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A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress
Author(s) -
Coleman Lewis Stanton
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.878.1
Subject(s) - endothelium , von willebrand factor , fibrin , mechanism (biology) , autonomic nervous system , biology , neuroscience , perfusion , thrombin , microbiology and biotechnology , anatomy , endocrinology , medicine , platelet , immunology , blood pressure , philosophy , heart rate , epistemology
This presentation describes the “Stress Repair Mechanism”(SRM) that enables the “Universal Theory of Medicine” predicted by Hans Selye. It explains the nature of embryology, physiology, pathology, and stress. SRM function comprises the autonomic nervous system, the vascular endothelium, and the dynamic enzymatic interaction of blood‐borne hepatic Factors VII, VIIIC, IX and X that produces thrombin, soluble fibrin and insoluble fibrin, whose combined effects account for all SRM manifestations. The vascular endothelium is a diaphanous neuroendocrine organ that lines all blood vessels and is the sole constituent of capillary walls. It secretes tissue factor into extravascular tissues, and insulates those tissues from the hepatic enzymes. Tissue disruption exposes tissue factor to the enzymatic interaction and activates tissue repair. The vascular endothelium also releases nitric oxide and von Willebrand Factor into blood in accord with autonomic balance to regulate the enzymatic interaction to govern tissue perfusion and organ function. Therefore, continuously fluctuating combinations of nervous stimuli that affect autonomic balance and forces that disrupt tissues determine SRM activity.