The Capillary Gate Mechanism

 “Most people say that it is the intellect which makes a great scientist. They are wrong. It is character. “---Albert Einstein

“One must still have chaos in oneself to be able to give birth to a dancing star.” ---Frederich Nietzsche 

A capillary gate mechanism regulates flow resistance efficiently, because pressures, flows, and turbulence are minimal in capillaries, and capillary surface area is greater than that of all larger vessels combined.(1-5) 

Sympathetic nervous activity releases von Willebrand Factor (VWF) from the capillary endothelium; VWF increases factor VIII activity, which generates insoluble fibrin in the capillary lumen to increase flow resistance (aka viscosity, or systemic vascular resistance).

Parasympathetic nervous innervation releases nitric oxide (NO) from the capillary endothelium, which binds to Ca+, inhibits thrombin, accelerates the disintegration of insoluble fibrin, and reduces flow resistance (aka "nitrergic neurogenic vasodilation") 

Hypoxia and hypercarbia open the capillary gate by releasing nitric oxide from the capillary endothelium.(6)  

The capillary gate mechanism governs cardiac output, cardiac efficiency, tissue perfusion, tissue oxygenation, and organ function. Its activity affects the turbulence mechanism that maintains arterial patency and explains blood pressure and the palpable pulse. 

Sympathetic activity releases epinephrine from the adrenal glands, which releases von Willebrand Factor from the capillary endothelium to close the capillary gate in peripheral tissues where direct sympathetic innervation is lacking. 

Parasympathetic activity releases insulin from the pancreas, which releases nitric oxide from the capillary endothelium to open the capillary gate in peripheral tissues where direct parasympathetic innervation is lacking.

The capillary gate explains why both "vasopressors" and "vasodilators" increase "fibrin split products".

Capillary gate activity does not normally cause tissue hypoxia, as evidenced by the rarity of infarction in youth. However, capillary senescence  undermines tissue perfusion and exaggerates the risk of infarction, diabetes, and congestive heart failure. Chronic stress causes accelerated capillary senescence.

Trauma disrupts the capillary endothelium and directly exposes tissue factor to blood, which triggers a synergistic enzymatic interaction of factors VII, VIII, IX and X that exaggerates insoluble fibrin generation to enable capillary hemostasis and viscoelastic clot formation. 

 

1. L. S. Coleman, Insoluble fibrin may reduce turbulence and bind blood components into clots. Med Hypotheses 65, 820-821 (2005).
2. L. S. Coleman, To the Editor: Is von Willebrand Factor a Hormone that Regulates a Coagulation Mechanism? World J Surg,  (2006).
3. L. S. Coleman, A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand's factor may function as a "capillary gate" and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance. Med Hypotheses 66, 773-775 (2006).
4. L. S. Coleman, A Stress Repair Mechanism that Maintains Vertebrate Structure during Stress. Cardiovasc Hematol Disord Drug Targets,  (2010).
5. L. S. Coleman, in Hypotheses in Clinical Medicine, e. a. Shoja MM, Ed. (Nova Biomedical, New York, NY, 2012),  chap. 29.
6. N. Toda, K. Ayajiki, T. Okamura, Cerebral blood flow regulation by nitric oxide: recent advances. Pharmacol Rev 61, 62-97 (2009).