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CSF acidosis augments ventilation through cholinergic mechanisms.
M D Burton1, D C Johnson, H Kazemi
1Medical Services (Pulmonary Unit), Massachusetts General Hospital, Boston 02114.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1989
Summary
Acidic brain conditions stimulate ventilation via acetylcholine (ACh) acting on muscarinic receptors. Blocking these receptors with atropine (ATR) inhibits this ventilatory response.
Area of Science:
- Neuroscience
- Respiratory Physiology
- Acid-Base Balance
Background:
- Ventilation is modulated by the brain's extracellular fluid (ECF) acid-base status.
- The precise mechanisms by which CO2 and acidity affect neuronal firing and ventilation are not fully understood.
- Investigating the role of endogenous neurotransmitters in response to altered brain ECF pH is crucial.
Purpose of the Study:
- To investigate the ventilatory effects of acetylcholine (ACh) and acidic cerebrospinal fluid (CSF) in dogs.
- To determine if acidic brain ECF activates ventilation through muscarinic cholinergic pathways.
- To elucidate the role of ACh in central respiratory control during acid-base disturbances.
Main Methods:
- Ventriculocisternal perfusion (VCP) was employed in anesthetized, spontaneously breathing dogs.
- Control CSF (pH ~7.4), eucapnic acidic CSF (pH ~7.0), and hypercapnic acidic CSF (pH ~7.1) were perfused.
- The effects of acetylcholine (ACh) and atropine (ATR) on minute ventilation (VE) were assessed.
Main Results:
- ACh administration significantly increased minute ventilation (VE) by 53%.
- Both eucapnic and hypercapnic acidic CSF increased VE by 41% and 47%, respectively.
- These increases in VE were abolished in the presence of atropine, indicating a cholinergic mechanism.
Conclusions:
- Acidic brain ECF stimulates ventilation through muscarinic cholinergic pathways.
- Acetylcholine plays a significant role in the central augmentation of ventilation during CSF acidosis.
- The findings highlight the importance of cholinergic neurotransmission in respiratory regulation under altered acid-base conditions.