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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
1977-4-15
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| pubmed:abstractText |
Autoregulation of the cerebral blood flow is a wellknown fact. In normal man the arterial pressure can vary from 80 mm Hg to 150 mm Hg without a change in the normal cerebral blood flow of 50 ml/100 g/min. The mechanism which is responsible for this autoregulation is not clearly understood. Several theories were proposed to explain this phenomenon. 1. The tissue pressure increases with an increase of the arterial pressure. A mechanical process should neutralize an increase of the cerebral blood flow. 2. The metabolic theory says that a decrease of the blood pressure, without a change of metabolism, involves an increase of the PaCO2, and a decrease of the PaO2. Those two factors provoke a decrease of the vascular tone. 3. The myogenic theory explains autoregulation by the fact that a change of the transmural pressure in the small vessels, involves a change in the activity of the smooth muscles of the vessels. 4. The exact mechanism of the autonomic nervous system in the autoregulation of the cerebral blood flow is still obscure. In some pathological conditions autoregulation is completely lost or is functioning not optimal: hypoxia, hypercapnia and brain contusion. We have measured the cerebral blood flow before and after an intravenous injection of 5 mg thiopental (Pentothal) on occasion of a carotid angiography in man. We noticed a decrease of the cerebral blood flow and at the same moment a decrease of the arterial pressure. We thought that maybe barbiturates could influence autoregulation. Our results could not prove this hypothesis. For ethical reasons we could not make the necessary measurements to prove or to reject this hypothesis (i.e. intracranial pressure, deep controlled hypotension). In the literature there are arguments which support this hypothesis although most workers found an intact autoregulation after a barbiturate anesthesia. Some workers saw that the increase of the cerebral blood flow by increasing the PaCO2 was depressed by barbiturates and exhausted by halothane and cyclopropane. As autoregulation is a more vulnerable mechanism than CO2 reactivity as seen in clinical situations, it could be true that anesthetics do influence autoregulation.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0001-5164
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
27
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
11-9
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading | |
| pubmed:year |
1976
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| pubmed:articleTitle |
Influence of anesthesia on autoregulation of the cerebral blood flow.
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| pubmed:publicationType |
Journal Article
|