Document Detail


Autonomic control of bronchial circulation in awake sheep during rest and behaviour.
MedLine Citation:
PMID:  9406660     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. We tested the hypothesis that the pattern and the intensity of autonomic mechanisms causing vasoconstriction in the resting bronchial circulation of awake dogs also exists in awake sheep. It was also postulated that sighing behaviour and the associated bronchovascular dilatation induced by non-adrenergic, non-cholinergic (NANC) mechanisms observed in the dog exist in sheep. 2. Bronchial arterial blood flow to lower airways of both lungs of awake sheep was measured continuously using pulsed Doppler flow probes mounted on the bronchial artery at prior thoracotomy. 3. Cumulative and factorial analysis of responses to randomized combinations of autonomic alpha 1-, alpha 2-, beta 1- and beta 2-adrenoceptors and cholinoceptor autonomic blockade suggests that resting vasoconstrictor activity is less in sheep than in dogs. At normal aortic pressure, the autonomic activity of these receptor groups in the sheep lowers bronchial blood flow and conductance by 30%, whereas in the awake dog, the corresponding autonomic effect is 50%. 4. Tonic autonomic control of bronchial conductance can be partitioned in sheep to show significant and separate alpha- and beta-adrenoceptor vasoconstrictor activity at a ratio of 1.8:1, an effect normally offset by a weaker vasodilator alpha-/beta-adrenoceptor interaction. In contrast to the situation in awake dogs, cholinoceptors do not play a role in awake sheep. 5. Nitric oxide (NO) synthase inhibition in sheep using NG-nitro-L-arginine following blockade of alpha- and beta-adrenoceptors and cholinoceptors causes hypertension, but minor changes, if any, in pulmonary pressures or heart rate. Bronchial flow and conductance, however, fall from a higher resting conductance by approximately 50%, suggesting that, normally, resting bronchial flow conductance is dominated by strong tonic NO vasodilator effects that interact with weaker tonic autonomic vasoconstrictor effects. 6. Superimposed (respiratory) behaviours of sighing, sneezing and coughing, which involve negative swings in intrathoracic pressure and the movement of inspired air, evoke large active bronchovascular dilator effects. These appear to be largely NANC in origin and appear to be dependent, in part, on mechanisms associated with NO release. It is postulated that the C-fibre axon reflex using substance P, calcitonin gene-related peptide and neurokinin A may be involved. Vocalization and eructation do not evoke bronchovascular effects.
Authors:
S McIlveen; S White; G Parsons
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental pharmacology & physiology     Volume:  24     ISSN:  0305-1870     ISO Abbreviation:  Clin. Exp. Pharmacol. Physiol.     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-01-12     Completed Date:  1998-01-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0425076     Medline TA:  Clin Exp Pharmacol Physiol     Country:  AUSTRALIA    
Other Details:
Languages:  eng     Pagination:  940-7     Citation Subset:  IM    
Affiliation:
Division of Pulmonary and Critical Care Medicine, School of Medicine, University of California, Davis, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Antagonists / pharmacology
Adrenergic beta-Antagonists / pharmacology
Animals
Autonomic Nervous System / physiology*
Behavior, Animal / physiology*
Blood Pressure / drug effects,  physiology
Bronchial Arteries / drug effects,  innervation*
Cholinergic Antagonists / pharmacology
Enzyme Inhibitors / pharmacology
Female
Nitroarginine / pharmacology
Pulmonary Circulation / drug effects,  physiology*
Receptors, Adrenergic, alpha / physiology
Receptors, Adrenergic, beta / physiology
Receptors, Cholinergic / physiology
Respiration / physiology
Rest / physiology*
Sheep
Vasoconstriction / physiology
Wakefulness
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Adrenergic beta-Antagonists; 0/Cholinergic Antagonists; 0/Enzyme Inhibitors; 0/Receptors, Adrenergic, alpha; 0/Receptors, Adrenergic, beta; 0/Receptors, Cholinergic; 2149-70-4/Nitroarginine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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