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Based on Capillary Gate Theory and Tissue Repair Theory, this presentation will explain the recently identified “Stress Repair Mechanism” (SRM) that enables the long-anticipated Universal Theory of Medicine postulated by Hans Selye in 1954. The SRM maintains and repairs vertebrate tissues and accounts for most of the mysterious manifestations of allostasis that remain unexplained by Hypothalamic-Pituitary-Axis (HPA) hormones. SRM activity explains hemodynamic physiology, capillary hemostasis, infarction, Korotkoff sounds, blood pressure, hypertension, diabetes, allostasis, allostatic load, anesthesia, analgesia, atherosclerosis, apoptosis, malignancy, eclampsia, sepsis, Multi-System Organ Failure (MSOF), the surgical stress syndrome, the fight or flight response, and numerous other manifestations of physiology, pathology, and allostasis. 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, so that 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.
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SurgeryTraumaBurnsSepsisRadiationChemicalsToxins
Stressful ForcesExtravascularTissue Disruption
TISSUE REPAIR COMPONENT
Tissue Factor Pathway InhibitorATIIIProtein C
MetabolismAngiogenesisChemokinesCytokinesProstaglandins
Malignancy
Apoptosis
BoneMuscle
PneumoniaInfluenza
AsthmaARDSMSOF
EclampsiaARF
PusScabsCasts
Exudates
Abscesses
SOLUBLEFIBRIN
TISSUEREPAIR
PlateletsInflammationChemotaxisMitosis
FIBRONIGENFactor X
ImmuneProteins
TemperatureCatabolismFeverImmune CellsEndotheliumOsteoblastsMyoblastsFibroblasts
Collagen
Factor XIII
VitronectinFibronectin
COAGULATION
SYSTOLICTURBULENTRESISTANCE
HyperviscosityHypercoagulableFlow ResistanceIncreased SWRCardiac WorkHypertensionDecreased COAtherosclerosis
Tissue IschemiaHypoxemiaOrgan QuiescenceIncreased SWROrgan StressHypertensionDecreased COIncreased HR
Tissue PerfusionHyperoxemiaOrgan ActivityDecreased SVROrgan PreservationHypotensionIncreased CODecreased HR
CAPILLARYHEMOSTASIS
CAPILLARYFLOW
SYSTOLICLAMINARFLOW
Optimal ViscosityNormocoagulableFlow FacilitationDecreased SVRCardiac RestHypertensionIncreased COHealth & Longevity
Cerebral Cortex
FibrinSplit Products
Insoluble Fibrin
TAFI
THROMBIN TISSUE FACTORThrombin ActivationFactor VII
Krebs
Cycle
Ca+
Factor VIIIC
ThrombinAcceleration
VON WILLIBRAND FACTOR
PAI
TPA
The Stress Repair Mechanism (SRM)
ThrombinAmplificationFactor IX
VASCULARENDOTHELIUM
EpinephrineNorepinephrineCortisol
HPA Axis
NitricOxide
Analgesia
Visual, OlfactoryAuditory, Tactile
Pain
CAPILLARY GATE COMPONENTStressful StimuliIntravascularNeurons Pathways
ATP
Nociception
Internuncial
Spinal Cord
Hypothalamus
Peripheral Nerves
PeripheralReceptors
Sensory Stressors
SPINAL PATHWAY
EmotionalMechanisms
Anesthesia
SYMPATHETIC
PARASYMPATHETIC
Insulin
COGNITIVE PATHWAY
FibrosisScar
Adhesion
The Universal Theory of Medicine of Hans Selye
Dr. Hans Selye 1907-1982
Capillary Gate Theory
Tissue Repair Theory
Coagulation Cascade
Stress Repair Mechanism
Factor VIII: The Missing Link
Von Willebrand’s Factor
Vascular Endothelium
Inert
Fluctuates with Nervous activity
Gigantic molecule
Factor VIIIC
liver
Labile enzyme
Generates Insoluble Fibrin
Gigantic molecule
THROMBIN
THROMBIN: THE UNIVERSAL ENZYME OF ENERGY TRANSDUCTION
Soluble Fibrin: The Universal Protein of Tissue Repair
Insoluble Fibrin: The Universal Polymer of Hemostasis
The Vascular Endothelium
TF
TF VWF
SNS
PNSNO
TF
Vascular Endothelium
Factor IX
Stressful Forces
Stressful Stimuli
FactorVIII Factor VII
Factor X
Thrombin
Soluble FibrinFactor XIII
Insoluble Fibrin
FibrinogenTAFI
Cell Activity
Capillary Gate Component
Tissue Repair Component
VWFTF
Capillary Gate Mechanism/Component
1. Operates in flowing blood2. Molecular level capillary gate that controls capillary flow3. Closed by SNS release of VWF that generates Insoluble Fibrin that binds to
red cells in capillary lumen4. Opened by PNS release of NO that disintegrates Insoluble Fibrin into fibrin
split products5. Turbulence Mechanism regulates viscosity & coagulability in larger vessels6. Controls blood pressure, heart rate, Cardiac Output, atherosclerosis7. Controls organ function8. Determines tissue perfusion and oxygenation
The Capillary Gate
Tissue Repair Mechanism/Component
1. Clot formation (seals flowing blood from damaged tissues)2. Inflammation (loosens cell connections)3. Chemotaxis (attracts repair cells to damaged tissues)4. Fibrin infiltration (forms structure for cell activity)5. Cell proliferation & differentiation (replaces damaged tissues)6. Production of collagen & bone7. Angiogenesis (perfuses developing tissues)8. Immune cell activity (removes debris & combats infection)9. Apoptosis of repair cells (shrinks wound & enables closure)
Insoluble Fibrin
The Coagulation Cascade
BurnsSurgeryTraumaSepsisRadiationChemicalsToxins
Stressful ForcesExtravascularTissue Disruption
TISSUE REPAIR COMPONENT
Tissue Factor Pathway InhibitorATIIIProtein C
MetabolismAngiogenesisChemokinesCytokinesProstaglandins
Malignancy
Apoptosis
BoneMuscle
PneumoniaInfluenza
AsthmaARDSMSOF
EclampsiaARF
PusScabsCasts
Exudates
Abscesses
SOLUBLEFIBRIN
TISSUEREPAIR
PlateletsInflammationChemotaxisMitosis
FIBRONIGENFactor X
ImmuneProteins
TemperatureCatabolismFeverImmune CellsEndotheliumOsteoblastsMyoblastsFibroblasts
Collagen
Factor XIII
VitronectinFibronectin
COAGULATION
SYSTOLICTURBULENTRESISTANCE
HyperviscosityHypercoagulableFlow ResistanceIncreased SWRCardiac WorkHypertensionDecreased COAtherosclerosis
Tissue IschemiaHypoxemiaOrgan QuiescenceIncreased SWROrgan StressHypertensionDecreased COIncreased HR
Tissue PerfusionHyperoxemiaOrgan ActivityDecreased SVROrgan PreservationHypotensionIncreased CODecreased HR
CAPILLARYHEMOSTASIS
CAPILLARYFLOW
SYSTOLICLAMINARFLOW
Optimal ViscosityNormocoagulableFlow FacilitationDecreased SVRCardiac RestHypertensionIncreased COHealth & Longevity
Cerebral Cortex
FibrinSplit Products
Insoluble Fibrin
TAFI
THROMBIN TISSUE FACTORThrombin ActivationFactor VII
Krebs
Cycle
Ca+
Factor VIIIC
ThrombinAcceleration
VON WILLIBRAND FACTOR
PAI
TPA
The Stress Repair Mechanism (SRM)
ThrombinAmplificationFactor IX
VASCULARENDOTHELIUM
EpinephrineNorepinephrineCortisol
HPA Axis
NitricOxide
Analgesia
Visual, OlfactoryAuditory, Tactile
Pain
CAPILLARY GATE COMPONENTStressful StimuliIntravascularNeurons Pathways
ATP
Nociception
Internuncial
Spinal Cord
Hypothalamus
Peripheral Nerves
PeripheralReceptors
Sensory Stressors
SPINAL PATHWAY
EmotionalMechanisms
Anesthesia
SYMPATHETIC
PARASYMPATHETIC
Insulin
COGNITIVE PATHWAY
FibrosisScar
Adhesion
The Universal Theory of Medicine of Hans Selye
Charles Atlas or 90lb Weakling?
Blood Acceleration & Turbulence
Systolic Acceleration
Diastolic Deceleration
Diastolic Turbulence
Pipe Flow TurbulenceLateral ForcesFast Faster Fastest
What Can It Do?1. Explains the manifestations of allostasis2. Promises a rapid and reliable cure for cancer3. Elimination of the Surgical Stress Syndrome 4. Advanced forms of invasive surgery5. Fresh explanation of Rheumatoid Disease and effective treatments6. Control of ARDS, MOFS, Eclampsia, Asthma, Pneumonia, Influenza, spinal
cord shock, and sepsis7. Control of plagues and epidemics8. Fresh insights to embryology, evolution, parasitology, psychology
The End
New Research Information
1. The Vascular Endothelium is a nervous gland that releases numerous hormones
2. The Vascular Endothelium releases VWF in accord with Sympathetic activity
3. Factor VIII consists of hepatic VIIIC plus VWF produced by the Vascular Endothelium
4. Thrombin energizes cell and enzyme activity 5. Thrombin requires both Ca+ and ATP6. Agents that bind to Ca+ inhibit thrombin activity7. The vascular endothelium releases Nitric Oxide in accord with
Parasympathetic activity to induce “nitrergic neurogenic vasodilation”8. All cells possess thrombin receptors in combinations that are characteristic
of the cell type9. Fibrinogen, soluble fibrin and insoluble fibrin can now be distinguished
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