Effects of Nω-nitro-L-arginine (L-NOARG) on blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension

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Abstract

The role of Nω-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60% of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1% DMSO and 0.9 mN NaOH, group 4). For groups 5 and 6, L-NOARG or its vehicle was superfused for 15 min without hemorrhage. In group 7, the vasodilator responses to the endothelium-dependent vasorelaxant acetylcholine (ACH) and the endothelium-independent vasorelaxant sodium nitroprusside (SNP) were assessed at rest and after 25 min of hemorrhagic hypotension. The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.

Original languageEnglish
Pages (from-to)69-74
Number of pages6
JournalShock
Volume12
Issue number1
DOIs
Publication statusPublished - 1999 Jan 1

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Nitroarginine
Microcirculation
Diaphragm
Hypotension
Arginine
Vasodilator Agents
Nitroprusside
Acetylcholine
Endothelium
Hemorrhage
Laser-Doppler Flowmetry
Dimethyl Sulfoxide
Nitric Oxide Synthase
Sprague Dawley Rats
Nitric Oxide
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

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title = "Effects of Nω-nitro-L-arginine (L-NOARG) on blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension",
abstract = "The role of Nω-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60{\%} of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1{\%} DMSO and 0.9 mN NaOH, group 4). For groups 5 and 6, L-NOARG or its vehicle was superfused for 15 min without hemorrhage. In group 7, the vasodilator responses to the endothelium-dependent vasorelaxant acetylcholine (ACH) and the endothelium-independent vasorelaxant sodium nitroprusside (SNP) were assessed at rest and after 25 min of hemorrhagic hypotension. The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.",
author = "Chang-Wen Chen and Tzuen-Ren Hsiue and Han-Yu Chang",
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T1 - Effects of Nω-nitro-L-arginine (L-NOARG) on blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension

AU - Chen, Chang-Wen

AU - Hsiue, Tzuen-Ren

AU - Chang, Han-Yu

PY - 1999/1/1

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N2 - The role of Nω-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60% of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1% DMSO and 0.9 mN NaOH, group 4). For groups 5 and 6, L-NOARG or its vehicle was superfused for 15 min without hemorrhage. In group 7, the vasodilator responses to the endothelium-dependent vasorelaxant acetylcholine (ACH) and the endothelium-independent vasorelaxant sodium nitroprusside (SNP) were assessed at rest and after 25 min of hemorrhagic hypotension. The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.

AB - The role of Nω-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60% of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1% DMSO and 0.9 mN NaOH, group 4). For groups 5 and 6, L-NOARG or its vehicle was superfused for 15 min without hemorrhage. In group 7, the vasodilator responses to the endothelium-dependent vasorelaxant acetylcholine (ACH) and the endothelium-independent vasorelaxant sodium nitroprusside (SNP) were assessed at rest and after 25 min of hemorrhagic hypotension. The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.

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