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C R Bainton

Publications and source records attributed to C R Bainton.

At least 19 recordsLinked to original sources
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↗
PubMed1979

The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones.

1. Extracellular micro-electrodes were used to measure the responses of expiratory bulbospinal neurones to CO2 in anaesthetized, paralyzed cats, ventilated with O2. Simultaneous measurements were made of phrenic nerve and intercostal nerve filament discharges. 2. Hypocapnia produced tonic activity in some of the expiratory neurones and in expiratory filaments but rendered the phrenic and inspiratory filaments silent. 3. A graded excitatory effect of CO2 on tonic activity of both the neurones and the filaments was seen which progressed smoothly and continuously to rhythmic activity as CO2 was increased and to zero as CO2 was decreased. 4. Increases in blood pressure produced effects which were opposite to those produced by CO2, and which had a faster time course. 5. The CO2 response curves of those units showing tonic activity were indistinguishable from the CO2 response curves of those which did not. 6. A mid line lesion in the medulla interrupted inspiratory activity, converting activity of expiratory bulbospinal neurones from periodic to ionic firing patterns. 7. Following such lesions the CO2 threshold for rhythmic excitation of medullary neurones was elevated and the slopes of their CO2 response curves were reduced. 8. These findings fully confirm the hypothesis put forward by Bainton, Kirkwood & Sears (1978b) that bulbospinal respiratory neurones convey both tonic and rhythmic excitation to spinal respiratory motoneurones and that the rhythmic excitation of expiratory muscles derives from a period inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.

Action Potentials↗
PubMed1978

On the transmission of the stimulating effects of carbon dioxide to the muscles of respiration.

1. Electromyography was used to measure the response of the diaphragm and intercostal muscles to CO2 in artificially ventilated decerebrate cats. 2. Hypocapnia produced tonic activity in either inspiratory or expiratory muscles or both, according to the preparation. 3. A graded effect of CO2 on both rhythmic and tonic activity was observed and for the latter this could be seen at as low as 10 torr PA,CO2. 4. In one human subject tonic firing of expiratory motoneurones was also induced by hypocapnia and this activity showed a graded increase with increasing (CO2. 5. A saggital incision of the medulla aimed at interrupting inspiratory bulbospinal axons abolished activity in inspiratory muscles and at eupnoeic levels of CO2 converted the activity of expiratory muscles from a periodic to a topic firing pattern. 6. Following such lesions the threshold for rhythmic excitation of expiratory muscles was elevated and this revealed that the graded effect of CO2 on tonic expiratory activity extends to as high as 60 torr. 7. The tonic activation of respiratory muscles in response to CO2 ceased after cervical cord transection or when the saggital incision in the medulla was extended caudally to the first cervical segment. 8. It is concluded that the CO2 dependent activation of spinal respiratory motoneurones is conveyed by bulbospinal axons which decussate in the vicinity of the obex and that this activation can be rhythmic or tonic. 9. It is suggested that the rhythmic excitation of expiratory muscles derives from a periodic inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.

Action Potentials↗
PubMed1978

Canine ventilation after acid-base infusions, exercise, and carotid body denervation.

We studied the effect of exercise and carotid body denervation on the ventilatory response which occurs following acute acid-base infusions. Studies were done in 6 dogs prepared with chronic tracheostomies and carotid loops. Ventilation (VE) and arterial pH were measured at rest and during exercise before and after infusions of lactic acid (70 meq), HCl (26 meq), NaHCO3 (45 and 90 meq), or normal saline alone (250 ml). The VE response to [H+] is expressed as 1.min-1/[H+] in nmol.kgH2O-1. Before carotid body denervation (CBD), the response was 0.1 l.min-1[H+] at rest, 1.2 1.min-1/[H+] during exercise. After CBD there was no ventilatory response to [H+] at rest or during exercise. We conclude that 1) Exercise potentiates the [H+] stimulus to breathing. 2) For small changes in arterial [H+], this exercise potentiation is a function of the carotid body. 3) Therefore, that exercise potentiates the carotid body response directly and/or the central projection of this input in the central nervous system. 4) Finally, since carotid body denervation eliminates only 7% (0.8 1.min-1) of ventilation at pH 7.35 in these dogs, that the effective threshold for this ventilatory response approximates a pH slightly greater than 7.35.

Acid-Base Imbalance↗
PubMed1977

Thermoregulatory responses to altering hypothalamic temperature in the harbor seal.

The rostral brainstem of the harbor seal Phoca vitulina was cooled and heated 33-41 degrees C while oxygen consumption and rectal, hypothalamic, flipper and dorsal skin temperatures were measured. These experiments were made on restrained seals at ambient temperatures -15 to 30 degrees C. Cooling the preoptic and hypothalamic (POH) tissue increased oxygen consumption in a way that could be approximated by a linear regression line with slope and threshold temperature at which the metabolic rate was minimal. The slope of the regression line was a function of ambient temperature and rectal temperature. At each ambient temperature, the slope was significantly higher for lower rectal temperature. At all rectal temperatures, the slope was significantly higher for lower ambient temperature. The threshold hypothalamic temperatures did not very consistently or significantly with either rectal temperature or ambient temperature. These results on the harbor seal are explicable by suggesting that the thermal-sensitive and reference neurons in the POH which regulate body temperature are inhibited equally by extrahypothalamic cold transducing neural elements.

Animals↗