Stress repair mechanism activity explains inflammation and apoptosis

作     者：Lewis S. Coleman 

作者机构：Barnes Dental Surgery Center 2626 S. Mooney Blvd Visalia Ca. 

出 版 物：《Advances in Bioscience and Biotechnology》 (生命科学与技术进展（英文）)

年 卷 期：2012年第3卷第4期

页      面：459-503页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：Selye Stress Inflammation Atherosclerosis Tissue Repair Hemodynamic 

摘      要：A review of modern evidence using Internet resources has identified the Stress Repair Mechanism (SRM) postulated by Hans Selye in 1951. SRM activity regulates thrombin generation to govern tissue maintenance, tissue repair, hemodynamic physiology, inflammation, and apoptosis. Thrombin utilizes ATP to energize coagulation, capillary hemostasis, chemotaxis, immune activity, mitosis, metabolism, angiogenesis, and the release of chemokines, cytokines, bradykinins, and prostaglandins that enable cell-to-cell communications, promote perfusion, loosen cell connections, and sensitize nociceptors during tissue repair. The orchestration of these diverse activities by the SRM explains the disparate elements of the inflammation syndrome, including dolor (pain), rubor (redness), calor (heat), tumor (swelling), and Functio laesa (loss of function). Inflammation resolves as tissue repair nears completion and declining SRM activity restores thrombin to maintenance levels. As thrombin levels decline below a critical threshold, repair cells undergo apoptosis and clots disintegrate. Apoptosis shrinks granulation tissues to enable wound closure. Apoptosis also facilitates embryological development. Occult systemic SRM hyperactivity due to sepsis, surgery, trauma, chemicals, pain, fear, and emotional memories causes inflammatory effects that manifest as the fever, edema, malignancy, organ disruption, eclampsia, Multi-System Organ Failure (MS-OF), Systemic Inflammatory Response Syndrome (SI-RS), Adult Respiratory Distress Syndrome (ARDS), Disseminated Intravascular Coagulation (DIC) and other pathologies.