liu.seSearch for publications in DiVA
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Microcirculation in skeletal muscle during hypoperfusion: An experimental study regarding some psysiological and pharmacological factors influencing blood flow and oxygen pressure distributions
Linköpings universitet, Institutionen för biomedicin och kirurgi, Hand och plastikkirurgi. Linköpings universitet, Hälsouniversitetet.
1995 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

The vascular bed in skeletal muscle plays an important role in the regulation of the systemic circulation. The present study was undertaken to investigate how capillary blood flow and oxygenation in skeletal muscle are affected by: a) a reduction in the levels of respiratory gases in blood, hypocapnia or hypoxia, and b) the interaction of anesthetics (pentobarbital, propofol, ketamine) during hemorrhage, and c) hypotension induced pharmacologically by adenosine, sodium nitroprusside or acetylcholine.

The experiments were performed on the vastus medialis muscle in mechanically ventilated anesthetized rabbits. Skeletal muscle microvascular perfusion was investigated with a local hydrogen clearance technique (LHC) (using a multi wire microelectrode) and laser-Doppler flowmetry (LDF). Skeletal muscle oxygen pressures (Pt02) and pH wereassessed using a multiwire Clark-type oxygen or an antimony (pH) microelectrode.

Hypocapnia (arterial PC02 2.3 kPa) decreased LDF flow and Pt02, whereasmuscle tissue pH remained unchanged. This was interpreted as being due to a reduction in microvascular perfllsion induced by vasoconstriction. This led to a decline in both tissue oxygenation and in the removal of acid metabolites, which counteracted a developing tissue alkalosis. Apart form the vasoregulatory role of carbon dioxide, it appears that muscle tissue pH is an important factor in the control of skeletal muscle perfusion. Hypoxia (arterial P02 4.0 kPa) reduced LHC flow and Pt02. This was reversed by the administration of ritanserin (serotonin antagonist), despite a further reduction in blood pressure. This supports the concept that the decline in capillary perfusion during systemic hypoxia is at least partly mediated by serotonin.

Hemorrhage was induced by withdrawal of blood to a mean arterial blood pressure of 40 mmHg, and measurements (LHC, LDF) were carried out during the spontaneous recovery period. When ketarnine wa<> used as anesthetic a higher capillary perfusion was found as compared to pentobarbital or propofol. These differences may be mediated, as suggested by the results from other studies, by the cardiovascular stimulating properties of ketamine, the effects on the renin-angiotensin system by pentobarbital and venomotor tone by propofol.

Hypotension, 20-25% reduction in mean arterial blood pressure, induced by adenosine, was associated with a decrease in skeletal muscle capillary blood flow and an increase in PtOz. This may be explained by a redistribution of capillary flow and/or a reduction in local oxygen demand. Hypotension induced by sodiuin nitroprusside to a similar level, on the other hand, increased capillary blood flow, mostly in the high flow range, whereas the oxygen pressure distributions were reduced. This may be caused by an increased local oxygen demand. Acetylcholine-induced hypotension decreased capillary blood flow which was most pronounced in the high flow range, while oxygen pressure distributions decreased homogeneously in a manner similar to that seen during hemorrhage.

The findings presented rnay be of importance in clinical situations with compromised skeletal muscle circulation.

sted, utgiver, år, opplag, sider
Linköping: Linköpings universitet , 1995. , s. 46
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 440
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-25651Lokal ID: 10027ISBN: 91-7871-289-0 (tryckt)OAI: oai:DiVA.org:liu-25651DiVA, id: diva2:246199
Disputas
1995-03-03, Berzeliussalen, Universitetssjukhuset, Linköping, 09:00 (svensk)
Merknad
Papers, included in the Ph.D. thesis, are not registered and included in the posts from 1999 and backwards.Tilgjengelig fra: 2009-10-08 Laget: 2009-10-08 Sist oppdatert: 2012-07-25bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

Av organisasjonen

Søk utenfor DiVA

GoogleGoogle Scholar

isbn
urn-nbn

Altmetric

isbn
urn-nbn
Totalt: 97 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf