Increased dermal perfusion after skin burn injury by d-myo-inositol-1,2,6-trisphosphate
Autor: | Jean Cassuto, Anders Jönsson, Peter Tarnow, G. Rimbäck |
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Rok vydání: | 1996 |
Předmět: |
Male
Burn injury Inositol Phosphates medicine.medical_treatment Ischemia Vasodilation Critical Care and Intensive Care Medicine Rats Sprague-Dawley Edema medicine Animals Infusions Intravenous Saline Skin Wound Healing business.industry Anti-Inflammatory Agents Non-Steroidal General Medicine Blood flow medicine.disease Thrombosis Rats Disease Models Animal Regional Blood Flow Anesthesia Emergency Medicine Surgery medicine.symptom Burns business Perfusion |
Zdroj: | Burns. 22:363-368 |
ISSN: | 0305-4179 |
DOI: | 10.1016/0305-4179(95)00173-5 |
Popis: | 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. |
Databáze: | OpenAIRE |
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