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C R Bainton

Publications and source records attributed to C R Bainton.

At least 19 recordsLinked to original sources
PubMed1994

Concentration dependence of lidocaine-induced irreversible conduction loss in frog nerve.

BACKGROUND: Concentration is a causal factor in local anesthetic nerve toxicity. Therefore, it is essential to define a concentration below which injury does not occur. We explored the relation of lidocaine concentration and nonreversible block after drug washout in frog sciatic nerve. METHODS: Frog sciatic nerve was mounted in sucrose-gap or extracellular recording chambers. The observed compound action potential in response to a supramaximal stimulus was used as a measure of nonreversible block after applying lidocaine in a range of concentrations (0.5-200 mM for 15 min) and then washing off (for as long as 180 min). RESULTS: Lidocaine causes a nonreversible block after washout that begins at concentrations as low as 40 mM and increases in a graded fashion with increasing concentrations to complete ablation of the compound action potential at 80 mM (approximately 2%). Extended storage of frogs (5 weeks) at 4 degrees C makes the nerves more resistant to the effects of lidocaine. The presence of nifedipine (10(-5) M), an L-type calcium-channel blocker, makes the nerves more resistant to lidocaine as well. CONCLUSIONS: Lidocaine induces a nonreversible loss of impulse activity in frog nerve in a progressive fashion with increasing drug concentration, beginning at 40 mM (approximately 1.0%). The range of lidocaine that produces such changes in mammalian nerve awaits determination.

Action Potentials↗
PubMed1994

A pressurized injection/suction system for ventilation in the presence of complete airway obstruction.

OBJECTIVE: To describe the design and ventilatory characteristics of a new mode of ventilation (pressurized injection/suction ventilation). DESIGN: Descriptive and analytical laboratory study. SETTING: Laboratory study. SUBJECTS: Simulated lung model and dogs. INTERVENTIONS: We tested the ability to maintain ventilation through a 2.5-mm internal diameter ventilating stylet in the setting of simulated complete airway occlusion. A microprocessor-controlled ventilator mode was used wherein injection of oxygen under high pressure (flow rate 95 L/min) alternates with suction of expired gas (flow rate 18 L/min) through the ventilating stylet. MEASUREMENTS AND MAIN RESULTS: In a lung model, we achieved a maximum minute ventilation of 12.9 L/min. In two dogs, we maintained stable oxygenation (mean PaO2 603 +/- 47 torr [80.4 +/- 6.3 kPa]) and ventilation (mean PaCO2 19 +/- 3 torr [2.5 +/- 0.4 kPa]) for 15 mins at maximum minute ventilation settings. No clinically important deleterious effects on the tracheal mucosa were observed. The ventilator system's safety-abort feature prevented overinflation or excessive deflation of the dogs' lungs in every test of simulated malfunction of the pressure-monitoring mechanism. CONCLUSIONS: Pressurized injection/suction ventilation can maintain adequate gas exchange in an animal model with near-complete airway obstruction. Further work is needed to develop the safety and clinical applications of pressurized injection/suction ventilation in the management of patients with near-complete airway occlusion.

Airway Obstruction↗
PubMed1994

Cricothyrotomy.

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Airway Obstruction↗
PubMed1988

Surface-induced hypothermia: effects on coronary blood flow autoregulation and vascular reserve.

