XXXX : processes in pathogenetic networks: a review.

@entity131 @entity5721 @entity855 @entity63
@entity5721 is a complex phenomenon involving not only intracellular injury processes but also an injurious inflammatory response. Both the intracellular injury processes and the injurious events of the inflammatory response are interconnected in pathogenetic networks. @entity131 predominates in the @entity63 phase. The decreased mitochondrial @entity855 generation impairs cellular ion homeostasis with activation of hydrolases and loss of selective permeability of cell membranes. Upon resupply of blood, the inflammatory response is initiated. Resident cells of the affected tissue, blood-derived cells, and noncellular elements such as the complement system are activated, and signalling and other molecules are formed at altered rates. @entity131 occurring in the reperfusion phase may either be a consequence of cellular alterations that were already initiated in the @entity63 phase or may result from the inflammatory response. The intracellular injurious alterations are in part the same as those involved in @entity131 . In addition, activation of intracellular signalling cascades and of apoptotic pathways may take place. Except for a large decrease in their rates, no significant difference exists between the injury processes during warm and cold @entity63 as they become evident during @entity63 itself. In contrast, the injury processes of the inflammatory response and of cell injury in the reperfusion phase significantly vary depending on pre-existent warm versus cold @entity63 . Because of the netlike characteristics of the pathomechanisms, a multifactorial approach is required to provide protection against @entity63 -reperfusion injury.
