| 1. |
- Lindblom, Lucky, 1947, et al.
(författare)
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Importance of nitric oxide in the regulation of burn oedema, proteinuria and urine output.
- 2000
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Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:1, s. 13-7
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Tidskriftsartikel (refereegranskat)abstract
- Burn injuries trigger a pronounced inflammatory response in the burned skin, resulting in oedema formation and impaired circulation. This response involves activation of the nitric oxide (NO) synthetic pathway, which could play a key role in the complex hemodynamic and hemostatic changes occurring as a result of a burn trauma. The results presented in full-thickness skin burns of rats show that the NO-precursor, L-arginine (n = 10), inhibit burn-induced plasma extravasation as compared to saline-treated burned controls (n = 10) (p<0.001) to a level not significantly different from nonburned animals. Administration of the NO-synthase inhibitor. NG-nitro-L-arginine (L-NNA) (n = 10), did not significantly influence burn extravasation compared to burned controls. Accumulated urine volume 90 min post-burn increased ten-fold in burned animals treated with L-arginine compared to saline-treated burned controls (p<0.001) and nonburned animals (p<0.001), while L-NNA had no significant effect on diuresis. A significantly increased proteinuria occurred in L-arginine treated burned animals as compared to burned controls and nonburned controls (p<0.001), whereas L-NNA did not significantly influence the leakage of protein in the urine. Activation of NO synthesis significantly suppresses burn edema and strongly increases diuresis along with increased proteinuria.
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| 2. |
- Lindblom, Lucky, 1947, et al.
(författare)
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Importance of vasoactive intestinal polypeptide in the regulation of burn perfusion.
- 2000
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Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:5, s. 435-42
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Tidskriftsartikel (refereegranskat)abstract
- Vasoactive intestinal polypeptide is one of the body's most potent vasodilators and has been shown to increase blood flow in a number of tissues. Its effects on postburn skin perfusion and progressive ischemia was investigated in rats exposed to partial- and full-thickness experimental skin burns. Systemic administration of VIP elicited a significant drop in mean arterial blood pressure versus saline (p<0.001) and VIP antiserum (p<0.001) both in burned and nonburned animals. VIP also decreased heart rate versus saline (p<0.05) and anti-VIP (p<0.001) in nonburned and burned animals. In contrast, VIP antiserum significantly increased blood pressure (p<0. 001) and heart rate (p<0.001) versus saline in all the groups. Skin perfusion in normal skin was significantly impaired by VIP infusions as compared to saline (p<0.01) while VIP-antiserum did not differ significantly from saline. Similarly, VIP significantly reduced blood flow versus saline-treatment in partial-thickness (p<0.01) and full-thickness burns (p<0.05) while VIP-antiserum had no significant effect on skin perfusion in any of the burned groups as compared to saline treatment. The present results show that VIP is directly involved in general cardiovascular control but plays a minor role in the maintenance of skin perfusion following a thermal injury as suggested by the lack of effect of VIP-antiserum. In contrast, exogenous administration of VIP significantly and dramatically impaired skin perfusion in normal and burned skin probably by increasing blood flow in organs of higher priority such as the brain and heart and concomitantly inducing a pronounced vasoconstriction in the skin, probably as a result of increased sympathetic effect on peripheral organs in order to maintain blood pressure.
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| 3. |
- Lindblom, Lucky, 1947, et al.
(författare)
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Role of nitric oxide in the control of burn perfusion.
- 2000
-
Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:1, s. 19-23
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 4. |
- Lindblom, Lucky, 1947, et al.
(författare)
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Role of vasoactive intestinal polypeptide in burn-induced oedema formation.
- 2000
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Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:5, s. 443-8
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Tidskriftsartikel (refereegranskat)abstract
- Vasoactive intestinal polypeptide has been demonstrated to lack inherent effects on capillary permeability, but also to potentiate the oedema promoting actions of other inflammatory mediators or even to strongly reduce organ damage and subsequent oedema in ischemic models of the lung and heart. This study investigated the role of VIP on oedema in partial- and full-thickness skin burns of anaesthetised rats in vivo by spectrophotometrical quantification of Evans blue albumin. Results show that systemic VIP elicited a significant drop in mean arterial blood pressure versus saline (p<0. 001) and VIP antiserum (p<0.001) both in burned and non-burned animals. VIP also decreased heart rate versus saline (p<0.05) and anti-VIP (p<0.01) in non-burned and burned animals. EB-albumin in normal skin was significantly inhibited by VIP as compared to saline (p<0.05), but did not differ significantly from VIP-antiserum. A significant inhibition of EB-albumin extravasation versus saline was also seen following administration of VIP-antiserum (p<0.01). Similarly, VIP significantly reduced EB-albumin extravasation versus saline treatment in partial-thickness (p<0.01) and full-thickness burns (p<0.001), while VIP-antiserum had no significant effect on skin perfusion in any of the burned groups as compared to saline treatment. The present results show that systemic VIP is a potent inhibitor of burn oedema. This effect could be secondary to constriction of skin vessels as a result of VIP-induced systemic hypotension or be mediated by the interaction of VIP with other oedema promoting mediators released following a thermal trauma to the skin.
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| 5. |
- Mattsson, Ulf, 1955, et al.
(författare)
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Intravenous lidocaine infusion in the treatment of experimental human skin burns - digital colour image analysis of erythema development.
- 2000
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Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:8, s. 710-5
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies have shown that local anaesthetics possess a wide range of effects on the pathophysiology of burns, including inhibition of burn oedema and inhibition of progressive burn ischemia. The present randomised double-blind cross-over study in six volunteers investigated the effects of intravenous lidocaine infusion on partial thickness skin burns. A thermoprobe was used to induce a standardised thermal injury (1 cm(2)) on the flexor side of one forearm and was repeated on the opposite side 1 week later. Subjects received either an intravenous bolus dose of lidocaine (1 mg kg(-1)) immediately after the thermal trauma followed by continuous intravenous infusion of lidocaine (40 microg kg(-1) min(-1)) during 4 h or equal volumes of isotonic saline. Macrophotographs of the experimental skin area were taken preburn and 1, 2, 3, 4, and 12 h postburn and evaluated by computerised image colour analysis using normalised rgb (n-rgb) and Hue-Saturation-Intensity (HSI) colour systems as a quantitative measure of pathophysiological events. Maximum erythema occurred 2-3 h postburn. Differences between lidocaine- and placebo-treated burns were not significant during the first 4 h postburn. At 12 h postburn, the lidocaine-treated burn demonstrated a significantly faster restitution of residual erythema compared to control sites. The present study shows that intravenous lidocaine significantly inhibits the long-term inflammation-induced tissue responses to thermal trauma.
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