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Role of nitric oxide in the control of burn perfusion.

Lindblom, Lucky, 1947 (author)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård,Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care
Cassuto, Jean (author)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård,Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care
Yregård, Liselotte (author)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård,Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care
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Mattsson, Ulf, 1955 (author)
Gothenburg University,Göteborgs universitet,Odontologiska institutionen, Avdelningen för endodonti med oral diagnostik,Institute of Odontology, Department of Endodontology/Oral Diagnosis
Tarnow, Peter, 1963 (author)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för plastikkirurgi,Institute of Surgical Sciences, Department of Plastic Surgery
Sinclair, Robert, 1951 (author)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård,Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care
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 (creator_code:org_t)
2000
2000
English.
In: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:1, s. 19-23
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Vascular changes following deep skin burns are characterised by vasoconstriction and progressive ischemia. Nitric oxide (NO) has been shown to be a potent regulator of vascular smooth muscle tone and tissue perfusion. We assessed the importance of NO on post-burn skin perfusion in rats using laser Doppler. The present results show that neither the NO-synthase inhibitor, NG-nitro-L-arginine (L-NNA) (n = 6) nor the NO precursor, L-arginine, significantly influenced skin perfusion in nonburned skin compared to saline-treated animals. In the area of full-thickness skin burn, neither L-arginine (n = 6) nor L-NNA (n = 6) had significant influence on post-burn perfusion compared to saline-treated controls (n = 6). Administration of L-NNA (n = 6) significantly impaired skin perfusion in the area adjacent to the contact burn representing a partial-thickness burn, while the NO precursor, L-arginine (n = 6) had no significant effect on burn perfusion as compared to saline-treated controls (n = 6). In conclusion, impairment of perfusion in a full thickness burn following administration of NO-synthase inhibitor suggests that nitric oxide is involved in the mechanisms responsible for maintaining adequate circulation post-burn. The lack of additional improvement of perfusion in response to L-arginine may suggest that NO synthesis in response to the thermal trauma is already at a peak.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Anestesi och intensivvård (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Anesthesiology and Intensive Care (hsv//eng)

Keyword

Animals
Arginine
pharmacology
Burns
physiopathology
Enzyme Inhibitors
pharmacology
Laser-Doppler Flowmetry
Male
Nitric Oxide
physiology
Nitric Oxide Synthase
antagonists & inhibitors
Nitroarginine
pharmacology
Rats
Rats
Sprague-Dawley
Skin
blood supply

Publication and Content Type

ref (subject category)
art (subject category)

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