeutic concentrations of quinidine are administered in dogs, depressed conduction and an acquired long QT syndrome with malignant ventricular arrhythmias may develop.

The electrophysiologic effects of amiodarone and halothane on canine Purkinje fibers.

Amiodarone may cause serious complications in patients receiving general anesthetics. Potentially adverse electrophysiologic interactions between amiodarone and halothane were studied with the use of standard microelectrode techniques to record intracellular action potentials (APs) from excised canine Purkinje fibers. A second dog (support dog) was anesthetized and a femoral arteriovenous bypass circuit created in which arterial blood from the support dog superfused the Purkinje fiber in a tissue bath. The applicability of this model was established by first comparing the AP effects of halothane during blood perfusion with those in Tyrode's solution. Halothane reduced AP duration (APD; P less than 0.05) during Tyrode's solution superfusion and blood cross-perfusion. After the blood perfusion-Purkinje fiber model was validated, the interaction between halothane and amiodarone was studied using Purkinje fibers from dogs chronically treated with oral amiodarone, superfused with blood from chronically amiodarone-treated support dogs. Amiodarone reduced resting membrane potential and prolonged APD. Depression of AP amplitude and reduction of the maximum rate of increase of phase 0 of the AP (Vmax) by halothane (both P less than 0.05) suggested risk of conduction defects if halothane is administered to patients receiving chronic amiodarone therapy.

Electrophysiological mechanisms for ventricular arrhythmias in patients with myocardial ischemia: anesthesiologic considerations, Pt II.

This is the second half of a two-part review article that discusses ventricular tachyarrhythmias, either induced by acute ischemia or consequent to chronic myocardial ischemia, and their anesthestic implications. The first half of the article was published in the June 1997 Issue of The Journal.

Effects of isoflurane on ouabain toxicity in canine Purkinje fibers. Comparison with halothane.

BACKGROUND: Although halothane reduces digitalis toxicity, other anesthetics, notably cyclopropane, increase toxicity. This study determined the effects of isoflurane on digitalis toxicity in isolated cardiac tissue and compared these effects with those of halothane. METHODS: Standard microelectrode techniques were used to record action potentials from excised canine Purkinje fibers. Fibers were paced at cycle lengths between 1,000 and 250 ms for 20 beats to induce delayed afterdepolarizations, which are membrane potential oscillations indicative of intracellular Na+ and Ca2+ overload, produced in these experiments by digitalis toxicity. The digitalis glycoside ouabain, 2 x 10(-7) M, was added to the Tyrode's solution superfusate to induce delayed after-depolarizations. Action potential variables and the coupling interval and amplitude of afterdepolarizations were then measured. Isoflurane (0.5%, 1%, or 2%) was added with a calibrated vaporizer (n = 8). In a second set of experiments (n = 10), isoflurane 1.25% or halothane 0.75% was added to the superfusate. After measurements had been made, the other agent was substituted. RESULTS: Ouabain produced primary and secondary delayed afterdepolarizations, which were reduced in amplitude by isoflurane in a dose-related manner (P = 0.0002). Action potential duration to 90% repolarization was shortened by ouabain (P = 0.009) and remained shortened during isoflurane administration. Action potential duration to 50% repolarization was shortened by isoflurane 2%. Halothane and isoflurane were equally effective in reducing the amplitude of delayed afterdepolarizations (both P = 0.0002). In three fibers, triggered extrasystoles appeared. Halothane and isoflurane each abolished extrasystoles. In two fibers, sustained triggered activity appeared. Isoflurane abolished the arrhythmia in each fiber. CONCLUSIONS: Isoflurane and halothane are equally effective in reducing delayed afterdepolarizations induced by ouabain toxicity.

The effects of halothane on ventricular tachycardia in intact dogs.

Halothane has either proarrhythmic or antiarrhythmic effects in a variety of clinical circumstances. This investigation tested the hypothesis that halothane would display different effects on ventricular tachycardia (VT) produced by different electrophysiologic mechanisms in intact dogs. Four models of VT produced by abnormal automaticity, reentry, delayed-afterdepolarization-induced triggered activity, and early-afterdepolarization-induced triggered automaticity (groups 1-4, respectively) were studied. In groups 1 and 2, the left anterior descending coronary artery (LAD) was ligated. In group 1 (n = 5), 24 h after LAD ligation and infarction, all dogs demonstrated incessant VT with 94.7 +/- 2.3% of beats of ventricular origin. This ectopy presumably was due to abnormal automaticity. Halothane reduced the frequency of ventricular ectopy until at 2% halothane only 34.8 +/- 15% of beats were of ventricular origin. One week after LAD ligation, programmed stimulation produced nonstimulated extrasystoles of presumably reentrant origin in six dogs. In three, halothane 1% abolished extrasystoles while increasing the ventricular refractory period by 23 +/- 3.8% (P less than 0.05). In the three other dogs, halothane had no effect (two dogs) or worsened the severity of VT (one dog), while the refractory period increased by 7.7% (P greater than 0.05). In group 3 dogs, ouabain was infused until VT secondary to triggered activity occurred. Halothane restored sinus rhythm in 4 of 5 dogs. Overall the percentage of sinus beats increased from 11.1 +/- 2.8 to 97.4 +/- 2.6% when halothane 2% was added during ouabain toxicity. Cesium chloride infusion increased the QT interval and produced complex VT in 5 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the electrophysiologic effects of acute and chronic amiodarone administration on canine Purkinje fibers.

