Smoking cessation reverses arterial endothelium-dependent relaxation injury

Bradley W. Mays, Timothy Ripple, Mark T. Eginton, Gary R. Seabrook, Robert A. Cambria, Jonathan B. Towne, Julie A. Freischlag

Research output: Contribution to journalArticle

Abstract

Chronic smoking is associated with acetylcholine-dependent endothelial dysfunction, an early marker of atherosclerosis. The purpose of this study was to determine whether this effect of smoke exposure on blood vessel endothelium is reversible. New Zealand White rabbits were placed in a 240 cubic-foot air flow chamber for 3 hours per day, 5 days per week, over a 4- week period and were exposed to smoke produced by a robotic smoke generator. After the 4-week period, rabbits (n=four, Smoked) were killed and their superficial femoral arteries (SFAs) were cut into 3-mm segments. The rings were suspended from tension transducers and the maximal contraction of one ring was recorded following stimulation with norepinephrine (NE). The remaining rings were contracted to 50% of the maximum. Relaxation of these rings was determined by adding increasing doses of acetylcholine. The remaining rabbits were placed in and out of the chamber without smoke exposure for an additional 4 weeks (n=five, Reverse-smoked), and then the SFAs were harvested. Control (n=six) SFAs were explanted from rabbits not exposed to smoke. KCl induced increased contractility in the smoked group when compared with the controls, and NE induced increased contractility in the smoked group when compared with the reverse-smoked rabbits. Acetylcholine-dependent relaxation was significantly reduced in the rings from the smoked rabbits when compared with the controls. The percentage ring relaxation in the reverse-smoked rabbits was similar to the control rings. The impaired acetylcholine-dependent endothelium relaxation in the smoked group verifies endothelial injury. However, the improved relaxation in the reverse-smoked group suggests that endothelial injury is reversible.

Original languageEnglish (US)
Pages (from-to)407-413
Number of pages7
JournalVascular Surgery
Volume32
Issue number5
StatePublished - 1998
Externally publishedYes

Fingerprint

Smoking Cessation
Endothelium
Smoke
Rabbits
Wounds and Injuries
Acetylcholine
Femoral Artery
Norepinephrine
Robotics
Transducers
Blood Vessels
Atherosclerosis
Smoking
Air

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Mays, B. W., Ripple, T., Eginton, M. T., Seabrook, G. R., Cambria, R. A., Towne, J. B., & Freischlag, J. A. (1998). Smoking cessation reverses arterial endothelium-dependent relaxation injury. Vascular Surgery, 32(5), 407-413.

Smoking cessation reverses arterial endothelium-dependent relaxation injury. / Mays, Bradley W.; Ripple, Timothy; Eginton, Mark T.; Seabrook, Gary R.; Cambria, Robert A.; Towne, Jonathan B.; Freischlag, Julie A.

In: Vascular Surgery, Vol. 32, No. 5, 1998, p. 407-413.

Research output: Contribution to journalArticle

Mays, BW, Ripple, T, Eginton, MT, Seabrook, GR, Cambria, RA, Towne, JB & Freischlag, JA 1998, 'Smoking cessation reverses arterial endothelium-dependent relaxation injury', Vascular Surgery, vol. 32, no. 5, pp. 407-413.
Mays BW, Ripple T, Eginton MT, Seabrook GR, Cambria RA, Towne JB et al. Smoking cessation reverses arterial endothelium-dependent relaxation injury. Vascular Surgery. 1998;32(5):407-413.
Mays, Bradley W. ; Ripple, Timothy ; Eginton, Mark T. ; Seabrook, Gary R. ; Cambria, Robert A. ; Towne, Jonathan B. ; Freischlag, Julie A. / Smoking cessation reverses arterial endothelium-dependent relaxation injury. In: Vascular Surgery. 1998 ; Vol. 32, No. 5. pp. 407-413.
@article{ce80ecf0ccde4509b820c9e7198a7c4f,
title = "Smoking cessation reverses arterial endothelium-dependent relaxation injury",
abstract = "Chronic smoking is associated with acetylcholine-dependent endothelial dysfunction, an early marker of atherosclerosis. The purpose of this study was to determine whether this effect of smoke exposure on blood vessel endothelium is reversible. New Zealand White rabbits were placed in a 240 cubic-foot air flow chamber for 3 hours per day, 5 days per week, over a 4- week period and were exposed to smoke produced by a robotic smoke generator. After the 4-week period, rabbits (n=four, Smoked) were killed and their superficial femoral arteries (SFAs) were cut into 3-mm segments. The rings were suspended from tension transducers and the maximal contraction of one ring was recorded following stimulation with norepinephrine (NE). The remaining rings were contracted to 50{\%} of the maximum. Relaxation of these rings was determined by adding increasing doses of acetylcholine. The remaining rabbits were placed in and out of the chamber without smoke exposure for an additional 4 weeks (n=five, Reverse-smoked), and then the SFAs were harvested. Control (n=six) SFAs were explanted from rabbits not exposed to smoke. KCl induced increased contractility in the smoked group when compared with the controls, and NE induced increased contractility in the smoked group when compared with the reverse-smoked rabbits. Acetylcholine-dependent relaxation was significantly reduced in the rings from the smoked rabbits when compared with the controls. The percentage ring relaxation in the reverse-smoked rabbits was similar to the control rings. The impaired acetylcholine-dependent endothelium relaxation in the smoked group verifies endothelial injury. However, the improved relaxation in the reverse-smoked group suggests that endothelial injury is reversible.",
author = "Mays, {Bradley W.} and Timothy Ripple and Eginton, {Mark T.} and Seabrook, {Gary R.} and Cambria, {Robert A.} and Towne, {Jonathan B.} and Freischlag, {Julie A.}",
year = "1998",
language = "English (US)",
volume = "32",
pages = "407--413",
journal = "Vascular and Endovascular Surgery",
issn = "1538-5744",
publisher = "SAGE Publications Inc.",
number = "5",

