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At least 73 records · Page 4Linked to original sources

PubMed2002

Intravenous colforsin daropate, a water-soluble forskolin derivative, prevents thiamylal-fentanyl-induced bronchoconstriction in humans.

OBJECTIVE: Forskolin, a direct activator of adenylate cyclase, can relax airway smooth muscle, similar to other agents that increase intracellular cyclic adenine monophosphate. However, the potential usefulness of forskolin in treating bronchospasm is limited by its poor water solubility. Colforsin daropate is a novel and potent water-soluble forskolin derivative. No clinical data have been published on the bronchorelaxant effects of this drug. The aim of this study was to investigate whether intravenous colforsin daropate prevents thiamylal-fentanyl-induced bronchoconstriction. DESIGN: Double-blind, prospective, placebo-controlled randomized study. SETTING: University teaching hospital. PATIENTS: Thirty-six patients were allocated randomly to two groups: the control group (n = 18) and colforsin daropate group (n = 18). INTERVENTIONS: Intravenous administration of colforsin daropate or placebo (normal saline). MEASUREMENTS AND MAIN RESULTS: Anesthesia was induced with thiamylal 5 mg/kg and vecuronium 0.3 mg/kg. A 15 mg x kg(-1) x hr(-1) continuous infusion of thiamylal followed anesthetic induction. Controlled ventilation was maintained, delivering 50% nitrous oxide in oxygen. Twenty minutes after the induction of anesthesia, the control group patients started to receive 7.5 mL/hr continuous infusion of normal saline, and the colforsin daropate group patients started to receive 0.75 microg x kg(-1) x min(-1) (7.5 mL/hr) continuous infusion of colforsin daropate for 60 min. After that, both groups received fentanyl 5 microg/kg. Systolic and diastolic arterial pressure, heart rate, mean airway resistance (Rawm), expiratory airway resistance (Rawe), and dynamic lung compliance (Cdyn) were measured at the baseline, just before the administration of fentanyl (T30), at three consecutive 6-min intervals after fentanyl injection (T36, T42, and T48) and 30 min after fentanyl injection (T60). At baseline, both groups had comparable Rawm, Rawe, and Cdyn values. In the control group, Rawm increased significantly at T36-60 compared with the baseline, Rawe increased significantly at T36-48 compared with the baseline, and Cdyn decreased significantly at T36-60 compared with the baseline. In the colforsin daropate group, there were no changes in Rawm, Rawe or Cdyn at T36-60. CONCLUSIONS: These observations suggest that intravenous colforsin daropate has a bronchodilator effect in humans.

Adult↗

PubMed2003

Intravenous nicorandil prevents thiamylal-fentanyl-induced bronchoconstriction in humans.

OBJECTIVE: Nicorandil has a hybrid property between nitrates and potassium channel openers and has been reported to cause a concentration-dependent relaxation of isolated guinea pig trachealis. Experimental asthma in a guinea pig model was also inhibited by nicorandil. However, no clinical data on the bronchorelaxant effects of this drug have been published. The aim of this study was to investigate whether intravenous nicorandil prevents thiamylal-fentanyl-induced bronchoconstriction. DESIGN: Double-blind, prospective, placebo-controlled, randomized study. PATIENTS: A total of 36 patients were randomly allocated to two groups: a control group (n = 18) and a nicorandil group (n = 18). INTERVENTIONS: Intravenous administration of nicorandil or a placebo (normal saline). MEASUREMENTS AND MAIN RESULTS: Anesthesia was induced with 5 mg/kg thiamylal and 0.3 mg/kg vecuronium. A continuous infusion of 15 mg x kg(-1) x hr(-1) thiamylal was then used to maintain the anesthesia. Controlled ventilation was maintained, delivering 50% nitrous oxide in oxygen. At 20 mins after the induction of anesthesia, the control group patients were given a 6 mL/hr continuous infusion of normal saline and the nicorandil group patients were given a 6 mg x hr(-1) (6 mL/hr) continuous infusion of nicorandil for 60 mins. At 30 mins after the start of the study, both groups received a 5-microg/kg dose of fentanyl. Systolic and diastolic arterial pressure, heart rate, mean airway resistance, expiratory airway resistance, and dynamic lung compliance were measured for the baseline condition, just before the administration of fentanyl (T30), at three consecutive 6-min intervals after the fentanyl injection (T36, T42, and T48) and 30 mins after the fentanyl injection (T60). Both groups had comparable baseline values for mean airway resistance, expiratory airway resistance, and dynamic lung compliance. In the control group, both mean airway resistance and expiratory airway resistance increased significantly at T36-60, compared with the baseline values, and dynamic lung compliance decreased significantly at T36-60, compared with the baseline value. In the nicorandil group, no changes in mean airway resistance, expiratory airway resistance, or dynamic lung compliance occurred at T36-60. CONCLUSIONS: Our observations suggest that the intravenous administration of nicorandil has a bronchodilator effect in humans.

