Breathing Pattern of Patients with COPD

Author(s):  
C. S. H. Sassoon ◽  
F. I. Hawari
Keyword(s):  
1991 ◽  
Vol 98 (1) ◽  
pp. 77-87 ◽  
Author(s):  
Wang Zhao-Xian ◽  
Ning-Zhen Sun ◽  
Wei-Ping Mao ◽  
Jie-Ping Chen ◽  
Gong-Qing Huang

2000 ◽  
Vol 49 (5) ◽  
pp. 319-333 ◽  
Author(s):  
J.N Han ◽  
R Schepers ◽  
K Stegen ◽  
O Van den Bergh ◽  
K.P Van de Woestijne

2001 ◽  
Vol 51 (2) ◽  
pp. 133-141 ◽  
Author(s):  
Alejandro Lucía ◽  
Jesús Hoyos ◽  
Javier Pardo ◽  
José L. Chicharro

2010 ◽  
Vol 22 (9) ◽  
pp. 24-28 ◽  
Author(s):  
Viviane Martins da Silva ◽  
Marcos Venícios de Oliveira Lopes ◽  
Thelma Leite de Araujo ◽  
Beatriz Amorim Beltrão ◽  
Nirla Gomes Guedes

1999 ◽  
Vol 45 ◽  
pp. 31A-31A
Author(s):  
H W Sundell ◽  
O Hafström ◽  
P A Minton ◽  
S Poole ◽  
J Milerad
Keyword(s):  

2014 ◽  
Vol 116 (8) ◽  
pp. 1006-1016 ◽  
Author(s):  
Hsiu-Wen Tsai ◽  
Paul W. Davenport

Respiratory load compensation is a sensory-motor reflex generated in the brain stem respiratory neural network. The nucleus of the solitary tract (NTS) is thought to be the primary structure to process the respiratory load-related afferent activity and contribute to the modification of the breathing pattern by sending efferent projections to other structures in the brain stem respiratory neural network. The sensory pathway and motor responses of respiratory load compensation have been studied extensively; however, the mechanism of neurogenesis of load compensation is still unknown. A variety of studies has shown that inhibitory interconnections among the brain stem respiratory groups play critical roles for the genesis of respiratory rhythm and pattern. The purpose of this study was to examine whether inhibitory glycinergic neurons in the NTS were activated by external and transient tracheal occlusions (ETTO) in anesthetized animals. The results showed that ETTO produced load compensation responses with increased inspiratory, expiratory, and total breath time, as well as elevated activation of inhibitory glycinergic neurons in the caudal NTS (cNTS) and intermediate NTS (iNTS). Vagotomized animals receiving transient respiratory loads did not exhibit these load compensation responses. In addition, vagotomy significantly reduced the activation of inhibitory glycinergic neurons in the cNTS and iNTS. The results suggest that these activated inhibitory glycinergic neurons in the NTS might be essential for the neurogenesis of load compensation responses in anesthetized animals.


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