Tissue Hydration Influences Bursting Pressure of Fused Arteries

Tissue fusion is a complex thermally driven reaction which, through the application of heat and pressure, bonds the extracellular matrix (ECM) of neighboring tissues together. While the mechanism of this reaction is unknown, several theories do exist. Collagen is largely thought to be responsible for the formation of the fusion bond [1–3]. During tissue fusion, as the tissue temperature is elevated (> 100 °C) [4–5], collagen denatures and water is forcibly evaporated out of the tissue [6–11]. Collagen in arterial tissue is comprised of a tightly wound triple helix held in place by crosslinking. Upon denaturation, the crosslinks are broken and the helix unwinds [6–8]. It is theorized that under applied heat and pressure the denatured molecules tangling with adjacent molecules [1], crosslinking to neighboring molecules [2], or a combination of these two mechanisms are responsible for the formation of the tissue fusion bond [3]. Water is also present in the ECM which can be classified as free or bound. Free water is able to diffuse and move freely around the ECM. Bound water is held to ECM proteins through dipole interactions. During tissue fusion, the water is forcibly removed and these charged sites which interact with water are now able to interact with adjacent molecules. These charged sites would not exist if not for the removal of water from the ECM. The goal of this study is to elucidate the importance of water in the formation of the tissue fusion bond.