Objective: An increase in transmural pressure reportedly depolarizes myocytes in various arterial blood vessels. We have examined the relationship between transmural pressure and membrane potential (E(m)) in human saphenous veins with a view to determine whether contractile force generation, hence spasmogenesis in vein grafts, involves a similar process of mechanoelectrical excitation.
Methods: Intracellular recordings were made by sharp glass microelectrodes in human isolated saphenous veins and parallel measurements were performed in ring preparations.
Results: E(m) values obtained in pressurized vessels at four different pressure levels were (mean+/-SD): -74.4+/-5.5 mV (0-6 cm H(2)O; n=10), -72.6+/-6.5 mV (11-14 cm H(2)O; n=27), -72.1+/-6.5 mV (26-27 cm H(2)O; n=30), and -72.9+/-4.0 mV (50-54 cm H(2)O; n=38), demonstrating the lack of an overt pressure-dependence. Except at the lowest transmural pressure tested, these values were significantly different from E(m) obtained in ring preparations (-77.8+/-4.0 mV; n=30). Raising extracellular K(+) to 80 mM produced a comparable depolarization in tissues either pressurized to 50-54 cm H(2)O (-64.9+/-4.3 mV; n=27) or set up as ring preparations (-64.06+/-6.9 mV; n=35).
Conclusions: Human saphenous veins respond to transmural pressure with a limited depolarization that lacks correlation with pressure. The absence of a pressure-induced graded depolarization suggests that pressure-dependent vasoconstriction does not play a primary role in blood flow regulation in lower limb large veins. Moreover, this raises doubts that mechanical stimuli per se would lead to development of vasospasm in the early stages of saphenous vein grafting into arterial vascular beds.