The electrophysiologic effects of acutely and chronically administered amiodarone on canine Purkinje fibers were assessed using microelectrode techniques to record intracellular action potentials. Chronically treated dogs received amiodarone for 3 weeks (serum levels, 0.91 +/- 0.09 microgram/ml or 1.42 X 10(-6) M). Acute studies were performed using fibers from untreated dogs superfused for 1 h with 5 X 10(-5) M amiodarone (32 micrograms/ml) in Tyrode's solution (KCl = 4 mM). Acute superfusion shortened the action potential duration to 50 and 90% repolarization by 41 and 8%, respectively (p less than 0.01), and decreased Vmax of phase 0 from 418 +/- 20 to 309 +/- 23 V/s (p less than 0.01) (paced cycle length of 500 ms). Prominent use-dependent depression of Vmax was noted. Acute exposure of fibers from untreated dogs to blood from dogs chronically treated with amiodarone using the blood cross-perfusion technique decreased the action potential duration to 50% repolarization and Vmax, similar to acute exposure in Tyrode's solution. Blood cross-perfusion was used to study fibers from treated dogs superfused with blood from another amiodarone-treated dog. Chronic amiodarone prolonged the action potential duration to 90% repolarization by 13% (p less than 0.02) and did not change Vmax when compared to control studies using fibers obtained from untreated dogs superfused with blood from untreated dogs. Thus, the effects of acutely superfused amiodarone on action potentials of canine Purkinje fibers differ from the effects of chronically administered amiodarone.

Effect of halothane on in vivo and in vitro cardiotoxicity of an aminocardenolide.

Halothane opposes cardiotoxicity of neutral-sugar digitalis compounds in intact animals, presumably by depressing a sympathetic component of arrhythmogenesis. However, halothane also produces a dose-related reduction in arrhythmogenicity of ouabain in isolated canine Purkinje fibers, suggesting that the anesthetic may oppose direct mechanisms of cardiotoxicity as well. The present study examined in vivo and in vitro the effect of halothane on the arrhythmogenicity of ASI-222 (3-beta-O[4-amino-4-6-dideoxy-beta-D-galactopyranosyl] digitoxigen in HCl), a highly polar aminocardenolide with no sympathetic component to cardiotoxicity. For in vivo studies, ASI-222 was infused at a rate of 1 microgram/kg/min until appearance of third-degree atrioventricular (AV) block or sustained ventricular arrhythmias in 5 conscious (control) and 6 halothane-anesthetized (1.4% end-tidal) dogs. For in vitro studies, standard microelectrode techniques were used to measure action potentials (AP) in seven excised canine Purkinje fibers superfused with oxygenated Krebs-Henseleit buffer. AP were recorded during control superfusion, after induction of toxicity with 10(-7) M ASI-222, and during exposure to 0.5, 1.0, and 2.0% halothane. Purkinje fibers were paced at 500-ms cycle lengths (CL) for 20 beats, and the amplitude of delayed afterdepolarizations (DAD) were recorded. Pacing at 250 ms CL was used to trigger ectopy. In vivo studies showed no difference in the cardiotoxic dose of ASI-222 between control dogs and those anesthetized with 1.4% halothane. However, in 4 of 6 anesthetized dogs, acutely increasing the inspired halothane concentration suppressed arrhythmias once end-tidal concentration were >2.2%.(ABSTRACT TRUNCATED AT 250 WORDS)

Halothane antagonizes ouabain toxicity in isolated canine Purkinje fibers.

Standard intracellular microelectrode techniques were used to study the effects of halothane on ouabain-induced delayed after depolarizations (DAD) in canine Purkinje fibers. Free running Purkinje fibers were superfused with 2 X 10(-7)M ouabain in Krebs-Henseleit buffer for 30-50 min until DAD appeared. Purkinje fibers were then paced for 20 beats at cycle lengths between 1,000 ms and 200 ms, and the amplitude of the DAD and coupling interval between the DAD and last paced beat were determined. Halothane (0.5, 1, and 2%) was then administered and measurements repeated. Halothane produced dose-related decreases in DAD amplitude without changing DAD coupling interval. The ability of calcium to antagonize the effects of halothane was evaluated by doubling buffer calcium concentration to 5 mM in the presence of halothane 2%. Doubling buffer calcium concentration to 5 mM antagonized the reduction of DAD amplitude caused by halothane. In several preparations, dysrhythmias occurred during ouabain superfusion. Halothane reversibly terminated these arrhythmias. Halothane antagonizes DAD and dysrhythmias induced in vitro by ouabain toxicity. This effect, in part, may account for the apparent effectiveness of halothane against ouabain-induced dysrhythmias in vivo.