Surface-induced hypothermia has been shown to exert a protective effect in canine models of myocardial infarction. However, its effects on coronary blood flow (CBF) autoregulation and coronary vascular reserve (CVR) have not been investigated. The effects of mild (32 degrees C) and moderate (27 degrees C) hypothermia on CBF autoregulation and CVR (at 60 mm Hg diastolic pressure) were studied using a chronically instrumented canine preparation. Coronary artery pressure-flow relations were obtained over a wide range of coronary diastolic pressures (10 to 106 mm Hg) with autoregulation intact and during adenosine-induced maximal coronary conductance (MCC) at 37, 32, 27 degrees C (n = 7 dogs), and after rewarming (n = 5 dogs). Halothane (1 MAC end-tidal concentration, temperature adjusted) was the anesthetic. Autoregulation remained intact during hypothermia. CBF remained relatively constant between diastolic pressures of 43.1 +/- 9.0 and 84.0 +/- 14.4 mm Hg (mean +/- SD). No significant differences were observed between temperatures in the autoregulated pressure range. CBF correlated well with myocardial oxygen consumption (MVO2) (r2 = 0.81, P less than 0.0001). There were no significant changes in MVO2, CBF, MCC, or CVR at 32 degrees C. At 27 degrees C, MVO2 (3.65 +/- 1.3 at 37 degrees C vs 2.35 +/- 1.4 ml O2.min-1 at 27 degrees C), autoregulated CBF (34.9 +/- 15.1 vs 19.5 +/- 10.8 ml.min-1), the slope of the line of MCC (4.31 +/- 0.7 vs 2.7 +/- 0.4 ml.mm-1.min-1), and CVR (147.1 +/- 24.6 vs 90.1 +/- 27.3 ml.min-1) were all less than control (P less than 0.05). After rewarming to 37 degrees C, no significant changes from control were noted. The authors conclude that coronary autoregulation remains intact at both 32 and 27 degrees C, although MCC and CVR are significantly decreased at 27 degrees C.

Animals↗
PubMed1988

Mechanism of age-related and nitrous oxide-associated anesthetic sensitivity: the role of brain catecholamines.

To provide a neurochemical basis for differences in their anesthetic requirements, the authors examined mice selectively bred for resistance (HI) and susceptibility (LO) to nitrous oxide anesthesia for brain levels of catecholamines. Concentrations of norepinephrine and dopamine in whole brain were 26% and 13% higher (P less than 0.001), respectively, in HI mice than in LO mice. Whole-brain levels of 3,4-dihydroxyphenylacetic acid, a major metabolite of dopamine, were the same for both HI and LO groups of mice. The authors then analyzed portions of the HI and LO mice brains for concentrations of norepinephrine and dopamine. A significant correlation was found between norepinephrine content in the medulla and nitrous oxide requirement. In other regions of the brain (cerebellum, cerebral cortex, hippocampus, pons, midbrain, hypothalamus), no significant differences in norepinephrine or dopamine levels could be detected. Differences in anesthetic requirements between resistant and susceptible mice decrease from 0.99 to 0.53 atm as they aged from 100 days to 600 days old, paralleling the decline in differences in norepinephrine levels in medulla oblongata between HI and LO mice from 1.6 to 0.73 ng/mg protein. Thus, the difference in anesthetic requirement between HI and LO mice may arise from alterations in catecholamine content in specific regions of the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

A new laryngoscope blade to overcome pharyngeal obstruction.

A new laryngoscope blade has been designed for emergency visualization of the pharynx and larynx when the pharyngeal space is restricted. The blade incorporates a 7-cm tube in the distal portion and an intraluminal light source protected from obstruction. It attaches to standard battery-powered light handles, making it practical for emergency use. The new blade has been tested on dogs and used successfully in 12 patients with edematous pharynges and in one patient with a bleeding pharyngeal tumor, where standard non-tubular blades failed to produce a view of the larynx.

Airway Obstruction↗
PubMed1986

Reflex prolongation of stage I of expiration.

Experiments were performed on anesthetized cats to test the theory that the interval between phrenic bursts is comprised of two phases, stage I and stage II of expiration. Evidence that these represent two separate neural phases of the central respiratory rhythm was provided by the extent to which stage duration is controlled individually when tested by superior laryngeal, vagus and carotid sinus nerve stimulation. Membrane potential trajectories of bulbar postinspiratory neurons were used to identify the timing of respiratory phases. Stimulation of the superior laryngeal, vagus and carotid sinus nerves during stage I of expiration prolonged the period of depolarization in postinspiratory neurons without significantly changing the durations of either stage II expiratory or inspiratory inhibition, indicating a fairly selective prolongation of the first stage of expiration. Changes in subglottic pressure, insufflation of smoke into the upper airway, application of water to the larynx or rapid inflation of the lungs produced similar effects. Sustained tetanic stimulation of superior laryngeal and vagus nerves arrested the respiratory rhythm in stage I of expiration. Membrane potentials in postinspiratory, inspiratory and expiratory neurons were indicative of a prolonged postinspiratory period. Thus, such an arrhythmia can be described as a postinspiratory apneic state of the central oscillator. The effects of carotid sinus nerve stimulation reversed when the stimulus was applied during stage II expiration. This was accompanied by corresponding changes in the membrane potential trajectories in postinspiratory neurons. The results manifest a ternary central respiratory cycle with two individually controlled phases occurring between inspiratory bursts.

