Biomedical subjects

E L Coates

Publications and source records attributed to E L Coates.

7 recordsLinked to original sources

PubMed1991

A decrease in nasal CO2 stimulates breathing in the tegu lizard.

Tegu lizards decrease ventilatory frequency (f) when constant CO2, as low as 0.4%, is delivered to the nasal cavities. In contrast, CO2, as high as 6%, pulsed into the nasal cavities during the expiratory phase of the breathing cycle does not alter f. The purpose of the present study was to investigate further the effect of nasal CO2 pattern on f in tegu lizards. Specifically, we tested: (1) whether f was affected by CO2 delivered to the nasal cavities during the inspiratory phase of the breathing cycle, and (2) whether pulsed decreases in nasal CO2 from 4% to 2% and from 4% to 0% would remove the f inhibition caused by constant nasal CO2. Ventilation was measured using a pneumotachograph and pressure transducer in-line with an endotracheal T-tube inserted through the glottis. CO2 was delivered to the nasal cavities through small tubes inserted into the external nares. Ventilatory frequency was not significantly altered when 4% CO2 was pulsed into the nasal cavities during inspiration. Dropping the CO2 in the nasal cavities from 4% to 0% at either 15 cycles/min (0.25 Hz) or for one cycle stimulated breathing. There was no significant difference between the f response to a drop in CO2 from 4% to 0% and that to a drop in CO2 from 4% to 2%. The failure to link the phasic CO2 ventilatory response to a phase in the respiratory cycle indicates that the nasal CO2 receptors do not participate in the breath-by-breath regulation of breathing in these lizards. The observation that small decreases in nasal CO2 abolished the f inhibition caused by constant nasal CO2 provides further evidence for the ability of the nasal CO2 receptors to distinguish between pulsed and constant CO2.

Animals↗

PubMed1991

The influence of venous CO2 on ventilation in garter snakes.

Garter snakes were used to study the effects of venous CO2 loading using the skin as an exchanger. The gaseous environment surrounding the snake's body was isolated by placing the body in a plethysmograph with the head out. While the animal breathed room air, the carbon dioxide concentration within the plethysmograph was varied between 0 and 80%. Room air was drawn through a funnel placed over the snake's head, thus collecting the exhaled gases, and this gas was analyzed by O2 and CO2 analyzers. The descending aorta was cannulated to measure blood gases. Expired CO2 flow rose linearly with increasing cutaneous CO2. Ventilation increased 3.5-fold at 80% cutaneous CO2 compared with no cutaneous CO2 load. Neither the mean CO2 concentration in exhaled air nor arterial PCO2 changed when the snake was exposed to high levels of CO2 at the skin. Thus ventilation increased in proportion to the CO2 load, and was not driven by arterial hypercapnia. Bilateral vagotomy eliminated arterial CO2 homeostasis during cutaneous CO2 loading, and ventilation increased with increasing arterial PCO2. Therefore, these snakes respond to extra-arterial elevations in CO2 or to a changing CO2 signal. Furthermore, receptors responsible for the increase in ventilation when venous CO2 is elevated have neurons in the vagus nerves.

Animals↗

PubMed1991

Acetazolamide on the ventral medulla of the cat increases phrenic output and delays the ventilatory response to CO2.

1. Acetazolamide (0.1 mM) applied to the surface of the rostral ventrolateral medulla or microinjected beneath the medullary surface in chloralose-urethane-anaesthetized, vagotomized, carotid-denervated, paralysed, servo-ventilated cats produced a long-lasting increase in integrated phrenic nerve activity. 2. Extracellular pH measured beneath the rostral ventrolateral medulla exhibited a long-lasting decrease after surface acetazolamide but was not a good predictor, in each individual animal, of changes in phrenic activity. 3. Medullary carbonic anhydrase inhibition reduced the slope and the half-time of the phrenic response to rapid step CO2 increases. Conversely, acetazolamide did not affect the phrenic response to steady-state CO2 increases. 4. These data indicate that localized inhibition of medullary carbonic anhydrase causes a centrally mediated increase in ventilation that we attribute to medullary tissue hypercapnia and acidosis. In addition, these data indicate that medullary carbonic anhydrase may play a role in central CO2 chemotransduction.

Acetazolamide↗

PubMed1990

Olfactory receptor response to CO2 in bullfrogs.

