Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 76: 2594-2601, 1994;
8750-7587/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bruandet, N.
Right arrow Articles by Quintin, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bruandet, N.
Right arrow Articles by Quintin, L.

Journal of Applied Physiology, Vol 76, Issue 6 2594-2601, Copyright © 1994 by American Physiological Society


ARTICLES

Systemic acidosis after controlled hypotension activates catechol activity in the vasomotor center

N. Bruandet and L. Quintin
Laboratoire de Physiologie de l'Environnement, Faculte de Medecine, Lyon, France.

Activation of the catechol metabolism, assessed with in vivo voltammetry, in the vasopressor area of the vasomotor center was investigated during systemic acidosis occurring after controlled hypotension. Rats anesthetized with halothane were mechanically ventilated. Sodium nitroprusside lowered mean arterial pressure to 55 mmHg for > or = 20 min. Arterial blood gases allowed us to group rats according to whether they showed symptoms of metabolic acidosis (pH < or = 7.34) immediately after controlled hypotension. To assess the effect of systemic acidosis independently of the progressive decline in pressure observed during the recovery period after controlled hypotension, we used phenylephrine infusion to maintain mean arterial pressure at baseline pressure during the recovery period after controlled hypotension in two groups of animals. Systemic acidosis increased the catechol signal in a prolonged manner [nitroprusside with acidosis (n = 7) vs. nitroprusside without acidosis (n = 5); P < 0.0001]. This catechol activation was greater when pressure was restored after hypotension [nitroprusside with acidosis plus phenylephrine (n = 5) vs. nitroprusside with acidosis over the whole interval (from -30 to +150 min); P < 0.05]. When the nitroprusside with acidosis group and nitroprusside with acidosis plus phenylephrine group were compared, hypercapnia had an involvement in the larger increase of the catechol signal observed in the nitroprusside with acidosis plus phenylephrine group [arterial PCO2: nitroprusside with acidosis vs. nitroprusside with acidosis plus phenylephrine over the whole interval (from -30 to +150 min) and at +30 and +60 min; all P < 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
N. Rentero, N. Bruandet, B. Milne, and L. Quintin
Catechol activation in rat rostral ventrolateral medulla after systemic isocapnic metabolic acidosis
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1998; 275(2): R350 - R356.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online