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Alpha 2-adrenocepto...
Alpha 2-adrenoceptor activation may trigger the increased production of endothelium-derived nitric oxide in skeletal muscle during acute haemorrhage
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- Ekelund, Ulf (författare)
- Lund University,Lunds universitet,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine
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Björnberg, J (författare)
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- Mellander, Stefan (författare)
- Lund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine
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(creator_code:org_t)
- 1998
- 1998
- Engelska.
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 164:3, s. 285-292
- Relaterad länk:
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https://lup.lub.lu.s...
Abstract
Ämnesord
Stäng
- Our previous studies indicated that acute haemorrhage leads to a pronounced increase in the release of endothelium-derived nitric oxide (EDNO) graded in relation to the magnitude of the blood loss. The EDNO-induced vasodilatation, confined selectively to the arterial 'feeder' vessels, attenuates the concomitant reflex adrenergic constriction and thereby prevents deleterious reduction of blood flow. The present study aimed at investigating whether the reflex release of blood-borne catecholamines might trigger this EDNO release via activation of endothelial alpha 2-adrenoceptors. The study was performed on the sympathectomized vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of resistance (tone) in consecutive vascular sections. Selection alpha 2-adrenoceptor blockade with idazoxan applied at steady state vasoconstriction after a 35% blood loss evoked an initial generalized dilator response (attributable to inhibition of post-synaptic smooth muscle alpha 2-adrenoceptors), followed by a constrictor response selectively in the arterial feeder vessels, the latter compatible with the hypothesis of reduced EDNO release by alpha 2-adrenoceptor blockade. More direct evidence for the hypothesis was obtained from studies of the vascular response to EDNO blockade (L-NAME) after haemorrhage in the presence and absence of alpha 2-adrenoceptor blockade. The constrictor response to EDNO blockade, which is a measure of the pre-existing EDNO dilator influence (EDNO production), was significantly smaller (P < 0.01) in the presence than absence of alpha 2-adrenoceptor blockade. The results indicate that blood-borne catecholamines, via activation of endothelial alpha 2-adrenoceptors, trigger the increase in the EDNO release in acute haemorrhage, implying a functionally important negative feedback in the integrated control of vascular tone in bleeding.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Anestesi och intensivvård (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Anesthesiology and Intensive Care (hsv//eng)
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