L773:1095 9319
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Endothelin-1 Reduces Microvascular Fluid Permeability through Secondary Release of Prostacyclin in Cat Skeletal Muscle.
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- Bentzer, Peter (författare)
- Lund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine
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- Holbeck, Staffan (författare)
- Lund University,Lunds universitet,Medicinska fakulteten,Faculty of Medicine
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- Grände, Per-Olof (författare)
- Lund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine
- (creator_code:org_t)
- Elsevier BV, 2002
- 2002
- Engelska.
- Ingår i: Microvascular Research. - : Elsevier BV. - 1095-9319 .- 0026-2862. ; 63:1, s. 50-60
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- The aim of the study was to analyze effects of various plasma concentrations of the vasoconstrictor endothelin-1 on microvascular fluid permeability and on transcapillary fluid exchange. We also analyzed whether the permeability-reducing substance prostacyclin is involved in the permeability effects of endothelin-1, as prostacylin is suggested to be released via ET(B) receptor stimulation. The study was performed on an autoperfused cat calf muscle preparation, and a capillary filtration coefficient (CFC) technique was used to estimate variations in microvascular fluid permeability (conductivity). Intraarterial infusion of endothelin-1 in low doses (5 and 10 ng/min/100 g muscle) caused transcapillary absorption, whereas higher doses (20-40 ng/min/100 g) induced filtration despite further vasoconstriction. Low-dose endothelin-1 had no significant effect on CFC, while CFC was reduced to at most 55% of baseline at higher doses (P < 0.01). Simultaneous local intraarterial infusion of the prostacyclin synthesis inhibitor tranylcypromine restored CFC to 114% of baseline (P < 0.01) and further increased vascular resistance. A low, nonvasodilator dose of prostacyclin given intravenously counteracted the tranylcypromine effect on CFC. The decreased CFC induced by a high dose of endothelin-1 was counteracted by the ET(B) receptor antagonist BQ-788 with no change in vascular resistance (P < 0.05). We conclude that the decreased CFC following high doses of endothelin-1 can be attributed to a decrease in microvascular hydraulic conductivity, mediated by secondary release of prostacylin via stimulation of the ET(B) receptor. Endothelin-1 may induce edema through postcapillary vasoconstriction. (c)2001 Elsevier Science.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine (hsv//eng)
Nyckelord
- Epoprostenol : antagonists & inhibitors : metabolism
- Male
- Microcirculation : metabolism
- Muscle Skeletal : cytology : metabolism
- Receptors Endothelin metabolism
- Support Non-U.S. Gov't
- Tranylcypromine : pharmacology
- Time Factors
- Endothelin-1 : biosynthesis
- Dose-Response Relationship Drug
- Cats
- Capillary Permeability
- Arteries : metabolism
- Capillaries : metabolism
- Animal
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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