Respiratory responses to progressive hypoxia in the Amazonian Oscar, Astronotus ocellatus

Author(s):  
G. Scott ◽  
C. Wood ◽  
K. Sloman ◽  
F. Iftikar ◽  
G. De Boeck ◽  
...  
2008 ◽  
Vol 162 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Graham R. Scott ◽  
Chris M. Wood ◽  
Katherine A. Sloman ◽  
Fathima I. Iftikar ◽  
Gudrun De Boeck ◽  
...  

1995 ◽  
Vol 79 (4) ◽  
pp. 1181-1189 ◽  
Author(s):  
F. Xu ◽  
J. Owen ◽  
D. T. Frazier

The general contribution of the cerebellum to hypoxic respiratory responses and the special role of the fastigial nucleus (FN) in the hypoxic respiratory reflex mediated via peripheral chemoreceptors were investigated in anesthetized and spontaneously breathing cats. Seven cats were exposed to isocapnic progressive hypoxia before and after cerebellectomy by decreasing the fractional concentration of end-tidal O2 (FETO2) from 15 +/- 0.3% to 7% while maintaining the pressure of end-tidal CO2 at a constant level of approximately 30 mmHg. Five additional cats inhaled five breaths of pure N2 (transient hypoxia) and received sodium cyanide (50 micrograms iv) before and after thermal lesions of the bilateral FN. The results showed that cerebellectomy or FN lesions failed to alter the respiratory variables (minute ventilation, tidal volume, respiratory frequency, and the peak of integrated diaphragm activity) during eupneic breathing. However, cerebellectomy significantly attenuated minute ventilation (FETO2 < or = 13%) and the peak of integrated diaphragm activity (FETO2 < or = 10%) compared with control. During progressive hypoxia, changes in respiratory frequency were noted earlier (FETO2 < or = 13%) than changes in tidal volume (FETO2 < or = 10%). Similarly, bilateral lesions of the FN resulted in a profound reduction in these respiratory responses to transient hypoxia and sodium cyanide. We conclude that the cerebellum can facilitate the respiratory response to hypoxia and that the FN is an important region in the modulation of the hypoxic respiratory responses, presumably via its effects on inputs from peripheral chemoreceptors.


1995 ◽  
Vol 268 (2) ◽  
pp. L201-L206 ◽  
Author(s):  
C. Vannier ◽  
T. L. Croxton ◽  
L. S. Farley ◽  
C. A. Hirshman

Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.


1999 ◽  
Vol 519 (2) ◽  
pp. 571-579 ◽  
Author(s):  
Renea V. Johnston ◽  
Daniel A. Grant ◽  
Malcolm H. Wilkinson ◽  
Adrian M. Walker

1977 ◽  
Vol 52 (2) ◽  
pp. 13P-13P
Author(s):  
D. C. Flenley ◽  
P. K. Wraith ◽  
A. G. Leitch ◽  
H. M. Brash

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