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Central vs. peripheral chemoreceptors in ventilatory stimulation by Hacetate
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1987
Summary
Acetate infusion in rabbits causes a larger decrease in cerebrospinal fluid bicarbonate and arterial carbon dioxide than other acids. This suggests acetate itself stimulates respiratory centers, independent of the carotid body.
Area of Science:
- Physiology
- Neuroscience
- Biochemistry
Background:
- Acid-base balance is critical for physiological function.
- Central and peripheral chemoreceptors regulate respiration.
- The role of acetate in modulating respiratory control is not fully understood.
Purpose of the Study:
- To investigate the differential effects of acetate versus other acids on respiratory control.
- To determine if acetate directly stimulates central chemoreceptors.
- To evaluate the contribution of the carotid body to acetate-induced ventilatory responses.
Main Methods:
- Intravenous and intracisternal infusions of acids (Hacetate, HCl, HNO3) in conscious rabbits.
- Measurement of cerebrospinal fluid (CSF) bicarbonate and arterial partial pressure of carbon dioxide (PaCO2).
- Comparison of responses in intact and chemodenervated rabbits.
Main Results:
- Hacetate infusion caused a greater decrease in CSF [HCO3-] and PaCO2 compared to HCl, HNO3, or Hacetate.
- Intracisternal HCl infusion, not Hacetate, decreased PaCO2, refuting direct central chemoreceptor stimulation by acetate.
- Hacetate induced a greater PaCO2 decrease than HCl even after carotid body denervation, indicating a non-carotid body mediated effect.
Conclusions:
- Acetate, not other acids, significantly stimulates ventilation.
- The ventilatory stimulation by Hacetate is independent of the carotid body.
- The hypothesis suggests nonionic diffusion of Hacetate into the brain or acetate replacing bicarbonate in CSF production affects central chemoreceptors.