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This Article Full Text Full Text (PDF) All Versions of this Article: 92/4/749    most recent expphysiol.2006.036673v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lin, S. Articles by Yu, J. Search for Related Content PubMed PubMed Citation Articles by Lin, S. Articles by Yu, J.

Departments of ¹ Medicine⁴ Pediatrics, University of Louisville, Louisville, KY 40292, USA ² Department of Respiratory Therapy, Bellarmine University, Louisville, KY 40205, USA ³Department of Mathematics and Statistics, James Madison University, Harrisonburg, VA 22807, USA

We tested the hypothesis that oleic acid-induced acute lung injury activates pulmonary nociceptors, that is, C fibre receptors (CFRs) and high-threshold A fibre receptors (HTARs). Single-unit activity was recorded in the cervical vagus nerve and assessed before and after injecting oleic acid (75 µl kg^–1 I.V.) into anaesthetized, open-chest, mechanically ventilated rabbits. Unit activities increased within seconds and peaked within a few minutes (from 0.3 ± 0.1 to 1.4 ± 0.9 impulses s^–1 for CFRs and from 0.5 ± 0.1 to 1.7 ± 0.3 impulses s^–1 for HTARs, both n = 8 and P < 0.05). These activities were sustained while pulmonary oedema developed and dynamic lung compliance decreased over the 90 min observation period. Activities in slowly adapting receptors and rapidly adapting receptors were also increased; however, their responsiveness to airway pressure stimulation decreased progressively. We conclude that pulmonary nociceptors are stimulated during acute lung injury. The dual nociceptor system, consisting of both non-myelinated CFRs and myelinated HTARs, may play an important role in the pathophysiological process of acute lung injury-induced respiratory responses.

(Received 21 November 2006; accepted after revision 13 March 2007; first published online 28 March 2007)
Corresponding author J. Yu: Pulmonary Division, Department of Medicine, University of Louisville, ACB-3, 530 South Jackson Street, Louisville, KY 40292, USA. Email: j0yu0001{at}louisville.edu

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