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Biomedical subjects

G O Ballam

Publications and source records attributed to G O Ballam.

8 recordsLinked to original sources

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

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

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

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

Effect of venous (gut) CO2 loading on intrapulmonary gas fractions and ventilation in the tegu lizard.

Studies were conducted to determine regional pulmonary gas concentrations in the tegu lizard lung. Additionally, changes in pulmonary gas concentrations and ventilatory patterns caused by elevating venous levels of CO2 by gut infusion were measured. It was found that significant stratification of lung gases was present in the tegu and that dynamic fluctuations of CO2 concentration varied throughout the length of the lung. Mean FCO2 was greater and FO2 less in the posterior regions of the lung. In the posterior regions gas concentrations remained nearly constant, whereas in the anterior regions large swings were observed with each breath. In the most anterior sections of the lung near the bronchi, CO2 and O2 concentrations approached atmospheric levels during inspiration and posterior lung levels during expiration. During gut loading of CO2, the rate of rise of CO2 during the breathing pause increased. The mean level of CO2 also increased. Breathing rate and tidal volume increased to produce a doubling of VE. These results indicate that the method of introduction of CO2 into the tegu respiratory system determines the ventilatory response. If the CO2 is introduced into the venous blood a dramatic increase in ventilation is observed. If the CO2 is introduced into the inspired air a significant decrease in ventilation is produced. The changes in pulmonary CO2 environment caused by inspiratory CO2 loading are different from those caused by venous CO2 loading. We hypothesize that the differences in pulmonary CO2 environment caused by either inspiratory CO2 loading or fluctuations in venous CO2 concentration act differently on the IPC. The differing response of the IPC to the two methods of CO2 loading is the cause of the opposite ventilatory response seen during either venous or inspiratory loading.

Animals

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

Breathing response of the tegu lizard to 1-4% CO2 in the mouth and nose or inspired into the lungs.

This study investigated the influence on ventilation of elevated CO2 in the nasal and buccal cavities (NaBuCO2) vs the effect of elevated CO2 levels inspired into the lungs (LuCO2). Separate gas sources were used to independently alter NaBuCO2 and LuCO2. As little as 1% NaBuCO2 or LuCO2 significantly increased the pause duration between the active expiratory-inspiratory cycles. Elevated NaBuCO2 caused minor changes in tidal volume, mean inspiratory and expiratory flow, and inspiratory and expiratory durations with a significant reduction in total ventilation. Elevated LuCO2 had little effect on inspiratory or expiratory durations but unlike CO2 in the upper airways, significantly increased tidal volume and mean inspiratory and expiratory flows. This study demonstrates that the increased pause duration seen in the tegu lizard to elevated environmental CO2 is due to a receptor response in the buccal or nasal cavities and also to elevated CO2 concentrations inspired into the lungs. Sensitivity of the ventilatory responses to CO2 in the upper airways is well within a physiologically relevant range.

Animals

Effect of sinusoidal forcing of ventilatory volume on avian breathing frequency.

Awake chickens were unidirectionally ventilated at 3.6 l . min-1 with 3.2-4.8% CO2 in air. The air sacs on each side were made confluent and implanted with exit tubes connected to the following three devices: 1) a system of constant-flow generators which remove air at exactly the same rate that it entered the trachea, allowing no port for spontaneous volume changes; 2) a sinusoidal pump to force volume changes in the chicken; and 3) a pressure transducer to record air sac pressure, which reflected the sum of two pressure components, the passive pressure changes created by the pump and the active pressure changes due to breathing efforts. Over a range of pump frequencies, the amplitude of measured air sac pressure changes varied inversely with frequency. Above and below this range, pressure showed a beat pattern, indicating a difference in the frequencies of the two pressure components. Within the range lacking a beat pattern, breathing movements and the pump stroke had the same frequency. This range was greater at increased stroke volume. Breathing efforts worked with the pump at the high end of the range and against the pump at the low end. These findings show further evidence of the presence of a response to volume forcing and fit a previously described volume threshold model.

Animals