Microvascular Changes in Cold Injury Edema

Abstract

The cold injury, originally introduced by Clasen and Klatzo has become the most commonly used model for traumatic vasogenic edema. It has been shown that the cortical injury is the site of focal increase in vascular permeability of protein. Removal of the cold injury completely eliminates the development of edema emphasizing the importance of an intact vascular bed. It has generally been assumed that traumatized blood vessels were the origin of the edema fluid in this model, but no attempts to define the vascular injury in detail are found in the voluminous literature which relates to this model. Since many functional studies of brain edema are based upon the cold injury model, it seems important to define the histology in detail. This report details a preliminary attempt to identify the morphological basis for the abnormal permeability which characterizes the cold injury model of vasogenic brain or spinal cord edema.