Animals↗
PubMed1985

Respiratory modulation of sympathetic activity.

Sympathetic activity recorded from cardiac and renal nerves was correlated with phrenic and internal intercostal nerve activity under normocapnea and hypercapnea. Cats were anesthetized with halothane for surgery switching to chloralose for recording. Both vagal and carotid sinus nerves were cut, animals were paralyzed and artificially ventilated. We found that sympathetic activity followed the rhythmic pattern of phrenic nerve discharge fairly closely except in two important respects: first, sympathetic activity was significantly depressed during early inspiration and second, it reached a minimum during post inspiration while phrenic activity was decaying but still active. These effects were accentuated when PACO2 was raised. In one cat early inspiratory depression was the only manifestation of respiratory modulation of sympathetic activity superimposed on an otherwise tonic pattern. In 4 cats sympathetic activity increased in an augmenting fashion in parallel with the augmenting discharge of expiratory alpha motoneurones. We suggest that respiratory-related, excitatory and inhibitory inputs modulate sympathetic activity at the brainstem level. Inspiratory and possibly expiratory interneurones may be the source of activation, and inhibitory inputs may derive from early inspiratory and postinspiratory interneurones. The inhibitory effects may be the only manifestation of respiratory modulation during strong tonic drive of the sympathetic activity.

Animals↗
PubMed1984

Potencies of barbiturates in mice selectively bred for resistance or susceptibility to nitrous oxide anesthesia.

To test the possibility that mice selectively bred for resistance (HI mice) and susceptibility (LO mice) to nitrous oxide anesthesia have general differences in central nervous system sensitivity to other depressants, we examined the effects of four barbiturates in these two lines of mice. LO mice given intraperitoneal injections of barbital (275 mg/kg), hexobarbital (120 mg/kg), pentobarbital (65 mg/kg), or secobarbital (50 mg/kg) had significantly (16-46%) longer sleep times than HI mice. Concentrations of barbiturates were significantly (12-73%) greater in the serum and 3-55% greater in the brain on awakening in HI mice than in LO mice. The largest separations in potency between the HI and LO lines occurred with pentobarbital and hexobarbital and the smallest separations with barbital and secobarbital. We concluded that HI and LO mice do have a general resistance and susceptibility to barbiturates, but that the magnitude of the difference in central nervous system sensitivity between the two lines varies among barbiturates.

Anesthesia↗
PubMed1982

Treatment of myocardial ischemia with halothane or nitroprusside-propranolol.

An experimental animal model was used to compare the effect of the two drug interventions on myocardial ischemia. Elevation of the ST segment on epicardial electrocardiogram in response to temporary occlusion of the coronary artery was used as an index of ischemia. For multiple sites distal to the left-anterior descending coronary artery (LADCA), ST segments were obtained, measured, and totaled (sigma ST). The effects of halothane (1.1% end-tidal concentration) were compared with those of a combination of nitroprusside and propranolol. The combination was given in a dosage that produced values for systemic blood pressure, heart rate, and maximal positive left-ventricular dP/dt (LV dP/dt) that were similar to those produced by halothane. Control measurements were obtained during chloralose-urethrane anesthesia. Both drug interventions reduced systemic blood pressure, heart rate, and left-ventricular dP/dt similarly. Occlusion of the left-anterior descending coronary artery alone did not change any of these hemodynamic variables. Although both drug interventions reduced sigma ST, the reduction was statistically significantly greater with halothane than with nitroprusside-propranolol.

Animals↗