Adult↗

PubMedDate not supplied

Circulatory changes in patients with coronary artery disease following thiamylal-succinylcholine and tracheal intubation.

Circulatory responses after thiamylal (4 mg/kg) and succinylcholine (SCh) (2 mg/kg) administration followed by direct laryngoscopy and tracheal intubation were measured in 20 patients before elective aortocoronary vein bypass graft operations. Compared with awake measurements, the mean arterial pressure (MAP) decreased 19 +/- 3 torr (mean +/- SE) and heart rate (HR) increased 9 +/- 3 bpm 1 minute after thiamylal-SCh. MAP was increased 39 +/- 4 torr and HR 20 +/- 3 bpm above awake levels in response to laryngoscopy and tracheal intubation. Blood pressure and HR returned spontaneously to near awake levels without additional anesthesia within 5 minutes of anesthetic induction. Stroke volume index was decreased significantly after tracheal intubation but cardiac index was not altered. The authors conclude that thiamylal-SCh followed by tracheal intubation is an acceptable anesthetic induction sequence for patients without evidence of left ventricular heart failure who require anesthesia for elective coronary artery revascularization.

Anesthesia, Intravenous↗

PubMed1990

[The effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves produced by cerebral ischemia in cats].

Spontaneous hippocampal electroencephalogram (EEG) was recorded in the pyramidal cell layer (PCL) and dentate gyrus (DG) during and after ischemia produced by bilateral clamping of the common carotid arteries in cats. Hippocampal theta waves, approximately 180 degree out of phase in PCL and DG, appeared within 4.3 +/- 2.3 seconds after the onset of bilateral carotid artery occlusion and continued for more than 60 minute. These hippocampal theta waves disappeared 34.2 +/- 10.2 seconds after 4 vessel occlusion. We could not find the clear difference between the two areas in the appearance and disappearance of the hippocampal theta waves. We further investigated the effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves during bilateral carotid artery occlusion. Thiamylal changed the two hippocampal theta waves to a similar pattern of EEG, which has irregular slow and fast waves, in both PCL and DG. Ketamine changed the two theta waves to irregular complex pattern of fast and slow waves and spike activity, which is independent at two areas. Nicardipine, a Ca antagonist, changed the theta waves to irregular slow waves which were similar to the pattern of EEG observed before carotid artery occlusion. These results indicate that thiamylal, ketamine and nicardipine have different effects on the ischemia of hippocampus.

Animals↗

PubMed1985

Effect of thiamylal and diazepam on release of myoglobin and creatine phosphokinase by succinylcholine chloride during halothane anesthesia.

The effects of thiamylal and diazepam on the release of myoglobin and creatine phosphokinase following the administration of succinylcholine chloride during halothane anesthesia were studied. Thirty patients receiving halothane anesthesia were divided into three groups. In Group I, 1.5-2 mg/kg of thiamylal were given intravenously as pretreatment before the injection of succinylcholine chloride. In Group II, 0.3 mg/kg of diazepam were given and, in Group III, only succinylcholine chloride was injected. A significant increase in the serum myoglobin and creatine phosphokinase levels was observed in all groups. However, the values in Group I were significantly lower than those in Groups II and III and a significant difference was not detected between Group II and III. Our results indicate that thiamylal has a considerable inhibitory effect on the release of myoglobin and creatine phosphokinase from the muscle following the administration of succinylcholine chloride.

