Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1976-8-23
pubmed:abstractText
It is generally believed that the reduction in plasma [HCO3] characteristic of chronic hypocapnia results from renal homeostatic mechanisms designed to minimize the alkalemia produced by.the hypocapneic state. To test this hypothesis, we have induced chronic hypocapnia in dogs in which plasma [HCO3] had previously been markedly reduced (from 21 to 15 meq/liter) by the prolonged feeding of HCl. The PaCO2 of chronically acid-fed animals was reduced from 32 to 15 mm Hg by placing the animials in a large environmental chamber containing 9% oxygen. In response to this reduction in PaCO2, mean plasma [HCO3] fell by 8.6 meq/liter, reaching a new steady-state level of 6.4 meq/liter. This decrement in plasma [HCO3] is almost identical to the 8.1 meq/liter decrement previously observed in normal (nonacid-fed) animals in which the same degree of chronic hypocapnia had been induced. Thus, in both normal and HCl-fed animals, the renal response to chronic hypocapnia causes plasma [HCO3] to fall by approximately 0.5 meq/liter for each millimeter of Hg reduction in CO2 tension. By contrast, the response of plasma [H+] in the two groups was markedly different. Instead of the fall in [H+] which is seen during chronic hypocapnia in normal animals, [H+] in HCl-fed animals rose significantly from 53 to 59 neq/liter (pH 7.28-7.23). This seemingly paradoxical response is, of course, an expression of the constraints imposed by the Henderson equation and reflects the fact that the percent fall in [HCO3] in the HCl-fed animals was greater than the percent fall in PaCO2. These findings clearly indicate that in chronic hypocapnia the kidney cannot be regarded as the effector limb in a homeostatic feedback system geared to the defense of systemic acidity.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-11344560, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-13376426, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-13376427, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-13736670, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-13951253, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-14207775, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-14254260, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-14437897, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-5032522, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-5838729, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-5901147, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-5937027, http://linkedlifedata.com/resource/pubmed/commentcorrection/6488-6079947
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1483-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Regulation of acid-base equilibrium in chronic hypocapnia. Evidence that the response of the kidney is not geared to the defense of extracellular (H+).
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.