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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Anestesi och intensivvård) ;pers:(Tarnow Peter 1963)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Anestesi och intensivvård) > Tarnow Peter 1963

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1.
  • Cassuto, Jean, et al. (författare)
  • Adrenoceptor subtypes in the control of burn-induced plasma extravasation.
  • 2005
  • Ingår i: Burns : journal of the International Society for Burn Injuries. - : Elsevier BV. - 0305-4179. ; 31:2, s. 123-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Burn trauma is known to induce a significant rise in circulating catecholamine levels and despite catecholamines being potent endogenous vasoactive agents with known actions on microvascular permeability, their effect on burn edema has been poorly investigated. The present study in rats investigated the role and importance of adrenergic receptor subtypes in the regulation of basal capillary permeability in normal skin and hyperpermeability in partial- and full-thickness skin burns. Edema was quantified by spectrophotometric analysis of extravasated Evans blue-albumin. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-receptor agonist), prazosin (alpha(1)-receptor antagonist), clonidine (alpha(2)-receptor agonist), yohimbine (alpha(2)-receptor antagonist), prenalterol (beta(1)-receptor agonist), terbutaline (beta(2)-receptor agonist), or propranolol (beta(1)- and beta(2)-receptor antagonist). Results showed increased capillary permeability in normal skin following administration of terbutaline (p<0.01) and yohimbine (p<0.01). In partial-thickness burns, clonidine significantly (p<0.05) reduced edema formation, whereas in full-thickness burns edema was significantly reduced by clonidine (p<0.05) and l-phenylephrine (p<0.01). In conclusion, the inhibition of postburn edema induced by stimulation of alpha(1)-receptors (l-phylephrine) and alpha(2)-receptors (clonidine) could be secondary to increased vascular resistance and reduced tissue perfusion pressure and/or suppressed inflammatory reaction in the burn injury. In the treatment of burn patients, clonidine is particularly interesting since the agent has previously been proven to induce potent analgesia in thermally injured.
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2.
  • Cassuto, Jean, et al. (författare)
  • Regulation of postburn ischemia by alpha- and beta-adrenoceptor subtypes.
  • 2005
  • Ingår i: Burns : journal of the International Society for Burn Injuries. - : Elsevier BV. - 0305-4179. ; 31:2, s. 131-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Deep skin burns are characterised by progressive ischemia secondary to vasoconstriction and thrombosis formation. Burn trauma elicits increased sympathetic activity and elevation of circulating catecholamines acting on adrenoceptors in vascular tissue playing an important role in the regulation of organ blood flow. The present study in rats investigated the role of alpha- and beta-adrenoceptors in the circulatory changes taking place in normal skin and in partial- and full-thickness skin burns using laser Doppler flowmetry. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-agonist), prazosin (alpha(1)-antagonist), clonidine (alpha(2)-agonist), yohimbine (alpha(2)-antagonist), prenalterol (beta(1)-agonist), terbutaline (beta(2)-agonist), and propranolol (beta(1)- and beta(2)-antagonist). Blood flow in normal skin was reduced by phenylephrine (p<0.001), clonidine (p<0.001) and propranolol (p<0.01), and increased by prazosin (p<0.05), yohimbine (p<0.05), prenalterol (p<0.05) and terbutaline (p<0.01). In partial-thickness burns, blood flow was reduced by phenylephrine (p<0.01), clonidine (p<0.01) and propranolol (p<0.05). In full-thickness burns, only clonidine reduced perfusion (p<0.05). In conclusion, beta(1)- and beta(2)-adrenoceptors play important role in the physiological regulation of skin perfusion but are of lesser importance for postburn skin perfusion. Vasoconstrictive alpha(1)- and alpha(2)-adrenoceptors were shown to be tonically active in normal skin and in partial-thickness burns, exerting a negative effect on skin perfusion which was further potentiated by exogenous administration of alpha(1)- and alpha(2)-agonists and reversed by selective alpha-blockers. In full-thickness burns, activation of alpha(2)-receptors was shown to significantly impair skin circulation, raising a flag of warning for the use of clonidine to treat pain in burn patients.
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3.
  • Jönsson, Anders, 1959, et al. (författare)
  • Effects of amide local anaesthetics on eicosanoid formation in burned skin.
  • 1999
  • Ingår i: Acta anaesthesiologica Scandinavica. - 0001-5172. ; 43:6, s. 618-22
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies have demonstrated potent inhibition of burn oedema and progressive ischaemia by local anaesthetics. Since eicosanoids have been suggested to play an important role in the pathophysiology of burns, we compared in the present ex vivo study the effects of topical lidocaine/prilocaine cream (EMLA, ASTRA, Sweden) and intravenous lidocaine with that of saline on eicosanoid formation by normal and burned rat skin.
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4.
