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Endogenous nitric oxide as a physiological regulator of vascular tone in cat skeletal muscle during haemorrhage

Ekelund, Ulf LU and Mellander, Stefan LU (1996) In Acta Physiologica Scandinavica 157(4). p.471-479
Abstract
The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tone in vivo was approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitor L-NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (RT) and in its consecutive sections, the proximal arterial resistance ('feeder') vessels (> 25 microns; Ra,prox), the small arterioles (< 25 microns) and the veins. NO blockade by close-arterial L-NAME infusion in the control situation increased RT from 16.3 to 33.0 PRU (+102%), because of a selective increase in Ra,prox... (More)
The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tone in vivo was approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitor L-NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (RT) and in its consecutive sections, the proximal arterial resistance ('feeder') vessels (> 25 microns; Ra,prox), the small arterioles (< 25 microns) and the veins. NO blockade by close-arterial L-NAME infusion in the control situation increased RT from 16.3 to 33.0 PRU (+102%), because of a selective increase in Ra,prox by 16.7 PRU. A 35% blood loss per se raised RT from 13.6 to 21.7 PRU. Superimposed NO blockade in this state caused a much stronger vasoconstriction than in the control situation, increasing RT to 60.9 PRU (+181%) and Ra,prox by 40.5 PRU, which indicated an approximately 2.4-fold increase (P < 0.001) in the NO dilator influence in the Ra,prox section above control. The effect was independent of autonomic nerves. The increased NO dilator influence during haemorrhage most likely was caused by an increased production of endothelium-derived nitric oxide (EDNO), The constrictor response to L-NAME was graded in relation to the blood loss (17.5 vs. 35%). The results indicate that EDNO functions as a physiological regulator of vascular tone in the arterial 'feeder' vessels during haemorrhage, serving to counterbalance to a significant extent the concomitant adrenergic constriction, and thereby preventing critical reduction of blood flow and untoward heterogeneous flow distribution within the tissue. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
arteries, capillary pressure, EDNO, EDRF, haemorrhage, microcirculation, noradrenaline, vascular resistance, vasodilation, veins
in
Acta Physiologica Scandinavica
volume
157
issue
4
pages
471 - 479
publisher
Wiley-Blackwell
external identifiers
  • pmid:8869730
  • scopus:0029759582
ISSN
0001-6772
DOI
10.1046/j.1365-201X.1996.516275000.x
language
English
LU publication?
yes
id
8d24949e-80a9-489c-8b72-7f727c8ff8e2 (old id 1110268)
date added to LUP
2008-07-23 08:15:33
date last changed
2017-01-01 07:16:38
@article{8d24949e-80a9-489c-8b72-7f727c8ff8e2,
  abstract     = {The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tone in vivo was approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitor L-NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (RT) and in its consecutive sections, the proximal arterial resistance ('feeder') vessels (&gt; 25 microns; Ra,prox), the small arterioles (&lt; 25 microns) and the veins. NO blockade by close-arterial L-NAME infusion in the control situation increased RT from 16.3 to 33.0 PRU (+102%), because of a selective increase in Ra,prox by 16.7 PRU. A 35% blood loss per se raised RT from 13.6 to 21.7 PRU. Superimposed NO blockade in this state caused a much stronger vasoconstriction than in the control situation, increasing RT to 60.9 PRU (+181%) and Ra,prox by 40.5 PRU, which indicated an approximately 2.4-fold increase (P &lt; 0.001) in the NO dilator influence in the Ra,prox section above control. The effect was independent of autonomic nerves. The increased NO dilator influence during haemorrhage most likely was caused by an increased production of endothelium-derived nitric oxide (EDNO), The constrictor response to L-NAME was graded in relation to the blood loss (17.5 vs. 35%). The results indicate that EDNO functions as a physiological regulator of vascular tone in the arterial 'feeder' vessels during haemorrhage, serving to counterbalance to a significant extent the concomitant adrenergic constriction, and thereby preventing critical reduction of blood flow and untoward heterogeneous flow distribution within the tissue.},
  author       = {Ekelund, Ulf and Mellander, Stefan},
  issn         = {0001-6772},
  keyword      = {arteries,capillary pressure,EDNO,EDRF,haemorrhage,microcirculation,noradrenaline,vascular resistance,vasodilation,veins},
  language     = {eng},
  number       = {4},
  pages        = {471--479},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Physiologica Scandinavica},
  title        = {Endogenous nitric oxide as a physiological regulator of vascular tone in cat skeletal muscle during haemorrhage},
  url          = {http://dx.doi.org/10.1046/j.1365-201X.1996.516275000.x},
  volume       = {157},
  year         = {1996},
}