Abstract
Chronic postsurgical pain (CPSP) is a chronic pain state that is difficult to be treated clinically. A series of complicated changes have been produced from nociceptive stimulation to the occurrence and development of postsurgical pain. Many mechanisms remain unclear. In order to study the role of intercellular gap junctions in inducing inflammatory microenvironment at the beginning of nociceptor after operation, the model of skin/muscle incision and retraction (SMIR) was established. We observed the changes of the expression of exchange proteins directly activated by cAMP-1 (Epac1) and p120 catenin (p120), the quantities of macrophages and endothelial cells, vascular endothelial permeability, and mechanical withdrawal threshold (MWT). It was found that macrophages and endothelial cells were functionally coupled through Epac1-p120. Adhesive linkage disorder remodeled the chronic, inflammatory, and eutrophic microenvironment at the beginning of nociceptor after operation through macrophages, endothelial cells, and endothelial paracellular pathways. It might be an early event and a key step in peripheral sensitization of CPSP. The expression of p120 in muscle tissue around the incision might become a prognostic marker for the conversion of acute postsurgical pain into CPSP. Targeted intervention of Epac1-p120 might be a clinical strategy for inhibiting the conversion of acute postsurgical pain into CPSP.
Highlights
In the persistent postsurgical pain, there is a series of complicated changes from nociceptive stimulation to the occurrence and development of postsurgical pain
In order to study the role of macrophages and endothelial cells in the remodeling of inflammatory microenvironment, the muscle tissue around the incision was taken on the 3rd, 7th, and 14th day after skin/muscle incision and retraction (SMIR) to detect the vascular endothelial permeability and the distribution of macrophages and endothelial cells
It was found that surgical wounds and repairs induced obstruction of the vascular endothelial barrier, maintenance of endothelial hyperpermeability, and increased distribution of macrophages and endothelial cells in muscle tissue around the incision in rats, and macrophages were not distributed in normal rats (Figure 2)
Summary
In the persistent postsurgical pain, there is a series of complicated changes from nociceptive stimulation to the occurrence and development of postsurgical pain. It is generally believed that peripheral sensitization and central sensitization caused by changes of neuronal plasticity are the mechanisms of chronic pain. Every kind of molecular change may affect CCC’s stability; CCC is involved in regulating a series of biological behavior changes such as cell adhesion, migration, invasion, and proliferation. Cyclic adenosine monophosphate (cAMP) regulates intercellular adhesion, migration, and inflammation through Epac [7]. Ere are two subtypes of Epac: Epac and Epac; Epac controls intercellular adhesion, links [8, 9], and regulates endothelial permeability barriers under injury [10] Cyclic adenosine monophosphate (cAMP) regulates intercellular adhesion, migration, and inflammation through Epac [7]. ere are two subtypes of Epac: Epac and Epac; Epac controls intercellular adhesion, links [8, 9], and regulates endothelial permeability barriers under injury [10]
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