  • Jönsson, Anders, 1959, et al. (författare)
  • Local anesthetics improve dermal perfusion after burn injury.
  • 1998
  • Ingår i: The Journal of burn care & rehabilitation. - 0273-8481. ; 19:1 Pt 1, s. 50-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Deep partial-thickness burn injury was induced in the abdominal skin of anesthetized rats. Dermal perfusion was assessed by laser Doppler flowmetry. In the first set of experiments, one group of rats (n = 15) was topically treated with a lidocaine-prilocaine cream 5% (25 mg of each in 1 g) for 6 hours, starting 5 minutes after inducing the burn injury. In one control group (n = 14), the thermal injury was treated with placebo cream. Results showed a markedly reduced perfusion in the skin of the control animals within the first hour after burn injury, with further decrease during the following 5 hours of observation. In animals treated with the lidocaine-prilocaine cream, skin perfusion in the burned area was significantly increased during the first 30 minutes after the burn injury compared to before the burn (p < 0.01), followed by a decrease to a level below the preburn stage but significantly higher than that of control animals during the first hour after burn injury (p < 0.05). As opposed to burned control animals, skin perfusion gradually recovered toward preburn levels at the end of the experiment in local anesthetic-treated animals. In the second experimental set, four groups of animals were burned and subsequently treated with a bolus dose of lidocaine intravenously (2 mg/kg), followed by continuous intravenous lidocaine infusions at a rate of 50 (n = 10), 100 (n = 11), or 150 (n = 10) micrograms.kg-1.min-1. The infusions were started 5 minutes after the burn injury and lasted for 6 hours. Corresponding volumes of saline solution were given to burned control animals (n = 10). Results showed a significantly improved skin perfusion in the lidocaine-treated group in a dose-response fashion as compared to control animals. A maximum improvement of dermal perfusion in the burned area was induced by intravenous lidocaine at an infusion rate of 150 micrograms.kg-1.min-1 as compared to burned controls treated with isotonic saline solution infusions (p < 0.01). Results showed that topical or systemic administration of local anesthetics can prevent progressive dermal ischemia after thermal injury.
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5.
  • Jönsson, Anders, 1959, et al. (författare)
  • Topical local anaesthetics (EMLA) inhibit burn-induced plasma extravasation as measured by digital image colour analysis.
  • 1998
  • Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 24:4, s. 313-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Amide local anaesthetics have previously been shown to reduce oedema and improve dermal perfusion following experimental burns. Previous studies have used invasive techniques for burn oedema quantification which do not allow continuous monitoring in the same animal. The present study used digital image colour analysis to investigate the effect of topical local anaesthetics on burn-induced extravasation of Evans blue albumin. A standardised full-thickness burn injury (1 x 1 cm) was induced in the abdominal skin of anaesthetised rats. The burn area was subsequently covered with 0.5 g of lidocaine-prilocaine cream 5% (25 mg of each in 1 g; EMLA, ASTRA, Sweden) or placebo cream during the first hour post-burn. One hour after the burn trauma, animals received Evans blue dye intravenously. Skin colour appearances were recorded by macrophotography before the burn and 5, 60. 65, 90, 120, 150, and 180 min post-burn. Colour slides were digitised and colour changes were analysed using the normalised red-green-blue (n-rgb) colour system. Results showed a significant inhibition of Evans blue extravasation between 60 and 180 min post-burn in EMLA-treated animals versus controls. Topical local anaesthetics are potent inhibitors of burn-induced plasma albumin extravasation, probably by direct action on vascular permeability and by inhibition of various steps of the pathophysiological response after burn injury.
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6.
  • Lindblom, Lucky, 1947, et al. (författare)
  • Importance of nitric oxide in the regulation of burn oedema, proteinuria and urine output.
  • 2000
  • Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 26:1, s. 13-7
  • 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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7.
  • Mattsson, Ulf, 1955, et al. (författare)
  • Digital image analysis of erythema development after experimental thermal injury to human skin: effect of postburn topical local anesthetics (EMLA).
  • 1999
  • Ingår i: Anesthesia and analgesia. - 0003-2999. ; 88:5, s. 1131-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Local anesthetics inhibit edema and improve circulation in experimental burns. We evaluated the effect of topical local anesthetics on human skin burns in volunteers using computerized color analysis that allowed repeated noninvasive quantitative measurements. A standardized partial-thickness burn (1 cm2) was induced in one forearm of 10 healthy volunteers and in the opposite forearm a week later. The burned areas were treated with lidocaine/prilocaine cream (EMLA; Astra, Sweden) or a placebo cream for 1 h. The experimental skin area was photographed before and 1, 2, 4, and 12 h postburn. Digitized images were evaluated using normalized red-green-blue and Hue-Saturation-Intensity. Differences in erythema between skin treated with EMLA and placebo were not significant during the first 4 h postburn. However, 12 h postburn, a pronounced decrease in the degree of erythema was observed in EMLA-treated skin compared with placebo-treated skin. We conclude that topical local anesthetics administered for 1 h postburn significantly reduces the duration of erythema after a mild thermal injury, which suggests a potential use in clinical practice in the treatment of minor skin burns.
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8.
  • Tarnow, Peter, 1963, et al. (författare)
  • [Disaster planning--lessons learned from the fire disaster in Gothenburg]
  • 2005
  • Ingår i: Läkartidningen. - 0023-7205. ; 102:4
  • Tidskriftsartikel (refereegranskat)abstract
    • The tragic fire disaster in Sweden 1998, killing 63 and wounding 213 teenagers was the result of arson fire in the basement of an overcrowded discotheque. Since the disaster occurred in a major city with substantial resources, all the injured could be hospitalised within two hours. The load on four local hospitals was initially severe due to the large number of injured. The patients suffered from inhalation injuries of different severity, whereas 25 of them also had deep skin burn injuries. Thirteen of the most severe burn injuries were transported to burn units in other parts of Sweden and to Norway. The vast psychosocial rehabilitation program initiated by health care staff, religious communions, schools and the community, has continued over the past years. This fire disaster emphasises the need for extensive preparation not only in the rescue and medical services, but also in many other areas of society.
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9.
  • Tarnow, Peter, 1963, et al. (författare)
  • Effects of D-myo-Inositol-1,2,6-triphosphate on eicosanoid formation in burned skin.
  • 1996
  • Ingår i: The Journal of surgical research. - 0022-4804. ; 62:1, s. 1-4
  • Tidskriftsartikel (refereegranskat)abstract
    • D-myo-Inositol-1,2,6-triphosphate (IP3) has been shown to reduce edema and progressive ischemia following experimental skin burns. The mechanism(s) are not identified but could be related to antiinflammatory effects of the agent. In the present ex vivo study we compared the effects of IP3 with those of saline and indomethacin on eicosanoid formation by normal and burned rat skin. In burned skin IP 3 treatment reduced the release of thromboxane B2 (TXB2) (P < 0.01) and leukotriene B4 (LTB 4) (P < 0.05) but there was only a weak trend for less prostaglandin E (PGE) compared to burned control animals receiving saline. Indomethacin reduced the release of TXB2 (P < 0.01), and PGE (P < 0.001), but not LTB 4 from burned skin compared to skin from saline-treated burned animals. In non-burned skin IP 3 increased the release of PGE (P < 0.01) and LTB 4 (P < 0.01), but did not significantly influence TXB2 accumulation in the incubation fluid compared to the saline-treated group. Indomethacin reduced the release of TXB2 (P < 0.001) and PGE (P < 0.001), but increased LTB 4 (P < 0.001) in normal skin compared to the saline-treated group. In conclusion, IP 3 inhibited the release of TXB2 and LTB 4 from burned skin ex vivo, but increased PGE and LTB 4 release from normal skin. These results suggest that the mode of action of IP 3 differs from that of nonsteroidal antiinflammatory drugs. The effects of IP 3 on the arachidonic acid cascade also seem to differ in burned versus normal skin.
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10.
  • Tarnow, Peter, 1963, et al. (författare)
  • Increased dermal perfusion after skin burn injury by D-myo-inositol-1,2,6-trisphosphate.
  • 1996
  • Ingår i: Burns : journal of the International Society for Burn Injuries. - 0305-4179. ; 22:5, s. 363-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Full-thickness burn injury results in a continuous deterioration of blood flow due to vascular sludging, thrombosis formation and oedema leading to irreversible ischaemia and tissue necrosis. D-myo-inositol-1,2,6-trisphosphate (IP3) has previously been shown to reduce burn-induced oedema formation and inflammation involved in the pathophysiology of progressive ischaemia. A full-thickness burn injury (1 cm2) was induced in the abdominal skin of anaesthetized rats using an electrically heated thermoprobe. Blood flow in the experimental area was measured by laser Doppler flowmetry during 6.5 h postburn. The experiments included five groups. Three burned groups were treated intravenously with IP3 and received respectively: a bolus dose of 4 mg/kg followed by a continuous intravenous infusion of 20 mg/kg/h, 8 mg/kg + 40 mg/kg/h or 16 mg/kg + 60 mg/kg/h. One burned and one unburned control group received a corresponding bolus dose and infusion of saline. Results showed a significant inhibition of dermal ischaemia in the burned groups receiving IP3 at all dose intervals as compared to saline-treated burned rats (all P < 0.001). We conclude that IP3 improved local dermal perfusion in burned skin. Probable mechanisms of action could be the vasodilatory and anti-inflammatory properties of the agent.
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