Effects of potassium depletion on control of breathing in awake rats.
Possible mechanisms for the variable ventilatory response to metabolic acid-base disturbances have been examined in normal and K-depleted rats. Ventilatory measurements are correlated with CSF acid-base data. The ratios VE/VO2 and 1/PaCO2 are utilized as indices of alveolar ventilation. The log of these indices correlates closely with CSF [H+] independent of [K+] except at very low CSF [H+] where the change in log 1/PaCO2 and log VE/VO2 per change in CSF [H+] is much diminished in low-K rats. This finding suggests the presence of an additional stimulus to breathing in the low-K rat opposing the inhibitory effect of low CSF [H+]. Otherwise the chemical control of ventilation appears to be normal. However, low-K rats always breath with a low-flight-Vt pattern and occasionally with abnormal rhythms. The similarity of the low K breathing pattern to that reported in awake animals with vagotomy and pneumotaxic center (PC) lesions suggests that the altered breathing pattern in depletion involves vagal and/or PC pathways. The similarity of the low-K breathing pattern to that observed with reserpine administration together with the known relationships of K and catecholamine metabolism lead to the speculation that K depletion alters breathing via an effect on central catecholamine metabolism. However, other mechanisms involving changes in membrane excitability and intracellular pH in K depletion might also be involved.
D000137:Acid-Base Imbalance / Q000503:physiopathology*; D000138:Acidosis; D000471:Alkalosis; D000818:Animals; D002245:Carbon Dioxide; D005260:Female; D006859:Hydrogen / Q000134:cerebrospinal fluid; D000860:Hypoxia; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012119:Respiration; D013990:Tidal Volume
D002245:Carbon Dioxide; D006859:Hydrogen; D011188:Potassium