In vivo electrophysiological recordings of olfactory receptor cells of the bullfrog (Rana catesbeiana) exhibit a receptor response to CO2 concentrations as low as 0.5%. The amplitude of the electroolfactogram (EOG) increased with an increase in the CO2 concentration delivered to the olfactory epithelium. Likewise, there was a significant increase in the decay time (time from 90 to 10% peak EOG amplitude) with an increase in CO2. The EOG rise time (time from 10 to 90% peak EOG amplitude) and the EOG response latency (time from beginning of CO2 pulse to beginning of EOG response) significantly decreased, whereas the plateau time (time from 90% rising phase to 90% falling phase of the peak EOG amplitude) was not significantly altered by an increase in CO2. These results indicate that low concentrations of CO2, below normal end expiratory CO2 concentrations, stimulate olfactory receptor cells. These results support our proposal that the ventilatory depression observed in response to upper airway CO2 in reptiles and amphibians is mediated by CO2-sensitive olfactory receptor cells.

Animals↗

PubMed1989

Breathing and upper airway CO2 in reptiles: role of the nasal and vomeronasal systems.

The ventilatory response of the garter snake, Thamnophis sirtalis, to 2% CO2 delivered to the upper airways (UA) was measured before and after the olfactory or vomeronasal nerves were transected. The UA (nasal cavities and mouth) were isolated from the gas source inspired into the lungs by inserting an endotracheal T tube into the glottis. CO2 was administered to the UA via a head chamber. The primary ventilatory response to UA CO2 was a significant decrease in ventilatory frequency (f) and minute ventilation. The decrease in f was caused by a significant increase in the pause duration. Tidal volume, expiratory duration, and inspiratory duration were not altered with UA CO2. The f response to UA CO2 was abolished with olfactory nerve transection, whereas vomeronasal nerve transection significantly increased the magnitude of the f depression. These results indicate that CO2-sensitive receptors are located in the nasal epithelium and that the olfactory nerves must be intact for the UA CO2 f response to be observed. In addition, the vomeronasal system appears to modulate the ventilatory response to UA CO2.

Animals↗

PubMed1989

Effect of upper airway CO2 pattern on ventilatory frequency in tegu lizards.

Nasal CO2-sensitive receptors are reported to depress ventilatory frequency in several reptilian species in response to constant low levels of inspired CO2. The purpose of this study was to determine the influence of phasic patterns of CO2 in the upper airways on ventilation. Awake lizards (Tupinambis nigropunctatus) breathed through an endotracheal tube from an isolated gas source. A second gas mixture was forced at constant flow into the external nares. A concentration of 4% CO2 was intermittently pulsed through the nares in a square-wave pattern with a frequency of 60, 12, 6, 4.2, 1.8, and 0.6 cycles/min. Concentrations of 2, 3, 4, and 6% CO2 were also pulsed through the nares at 12 cycles/min and compared with sustained levels of 1, 1.5, 2, and 3%. Additionally, 0 or 3% CO2 was forced through the upper airways with a servo system designed to mimic normal ventilatory flow and gas concentrations. No changes in breathing pattern were noted during any of the pulsing protocols, although a significant breathing frequency depression was present with sustained levels of CO2 of comparable mean concentrations. We conclude that ventilatory control is selectively responsive to sustained levels of environmental CO2 but not to phasic changes in upper airway CO2 concentration.

Animals↗

PubMed1987

Upper airway CO2 receptors in tegu lizards: localization and ventilatory sensitivity.

1. Tidal volume, end-tidal CO2, and ventilatory frequency in Tupinambis nigropunctatus were measured in response to CO2 (1-4%) delivered to either the mouth or nares. Additionally, the sensitivity of the ventilatory response to nasal CO2 was evaluated at CO2 concentrations less than 1%. The ventilatory parameters were also measured in response to CO2 (1-4%) delivered to the nares after the olfactory peduncle was transected. 2. It was found that (0.4-4%) nasal CO2 depressed ventilatory frequency by 9% to 83% respectively, while tidal volume was not significantly altered. CO2 (1-4%) delivered to the mouth produced no apparent changes in any of the ventilatory parameters. Following transection of the olfactory peduncle, nasal CO2 was ineffective in producing any change in ventilatory frequency or depth. 3. These findings indicate that CO2-sensitive receptors are located in either the nasal or vomeronasal membranes of tegu lizards and that the olfactory peduncle must be intact for these receptors to affect ventilatory changes in response to elevated CO2 concentrations. The receptors are capable of mediating a ventilatory response to CO2 concentrations lower than those found in either expired air or in confined spaces such as occupied burrows. 4. The discrepancies in the ventilatory responses of lizards and snakes to inspired CO2 reported in past experiments may be partially explained by the presence of nasal or vomeronasal CO2-sensitive receptors.

Administration, Intranasal↗