Linked Life Data

8785137

Source:http://linkedlifedata.com/resource/pubmed/id/8785137

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-9-26
pubmed:abstractText
Short-term potentiation (STP) of breathing refers to respiratory activity that persists at termination of a primary stimulus and is not related just to the dynamics of chemoreceptors. In humans, STP is activated by brief episodes of hypoxia and voluntary hyperventilation (VHV). STP exerts a stabilizing influence on breathing pattern. To investigate the effects of a subanaesthetic concentration of isoflurane on STP, we studied recovery from mild and moderate hypoxic hyperpnoea and VHV. Experiments were performed in eight healthy volunteers. If necessary, subjects were aroused to maintain a state of wakefulness. In the hypoxic studies, a control study involved 1 min of isocapnic hypoxia (end-tidal PO2 (PE'O2 6.1) kPa) followed by sudden transition to normoxia. In the isoflurane studies, 1 min of mild hypoxia (Iso-1 study: PE'O2 6.2 kPa) and 1 min of moderate hypoxia (Iso-2 study: PE'O2 5.7 kPa) were followed by sudden transition to normoxia during inhalation of 0.1 minimum alveolar concentration (MAC) of isoflurane. PE'CO2 was maintained at 5.9 kPa. In the VHV study, ventilatory recovery from 1 min of normoxic VHV was monitored before and during inhalation of 0.1 MAC of isoflurane. Subjects performed multiple transitions in each study. In the hypoxic studies, peak ventilation after 1 min of hypoxic stimulation did not differ between treatments. The averaged responses reached normoxic baseline after 56.3 (SEM 10.7) s in the control study (n = 47 transitions), 18.0 (3.3) s in the Iso-1 study (n = 41; P < 0.05 vs control) and 15.3 (2.4) s in the Iso-2 study (n = 23; P < 0.05 vs control). In the VHV studies, VE at termination of VHV was not different from baseline after 36 s in the control study. An immediate reduction to less than baseline ventilation, lasting 24 s, was present in the isoflurane study. We believe that shortening of the time required to reach baseline in the hypoxic studies, and hypoventilation at cessation of VHV in the isoflurane studies, are related to the inability to activate STP of breathing via an effect of isoflurane on respiratory neurones in the brain stem. Increasing the stimulus intensity during isoflurane inhalation (Iso-2 study) did not (re)-activate STP.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0007-0912
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
374-81
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Slow ventilatory dynamics after isocapnic hypoxia and voluntary hyperventilation in humans: effects of isoflurane.
pubmed:affiliation
Department of Anaesthesiology, Leiden University Hospital, The Netherlands.
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial