HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bieger, D. Articles by Tabrizchi, R. Search for Related Content PubMed Articles by Bieger, D. Articles by Tabrizchi, R. Related Collections Great vessels Peripheral vascular

Transmural pressure and membrane potential in human saphenous vein

^a Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada
^b Discipline of Surgery, Health Care Corporation of St. John's, St. John's, NL, Canada

Received 24 September 2007; received in revised form 26 March 2008; accepted 27 March 2008.

^_* Corresponding author. Address: Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, Health Sciences Centre, St. John's, NL, Canada A1B 3V6. Tel.: +1 709 777 6864; fax: +1 709 777 7010. (Email: rtabrizc{at}mun.ca).

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 H₂O; n = 10), –72.6 ± 6.5 mV (11–14 cm H₂O; n = 27), –72.1 ± 6.5 mV (26–27 cm H₂O; n = 30), and –72.9 ± 4.0 mV (50–54 cm H₂O; 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 H₂O (–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.

Key Words: Vascular smooth muscle • Pressurized vessels • Ring preparation