Adolescent↗

PubMed1985

Epinephrine-induced ventricular arrhythmias in dogs anesthetized with halothane: potentiation by thiamylal and thiopental.

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.

Anesthesia, General↗

PubMed1985

Catecholamine infusion in vagotomized dogs during thiamylal-halothane and pentobarbital anesthesia.

The cardiac arrhythmogenic infusion rate of epinephrine, dopamine, and dobutamine in vagotomized dogs was determined during thiamylal-halothane and pentobarbital anesthesia. Epinephrine, dopamine, and dobutamine were administered until 4 or more ventricular arrhythmias on duplicated trials were produced or until a predetermined maximum infusion rate was attained. The mean ventricular arrhythmogenic infusion rates (micrograms X kg-1 X min-1) during thiamylal-halothane anesthesia were: epinephrine, 0.57 +/- 0.24; dopamine, 23.7 +/- 8.26; and dobutamine, 10.21 +/- 3.54. Few arrhythmias were produced at the maximum administered infusion rate during pentobarbital anesthesia (2 of 6 with epinephrine, 3 of 6 with dopamine, and 0 of 6 administered dobutamine). Heart rate and blood pressure increased progressively with increasing infusion rates for all 3 catecholamines during thiamylal-halothane anesthesia. Heart rate and blood pressure changes were similar during pentobarbital anesthesia except for blood pressure changes during dobutamine infusion.

Anesthesia, General↗

PubMed1983

Effects of halothane, thiamylal, and ketamine on central sympathetic and vagal tone.

The effects of increasing doses of halothane, thiamylal, and ketamine on central sympathetic tone (ST) and vagal tone (VT) in cats were studied. Compound action potentials were recorded simultaneously from the cervical sympathetic trunk and the vagus nerve. After full-wave rectification, they were integrated for continuous monitoring of the tonic levels of activity. ST and VT changed characteristically with different anesthetics. Halothane depressed ST and VT equally to approximately 70%, 60%, and 30% of the control level (70% N2O in O2) at end-tidal halothane concentrations of 0.5%, 1.0%, and 2.0%, respectively. When thiamylal was given intravenously at incremental doses (3, 6, 9, and 12 mg/kg), ST was markedly reduced to 10% of the control level. The reduction in VT was relatively small and the autonomic balance shifted in the vagodominant direction. Intravenous ketamine (2, 4, 6, and 8 mg/kg) changed neither ST nor VT significantly. Halothane and thiamylal markedly reduced central sympathetic and vagal outflows that play a role in peripheral homeostatic regulation. We suggest that these two anesthetics effect attenuated or altered autonomic regulation. Ketamine produced little change in central autonomic outflow.

Action Potentials↗

PubMedDate not supplied

Influence of pancuronium or d-tubocurarine on circulatory responses during thiamylal-N2O-halothane anesthesia.

Circulatory responses after thiamylal (4 mg/kg) and pancuronium (0.08 mg/kg, 20 patients) or d-tubocurarine (dTc, 0.5 mg/kg, 20 patients) followed by tracheal intubation and nitrous oxide-halothane administration were measured. Three minutes after thiamylal, the mean arterial pressure (MAP) and cardiac index (CI) decreased significantly only in patients receiving dTc. Heart rate (HR) was increased 12 bpm in both groups. The magnitude of reduction in MAP and CI was similar and the HR was not greatly different between groups after 5 minutes of N2O-halothane administration. MAP and CI were better maintained following thiamylal in patients receiving pancuronium as compared with dTc. However, circulatory responses during early anesthetic maintenance were not influenced by the choice of neuromuscular blocker.

Anesthesia, Inhalation↗

PubMed2005

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: a comparative ultrastructural and cytochemical study.

