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.

The sympathetic nervous system (SNS) may directly or indirectly govern the release of von Willebrand's factor (VWB), which may be a hormone, from the vascular endothelium, which may be a gland. VWB is known to stabilize the labile VIIIC component of Factor VIII complex, and may thereby determine its half-life and activity level in the blood. Rising blood levels of Factor VIII may increase the speed of thrombin production during the "propagation" phase of blood coagulation and thereby elevate peak levels and duration of thrombin activity to produce and stabilize insoluble fibrin in quantities necessary to initiate clot formation. At the capillary level, microvascular receptor sites may bring fibrinogen and fibronectin, which are basic "building blocks" of insoluble fibrin, into close proximity with rising levels of Factor VIII to facilitate insoluble fibrin production and serve as binding sites for an expanding mass of insoluble fibrin that adheres to blood components to cause capillary hemostasis. Capillary hemostasis may serve as a "capillary gate mechanism" (CGM) that increases systemic vascular resistance and blood pressure and decreases cardiac output in accord with increased tone and activity levels of the SNS by obstructing capillary bed flow. Angiodysplasia may be caused by persistent defects in the VWB molecule that impair CGM function and cause visible capillary damage. Angioneurotic edema may be caused by sudden complement system attack on VWB that results in widespread paralysis of CGM function and sudden shift of blood from arteries and arterioles to capillaries to cause tissue edema and hypotension. The hypothesis may offer improved insight into the nature of circulatory physiology, the surgical stress syndrome, "vasoactive" drugs, and numerous disease states. It may be tested by using videomicroscopy to monitor changes in bowel capillary flow in response to stepwise increases of VWB or Factor VIII intravenous boluses in animals anesthetized using combined epidural-general technique to minimize SNS activity levels.