Ventilatory compensation for lactacidosis in ponies: role of carotid chemoreceptors and lung afferents.

This study examines how the introduction of lactic acid into the blood stream affecting breathing rates and acid concentration in ponies, specifically focusing on the roles of carotid chemoreceptors and lung afferents.

Methodology

• The researchers observed changes in arterial PCO2 (Partial pressure of carbon dioxide) and pulmonary ventilation (VE) in three groups of ponies: normal, carotid chemoreceptor-denervated, and hilar nerve-denervated ponies.
• The ponies were subjected to intravenous lactic acid infusion at rest and during treadmill exercise with two levels of difficulty. Lactic acid infusion took place at different rates under different conditions.

Results

• The infusion of lactic acid produced a linear increase in arterial acidity throughout the 10-minute infusion in each condition and pony group, with an average increase of about 20 nmol/l (0.2 pH units).
• The pattern of PaCO2 (an indicator of carbon dioxide in the blood) was generally biphasic under most conditions. This means that, initially, PaCO2 increased in the first two minutes, then at later stage, between 2 and 10 minutes, PaCO2 decreased. This happened both at rest and during exercise in all groups.
• During the first 2 minutes, the PaCO2 increased by about 2 Torr in all ponies except normal ponies during moderate exercise.
• Between 2 and 10 minutes of infusion, there was a significant decrease in PaCO2 by 5 Torr in all groups, whether the ponies were at rest or exercising.
• Also, VE (breathing rate) increased between 15-30 seconds and 2 minutes during the infusion, but there was little change between 2 and 10 minutes of infusion, regardless of whether the ponies were at rest or exercising.

Conclusion

• The study concludes that lactacidosis, the increased level of lactic acid in the blood, does augment breathing rates both at rest and during submaximal exercise in ponies.