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Biomedical subjects

C R Bainton

Publications and source records attributed to C R Bainton.

36 records · Page 2Linked to original sources
PubMed1981

Mice tolerant to nitrous oxide are not tolerant to barbiturates.

Mice continuously exposed to 50% nitrous oxide for 2 weeks or more become tolerant to nitrous oxide, as measured by an 8% to 19% increase in their nitrous oxide ED50 (the dose required to abolish the righting reflex in 50% of the animals). Control mice tolerant to nitrous oxide were given intraperitoneal injections of secobarbital (50 mg/kg), phenobarbital (120 mg/kg), or pentobarbital (55 or 65 mg/kg). Sleep onset times, sleep times, and serum levels of barbiturates upon awakening did not differ between the two groups. These results suggest that nitrous oxide and barbiturates do not share a common mechanism of action.

Anesthesia, Inhalation↗
PubMed1981

Adrenergic response to morphine-diazepam anesthesia for myocardial revascularization.

To evaluate sympathetic nervous system activity during narcotic-hypnotic "balanced anesthesia," plasma catecholamine concentrations and hemodynamic variables were assessed simultaneously in 10 men with coronary artery disease who received, sequentially, morphine sulfate, 3 mg/kg IV, and diazepam, 0.25 to 0.35 mg/kg IV, for myocardial revascularization surgery. Infusion or morphine sulfate rates of 5 to 10 mg/min significantly decreased both mean systemic arterial pressure (from 98 plus or minus 6 to 84 plus or minus 5 torr, p less than 0.01) and systemic vascular resistance index (from 38 plus or minus 3 to 30 plus or minus 5 units, p less than 0.05). These changes were associated with 2-fold increases in plasma norepinephrine levels (from 246 plus or minus 31 to 488 plus or minus 85 pg/ml, p less than 0.01) and 4-fold increases in plasma epinephrine levels (from 129 plus or minus 20 to 570 plus or minus 182 pg/ml, p less than 0.01). Addition of diazepam further decreased systemic arterial pressure (from 84 plus or minus 5 to 73 plus or minus 3 torr, p less than 0.01) and was associated with significant decreases in cardiac and stroke volume indices when compared with values obtained after morphine sulfate alone. Plasma concentrations of both norepinephrine and epinephrine also declined in association with these hemodynamic changes. Following skin incision, systemic arterial pressure and systemic vascular resistance index increased, the latter to the highest measured value (50 units). Norepinephrine concentrations increased significantly more than it had after morphine-diazepam anesthesia (321 plus or minus 63 pg/ml). It was concluded that the administration oif high dose morphine anesthesia acutely activates the sympathoadrenal system while producing peripheral vasodilation. Diazepam, when used following morphine to assure loss of consciousness, exacerbates the hypotensive effects produced by morphine and is associated with decreased levels of plasma catecholamines. Surgical incision produces significant peripheral sympathetic activation and increases vascular resistance during morphine-diazepam anesthesia.

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↗