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The effects of prolonged static inflation on the discharge characteristics of pulmonary stretch receptors in turtles McLean, Heather Ann

Abstract

Both the tonic and phasic discharge characteristics of single slowly adapting pulmonary stretch receptors (SARs) were examined before and after a one hour period of maintained lung volume in freshwater turtles, Pseudemvs scripta and Chrysemys picta. Lung volume was maintained at either resting volume (airway pressure = 0 cmH20) or at an elevated lung volume (airway pressure = 10 cmH20). Pressure inflations were performed with both air and 5% C02 in air. Two populations of receptors were recorded from: low threshold SARs (those that exhibited tonic discharge at resting lung volume) and high threshold SARs (those that did not exhibit tonic discharge at resting lung volume). During the one hour period of maintained lung inflation with air, low and high threshold SARs adapted up to 80% and 30% respectively. Following this period, the peak discharge rate attained with step inflation was unchanged in both groups. The low threshold SARs demonstrated a decrease in the phasic component of discharge associated with dynamic lung inflations following one hour of maintained lung inflation with air but the high threshold receptors did not. During one hour of maintained lung inflation with 5% C02 in air, low and high threshold SARs adapted more than they did during maintained lung inflation with air. Furthermore, there was an overall decrease in both the peak discharge attained with static lung inflation and the phasic responses to dynamic lung infaltions following maintained lung inflation with 5% C02 in both groups of receptors. During the one hour period of maintained lung inflation with air, there were significant increases in both lung gas and blood gas levels of C02, decreases in arterial pH and decreases in lung gas oxygen levels. The decreases in tonic and phasic components of SAR discharge seen during the one hour period of maintained lung inflation with air are due in part to an accumulation of metabolic (lung gas) C02.

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