Microvascular permeability to macromolecules in thermal injury.
Thermal injury of the skin causes an inflammatory reaction with formation of edema, mainly due to vasodilatation, increased extravascular osmotic activity and increased microvascular permeability to macromolecules. These reactions are due to local and systemic effects . At the site of injury heat itself causes microvascular damage. Vascular changes may also be mediated by vasoactive compounds, e.g. liberation of histamine and increased synthesis of prostaglandins. Reflex mechanisms elicited via the nervous system must also be considered. Morphological studies revealed increased number of vacuoles, a large number of open endothelial intercellular junctions and changes of the interstitial tissue at the site of thermal injury. The vascular reactions described can be modified by drugs, especially indomethacin which inhibits the synthesis of prostaglandins and drugs which competitively antagonize the effects of histamine at H2-receptors.
D000818:Animals; D002056:Burns / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002199:Capillary Permeability; D006224:Cricetinae; D003911:Dextrans; D004285:Dogs; D004487:Edema / Q000209:etiology; D004727:Endothelium / Q000648:ultrastructure; D006636:Histamine Release; D006801:Humans; D006874:Hydrostatic Pressure; D007365:Intercellular Junctions / Q000648:ultrastructure; D008196:Lymph / Q000032:analysis / Q000502:physiology; D046911:Macromolecular Substances; D008833:Microcirculation / Q000503:physiopathology* / Q000648:ultrastructure; D009997:Osmotic Pressure; D011453:Prostaglandins / Q000096:biosynthesis
D003911:Dextrans; D046911:Macromolecular Substances; D011453:Prostaglandins