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J Appl Physiol 88: 1247-1253, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 4, 1247-1253, April 2000

Vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism in dogs

H. F. Chen1 and Y. R. Kou2

1 Department of Early Childhood Care and Education, Cheng Shiu Junior College of Technology and Commerce, Kaohsiung 833; and 2 Institute of Physiology, School of Medicine and Life Science, National Yang-Ming University, Taipei, Taiwan 11221, Republic of China

We investigated the vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism (PAE) in anesthetized and spontaneously breathing dogs. PAE was induced by infusion of air into the right atrium (0.2 ml · kg-1 · min-1 for 10 min). The first PAE induction caused an increase in respiratory frequency accompanied by a decrease in tidal volume in each of the 30 animals studied. Subsequently, animals were evenly divided into five groups, and a second PAE induction was repeated after various experimental interventions. The tachypneic response to PAE was not significantly altered by pretreatment with a saline vehicle but was largely attenuated by either perivagal capsaicin treatment (a technique that selectively blocks the conduction of unmyelinated C fibers), pretreatment with ibuprofen (a cyclooxygenase inhibitor), or pretreatment with dimethylthiourea (a hydroxyl radical scavenger). Ultimately, the tachypneic response was nearly abolished by a bilateral cervical vagotomy. These results suggest that 1) lung vagal unmyelinated C-fiber afferents play a predominant role in evoking the reflex tachypneic response to PAE and 2) both cyclooxygenase products and hydroxyl radical are important in eliciting this vagally mediated response.

lung vagal sensory receptors; microembolism; reflex tachypnea; ibuprofen; dimethylthiourea; cyclooxygenase products; hydroxyl radical


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