The pulmonary intravascular macrophages (PIMs) of equines contain a unique electron-dense surface coat that is predominantly composed of lipoproteins. A single exposure of inhalatory halothane causes mobilization of the surface coat into the endocytotic system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. Simultaneously, the cells of the lymphocytic series show hyperplasia in the form of mitotic changes inside the microvascular compartment of the lung. Halothane is known to cause acute and chronic hepatotoxicity because of its biotransformation into trifluoroacytelated polypeptides. The present study was designed to examine the comparative effects of reexposures of inhalatory doses of halothane, isoflurane, and the intravenous barbiturate thiamylal sodium in ponies to evoke a stronger response in the PIMs after four exposures at increasing intervals of 1, 2, and 6 weeks. Ultrastructural and cytochemical evidence is presented that halothane induced translocation of the surface coat into the vacuolar system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. The cell membrane was thrown into extraordinary lamellipodial extensions, which enabled the PIMs to interact with platelets within the narrow confines of the pulmonary capillaries. The relationship between PIMs and platelets developed into large platelet aggregates. Isoflurane and thiamylal sodium did not affect the circulating platelets, although the surface coat was translocated into the endolysosomes in both situations. Although isoflurane is a lipid-soluble inhalant anesthetic similar to halothane, it is subject to very little biotransformation after use and in the present model demonstrates no immune response.

Acid Phosphatase↗

PubMed1996

Differential effects of propofol, thiamylal and ketamine on the cricothyroid and posterior cricoarytenoid muscles of the canine larynx.

PURPOSE: To measure the electromyographic (EMG) responses of the phasic discharge in the cricothyroid (CT; a tensor muscle of the vocal folds) and the posterior cricoarytenoid (PCA; sole abductor muscle of the vocal folds) following intravenous infusion of propofol 1.0 mg.kg-1.min-1, thiamylal 1.0 mg.kg-1.min-1, or ketamine 0.5 mg.kg-1.min-1 for five minutes. DESIGN: Prospective, nonrandomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Fifteen mongrel dogs, including three groups of five animals in each group. INTERVENTIONS: Under 0.2-0.3% halothane and oxygen anesthesia with spontaneous ventilation, phasic EMG activities of the CT and PCA muscles were recorded in an identical manner after the administration of each drug. MEASUREMENTS AND MAIN RESULTS: Propofol infusion produced almost equal suppression of EMG activity of the CT and the PCA with time and three minutes after the start of infusion of propofol there was a significant depression of the phasic activities in the both muscles; EMG activity of the CT and the PCA was 33.8 +/- 21.2 and 36.6 +/- 22.9% (% of control, mean +/- SD) respectively P < 0.05). Thiamylal selectively reduced rhythmic discharges in the CT muscle during spontaneous breathing and significant depression of discharge in the CT muscle was observed three minutes after the drug (47.3 +/- 24.9%, P < 0.05). In contrast, both phasic EMG activities of the CT and the PCA were rhythmically active and the differential sensitivity between the CT and the PCA muscles was not observed after ketamine, even after ten minutes of administration. CONCLUSIONS: This study confirms a difference in sensitivity between the CT and the PCA muscles, demonstrating that the intrinsic laryngeal muscles do not behave similarly after the administration of conventional intravenous anaesthetic agents.

Anesthetics, Dissociative↗

PubMed1976

Inhibition by six somatostatin analogs of plasma growth hormone levels stimulated by thiamylal and morphine in the rat.