}

TY - JOUR

T1 - Smoking cessation reverses arterial endothelium-dependent relaxation injury

AU - Mays, Bradley W.

AU - Ripple, Timothy

AU - Eginton, Mark T.

AU - Seabrook, Gary R.

AU - Cambria, Robert A.

AU - Towne, Jonathan B.

AU - Freischlag, Julie A.

PY - 1998

Y1 - 1998

N2 - Chronic smoking is associated with acetylcholine-dependent endothelial dysfunction, an early marker of atherosclerosis. The purpose of this study was to determine whether this effect of smoke exposure on blood vessel endothelium is reversible. New Zealand White rabbits were placed in a 240 cubic-foot air flow chamber for 3 hours per day, 5 days per week, over a 4- week period and were exposed to smoke produced by a robotic smoke generator. After the 4-week period, rabbits (n=four, Smoked) were killed and their superficial femoral arteries (SFAs) were cut into 3-mm segments. The rings were suspended from tension transducers and the maximal contraction of one ring was recorded following stimulation with norepinephrine (NE). The remaining rings were contracted to 50% of the maximum. Relaxation of these rings was determined by adding increasing doses of acetylcholine. The remaining rabbits were placed in and out of the chamber without smoke exposure for an additional 4 weeks (n=five, Reverse-smoked), and then the SFAs were harvested. Control (n=six) SFAs were explanted from rabbits not exposed to smoke. KCl induced increased contractility in the smoked group when compared with the controls, and NE induced increased contractility in the smoked group when compared with the reverse-smoked rabbits. Acetylcholine-dependent relaxation was significantly reduced in the rings from the smoked rabbits when compared with the controls. The percentage ring relaxation in the reverse-smoked rabbits was similar to the control rings. The impaired acetylcholine-dependent endothelium relaxation in the smoked group verifies endothelial injury. However, the improved relaxation in the reverse-smoked group suggests that endothelial injury is reversible.

AB - Chronic smoking is associated with acetylcholine-dependent endothelial dysfunction, an early marker of atherosclerosis. The purpose of this study was to determine whether this effect of smoke exposure on blood vessel endothelium is reversible. New Zealand White rabbits were placed in a 240 cubic-foot air flow chamber for 3 hours per day, 5 days per week, over a 4- week period and were exposed to smoke produced by a robotic smoke generator. After the 4-week period, rabbits (n=four, Smoked) were killed and their superficial femoral arteries (SFAs) were cut into 3-mm segments. The rings were suspended from tension transducers and the maximal contraction of one ring was recorded following stimulation with norepinephrine (NE). The remaining rings were contracted to 50% of the maximum. Relaxation of these rings was determined by adding increasing doses of acetylcholine. The remaining rabbits were placed in and out of the chamber without smoke exposure for an additional 4 weeks (n=five, Reverse-smoked), and then the SFAs were harvested. Control (n=six) SFAs were explanted from rabbits not exposed to smoke. KCl induced increased contractility in the smoked group when compared with the controls, and NE induced increased contractility in the smoked group when compared with the reverse-smoked rabbits. Acetylcholine-dependent relaxation was significantly reduced in the rings from the smoked rabbits when compared with the controls. The percentage ring relaxation in the reverse-smoked rabbits was similar to the control rings. The impaired acetylcholine-dependent endothelium relaxation in the smoked group verifies endothelial injury. However, the improved relaxation in the reverse-smoked group suggests that endothelial injury is reversible.

UR - http://www.scopus.com/inward/record.url?scp=0031751910&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031751910&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0031751910

VL - 32

SP - 407

EP - 413

JO - Vascular and Endovascular Surgery

JF - Vascular and Endovascular Surgery

SN - 1538-5744

IS - 5

ER -