These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The pattern of sympathetic neurone activity during expiration in the cat.
    Author: Bachoo M, Polosa C.
    Journal: J Physiol; 1986 Sep; 378():375-90. PubMed ID: 3098968.
    Abstract:
    The properties of sympathetic preganglionic neurone activity during expiration were studied in pentobarbitone-anaesthetized (n = 26) and in non-anaesthetized, mid-collicular decerebrate (n = 5), paralysed, artificially ventilated cats in which the electrical activity of the phrenic nerve and of the cervical sympathetic trunk was recorded. In control conditions (end-tidal PCO2 between 35 and 40 mmHg, zero end-expiratory pressure) sympathetic activity during expiration was either steady at a low level (n = 11) or showed a modest progressive increase from a low level in early expiration (n = 17). Very infrequently (n = 3), it showed a transient increase during the second half of expiration. Artificial ventilation with positive end-expiratory pressures in the range from 2.1 +/- 0.4 (mean +/- S.D.) to 6.7 +/- 0.6 cmH2O caused, in cats with intact vagus nerves, an increase in sympathetic neurone activity during the second half of expiration. Within this range of pressures, the magnitude of the increase was related to the magnitude of the positive end-expiratory pressure. This effect reversed at higher positive end-expiratory pressures. Pressures in excess of 10.2 +/- 1.8 cmH2O caused inhibition of sympathetic activity. The sympatho-excitatory effect of positive end-expiratory pressure disappeared after bilateral cervical vagotomy. With intact vagus nerves, it also disappeared at levels of systemic hypocapnia (end-tidal PCO2 less than or equal to 15 mmHg) which abolished phrenic nerve activity. In hypocapnia, artificial ventilation with peak tracheal pressures greater than 7.2 +/- 1.1 cmH2O caused inhibition of sympathetic activity, while ventilation with lower end-expiratory pressures had no effect on sympathetic activity. It may be concluded that the sympatho-excitatory effect of positive end-expiratory pressure is mediated by vagal afferents and requires a certain level of brain-stem respiratory neurone activity. Sympatho-excitation during expiration was also observed, in normocapnic conditions, during short-duration static lung inflation with tracheal pressures in the range from 2.5 +/- 0.3 to 7.0 +/- 0.8 cmH2O as well as during artificial ventilation with zero end-expiratory pressure when lung inflation occurred in expiration. These responses were abolished by bilateral cervical vagotomy and during systemic hypocapnia. Sympatho-excitation during expiration was also observed when systemic hypercapnia was produced in vagotomized cats by artificial ventilation with gas mixtures containing 5 or 10% CO2.(ABSTRACT TRUNCATED AT 400 WORDS)
    [Abstract] [Full Text] [Related] [New Search]