Administration of sodium thiamylal (50 mg/kg,i.p.) and morphine (3 mg/animal,s.c.) leads to high plasma levels of growth hormone (GH) with a maximum measured approximately 30 min after injection. When the same dose of morphine is administered 60 and 120 min later and small additional doses of thiamylal are injected to maintain the animals deeply anesthetized, constant high levels of plasma GH are maintained up to the last interval studied (3 h). This in vivo model has been used to evaluate the potency and duration of action of somatostatin and of six of its analogs by serial blood sampling of animals bearing a cannula inserted into the right superior vena cava. A significant inhibitory effect of somatostatin (45% inhibition) is observed 15 min after a s.c. injection of 1 mug of the peptide while a near maximal effect (90-95% inhibition) is found at a dose of 25 mug. Both the degree of inhibition and duration of action of somatostatin are dose-dependent. Inhibitory activities equivalent to 1-250 mug of somatostatin can be measured with the model described. [Tyr1] somatostatin, [D-Ala1]somatostatin, [N-acetyl-Cys3] somatostatin and [N-benzoyl-Cys3] somatostatin have activities indistinguishable from somatostatin itself while [D-Lys4] somatostatin and [des-amino1, des-carboxy14] somatostatin have approximately 10% the activity of the natural hypothalamic peptide. This in vivo model offers advantageous characteristics of precision and reproducibility for the evaluation of potency of inhibitors of GH release.

Animals↗

PubMed1988

Toxicological analysis of thiamylal in biological materials by gas chromatography/mass spectrometry.

A reliable and sensitive method to analyze thiamylal in biological materials was developed, using gas chromatography/mass spectrometry (GC/MS). A quantitative determination was made by use of mass fragmentography with the lower detection limit of 0.01 microgram/g. Thiopental was used as the internal standard. Distribution of the drug in the blood and body tissues of rats was examined. The method was then used to detect thiamylal in tissues from an autopsied patient and concentration of this drug in the body materials was evaluated, from medico-legal aspects.

Adipose Tissue↗

PubMed1988

Comparison of propofol and thiamylal for induction and maintenance of anaesthesia for outpatient surgery.

In an open, randomized study we have compared the safety and efficacy of propofol with thiamylal for induction and maintenance of anaesthesia supplemented by nitrous oxide in elective termination of pregnancy. Induction of anaesthesia was achieved with either propofol 2.5 mg kg-1 or thiamylal 4.0 mg kg-1 followed by maintenance with 70% nitrous oxide in oxygen and repeat boluses of 25% of the induction dose i.v. as indicated clinically. Both drugs induced and maintained anaesthesia reliably, with some minor differences. Recovery from propofol was significantly more rapid. The patients in the propofol group were alert and orientated early in the postoperative period, with less nausea or vomiting. Propofol has properties that are of particular benefit in anaesthesia for ambulatory surgery.

Abortion, Induced↗

PubMed1992

Flumazenil does not antagonize halothane, thiamylal or propofol anaesthesia in rats.

We have studied the effects of flumazenil on sleep time and EEG in rats anaesthetized with 1.5% halothane, propofol 20 mg kg-1, thiamylal 30 mg kg-1, or combinations of diazepam 5 mg kg-1 and anaesthetic agents. We also studied the effects of flumazenil 0.3, 3 and 30 mg kg-1 on behaviour and EEG. Flumazenil 0.3 and 3 mg kg-1 alone had no effect on behaviour or EEG, but flumazenil 30 mg kg-1 had depressive effects similar to those of diazepam on behaviour and EEG. Flumazenil 0.3, 3 and 30 mg kg-1 i.v., antagonized the effects of diazepam 10 mg kg-1 i.v. on behaviour and EEG. Flumazenil had no antagonistic effect on sleep time induced by anaesthetic agents, but flumazenil 30 mg kg-1 potentiated propofol-induced anaesthesia. Flumazenil did not affect anaesthesia-induced EEG changes. Diazepam 5 mg kg-1 potentiated anaesthesia. Flumazenil antagonism of diazepam potentiation varied with anaesthetic agent: flumazenil 0.3 mg kg-1 antagonized diazepam action in halothane anaesthesia, but 30 mg kg-1 was required in propofol anaesthesia; this large dose was insufficient in thiamylal anaesthesia.

Anesthesia, Inhalation↗

PubMed1989

Interactions between chloramphenicol, acepromazine, phenylbutazone, rifampin and thiamylal in the horse.

