Linked Life Data

5480859

Source:http://linkedlifedata.com/resource/pubmed/id/5480859

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1971-1-11
pubmed:abstractText
Alterations in human cerebral blood flow and related blood constituents were studied during exposure to acute hypoxia. Observations were made during serial inhalation of decreasing O(2) concentrations with and without maintenance of normocarbia, during 8 min inhalation of 10% O(2), and after hyperventilation at an arterial P(O2) of about 40 mm Hg. In the range of hypoxemia studied, from normal down to arterial P(O2) of about 40 mm Hg, the magnitude of the cerebral vasodilator response to hypoxia appeared to be largely dependent upon the coexisting arterial CO(2) tension. The mean slope of the increase in cerebral blood flow with decreasing arterial O(2) tension rose more quickly (P < 0.05) when eucapnia was maintained when compared with the slope derived under similar hypoxic conditions without maintenance of eucapnia. When 12 subjects inhaled 10% oxygen, cerebral blood flow rose to more than 135% of control in four whose mean decrease in arterial CO(2) tension was - 2.0 mm Hg. The remaining eight had flows ranging from 97 to 120% of control, and their mean decrease in CO(2) tension was - 5.1 mm Hg. When mean arterial P(O2) was 37 mm Hg, hyperventilation was carried out in 10 subjects. Arterial P(O2) increased insignificantly, arterial P(CO2) declined from 34 to 27 mm Hg (P < 0.05), and cerebral blood flow which had been 143% of control decreased to 109%, a figure not significantly different from control.These data demonstrate the powerful counterbalancing constrictor effects of modest reductions in CO(2) tension on the vasodilator influence of hypoxia represented by arterial P(O2) reductions to about 40 mm Hg. Indeed, mild hyperventilation completely overcame the vasodilator effect provided by an arterial O(2) tension as low as 40 mm Hg. The effects of hypoxia on the control of the cerebral circulation must be analyzed in terms of the effects of any associated changes in CO(2) tension.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-13563360, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-13587443, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-13783303, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-14117646, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-14318482, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-16695569, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-5913299, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-5914844, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-5954123, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-6016780, http://linkedlifedata.com/resource/pubmed/commentcorrection/5480859-6031186
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2362-8
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1970
pubmed:articleTitle
Cerebrovascular response to acute hypocapnic and eucapnic hypoxia in normal man.
pubmed:publicationType
Journal Article