Key result
Electrical potentials above 2.0 V trigger in vivo venous thrombosis in canine models.
Electrical thrombosis is a voltage-dependent phenomenon requiring a critical potential difference of >2.0 v, suggesting transmural potential changes do not initiate normal thrombosis.
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Critical 2.0 V threshold for canine venous thrombosis does not extend to clinical practice; leaves open voltage role in human coagulation mechanisms.
The in vitro coagulation of dog whole blood and the in vivo thrombosis of blood vessels by means of an electric current were found to be voltage-dependent phenomena. The critical potential difference below which they do not occur appears to be 2.0 v. Electrolytic decomposition potentials of several salt- and protein-containing solutions between smooth Pt electrodes were found to cluster between 2.0 and 2.3 v as determined by their voltage-current curves. Below 2.0 v whole blood was not found to deposit as a coagulum on the positive electrode even when the amount of charge allowed to flow was greater than that which caused coagulation at higher voltages. In vivo electrical thrombosis was found to have similar voltage dependence in femoral vein pairs in the dog. Those at 2.5 v thrombosed whereas those at 2.0 did not—even though the current was the same in each instance. Attention is called to the fact that a change in transmural potential cannot then be the initiating factor of "normal" thrombosis.
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Lamb et al. (1965) studied Thrombosis. Electric current vs. 2.0 v was evaluated on Thrombosis. In vivo electrical thrombosis in dog femoral veins occurred at 2.5 V but not at 2.0 V, indicating a critical potential difference of 2.0 V for thrombosis.
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