The potential for interactions between chloramphenicol, phenylbutazone, acepromazine and thiamylal and chloramphenicol, rifampin, and phenylbutazone were evaluated in two groups of experiments. In the first, five horses were given thiamylal intravenously (iv) (6.6 mg/kg) after pretreatment with acepromazine, and the time of recumbency was determined. Administration of chloramphenicol iv (25 mg/kg) 1 h prior to anaesthesia significantly lengthened the recumbency time from 21.8 +/- 4.8 mins to 36.0 +/- 8.3 mins. There was an apparent but not statistically significant decrease in recumbency time when phenylbutazone (4.4 mg/kg) was administered iv daily for 4 days prior to anaesthesia. In the second series of experiments, phenylbutazone (4.4 mg/kg), chloramphenicol (25 mg/kg) and rifampin (10 mg/kg) were administered in various sequences to five different horses. Chloramphenicol pretreatment produced a significant decrease in the elimination rate and rifampin a significant increase in the elimination rate of phenylbutazone. The half-life of elimination of phenylbutazone alone was about 4 h. Following four days pretreatment with rifampin it was approximately 2.7 h, it was approximately 5.6 h and 9.5 h, respectively, when chloramphenicol was administered in one dose 1 h before or two doses 12 h and 1 h before phenylbutazone.

Acepromazine↗

PubMed1984

Effect of thiamylal on the response to carotid occlusion and mild hemorrhage in rabbits.

The effects of anesthesia (thiamylal, 30 mg/kg) on steady-state mean arterial pressure responses to bilateral carotid occlusion (BCO) and rapid 8% hemorrhage were studied in 11 rabbits chronically instrumented with an arterial pressure catheter and balloon occluders on the common carotid arteries. The BCO was repeated in the conscious and anesthetized states both before and after transecting the aortic nerves (AN). With the AN intact, the BCO response was an increase in mean systemic arterial pressure of 23.6 +/- 2.1 (SE) mmHg in the conscious state and 24.7 +/- 1.2 in the anesthetized state. With the AN cut (AN) BCO response was 46.2 +/- 1.7 mmHg in conscious state and 45.7 +/- 2.6 in anesthetized state. There was no significant difference in BCO response between conscious and anesthetized states, whether the AN was present or absent. The hemorrhage experiment was repeated on separate days under various conditions, including carotid sinus reflex elimination (CS). With AN intact the posthemorrhage fall in mean arterial pressure (delta MAPh) was 3.2 +/- 0.6 mmHg in the conscious state. Under anesthesia, delta MAPh was 3.4 +/- 0.6 mmHg in the AN intact condition, 7.3 +/- 0.9 in AN, and 34.5 +/- 6.8 in (AN + CS). There was no significant difference in delta MAP between the conscious and anesthetized states under the intact AN condition. We conclude that, in the rabbit, thiamylal anesthesia has little effect on the BCO response and the restoration of arterial pressure after a mild hemorrhage.

Anesthesia, General↗

PubMedDate not supplied

Circulatory changes during anesthetic induction: impact of d-tubocurarine pretreatment, thiamylal, succinylcholine, laryngoscopy, and tracheal lidocaine.

Circulatory changes after IV d-tubocurarine (3 mg), thiamylal (4 mg/kg) plus succinylcholine (2 mg/kg) and followed by direct laryngoscopy with or without intratracheal lidocaine spray (2 mg/kg) just before endotracheal intubation (EI), were measured in 40 adult patients. Pretreatment with d-tubocurarine did not alter mean arterial pressure (MAP), heart rate (HR), or central venous pressure (CVP). One minute after thiamylal-succinylcholine and just before laryngoscopy, MAP was 15 torr less than the awake value (p less than 0.05) and HR was 13 beats/min greater than the awake value (p less than 0.05). Laryngoscopy and EI elevated MAP above awake levels and further increased HR in all patients. The magnitude of these responses immediately following EI was not altered by tracheal lidocaine. However, the pressor and HR changes following EI were more transient when tracheal lidocaine was used (20 patients) and these patients were more likely to tolerate the tracheal tube without immediate additional anesthesia. The incidence of ventricular dysrhythmias was not altered by tracheal lidocaine. Compared with awake values, the cardiac index did not change significantly following intubation but stroke volume was decreased (p less than 0.05), with or without tracheal lidocaine.

Adult↗