Chest
Laboratory and Animal InvestigationsSecondhand Tobacco Smoke Impairs Rabbit Pulmonary Artery Endothelium-Dependent Relaxation
Section snippets
Protocol
The study protocol was approved by the Committee for Animal Research of the University of California at San Francisco, and was performed in accordance with the recommendations of the American Association for Accreditation of Laboratory Animal Care. Rabbits ingested a standard rabbit chow diet throughout the study. Thirty-two rabbits were randomized in a two-by-two design (with SHS and long-term l-arginine as factors) into four groups: normal rabbits, SHS exposure, l-arginine exposure, and SHS/l
Animal Data
SHS and l-arginine did not influence body weight. l-Arginine ingestion by the two groups of arginine-supplemented animals was similar. SHS exposure reduced average food ingestion. l-Arginine supplementation did not affect food ingestion, but did block the SHS-induced reduction in food intake (Table 1).
SHS exposure markedly increased smoking-chamber carbon monoxide and particulate matter levels, and serum nicotine and cotinine levels. Neither SHS nor l-arginine affected levels of total
Discussion
This study demonstrates that (1) SHS reduces rodent conduit pulmonary artery endothelium-dependent relaxation, (2) SHS reduces rodent pulmonary artery endothelial constitutive nitric oxide activity, (3) a correlation between endothelial L-arginine content and endothelium-dependent relaxation exists, (4) SHS reduces endothelial L-arginine and long-term L-arginine supplementation increased endothelial L-arginine content, and (5) long-term L-arginine supplementation protects against SHS-induced
Conclusion
SHS exposure reduces rodent pulmonary artery endothelial NOS activity, lowers l-arginine content through a mechanism independent of l-arginase, and impairs pulmonary artery endothelium-dependent relaxation. Long-term dietary l-arginine supplementation increases serum and endothelial l-arginine content and prevents SHS-induced endothelial dysfunction. Although l-arginine supplementation addresses SHS-induced loss of substrate, the SHS-induced loss of NOS activity, if progressive, would not be
References (31)
- et al.
Testosterone worsens endothelium dependent relaxation of tobacco smoke exposed hypercholesterolemic male rabbit aorta
J Am Coll Cardiol
(1997) - et al.
Passive smoking increases experimental atherosclerosis in cholesterol-fed rabbits
J Am Coll Cardiol
(1993) - et al.
Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation
Chest
(1993) - et al.
Effects of smoking and vitamin E on blood antioxidant status
Am J Clin Nutr
(1991) - et al.
Role of nitric oxide in the local regulation of pulmonary vascular resistance in humans
Circulation
(1996) - et al.
Evidence that nitric oxide from the endothelium attenuates inherent tone in isolated pulmonary arteries from rats with hypoxic pulmonary hypertension
Br J Pharmacol
(1995) - et al.
Effect of inhibitors of nitric oxide release and action on vascular tone in isolated lungs of pig, sheep, dog and man
J Physiol (Lond)
(1994) - et al.
Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans
Circulation
(1994) - et al.
Endothelial control of the pulmonary circulation in normal and chronically hypoxic rats
J Physiol (Lond)
(1993) - et al.
Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults
Circulation
(1993)
Passive smoking is associated with impaired endothelium-dependent dilation in healthy young adults
N Engl J Med
Chronic dietary L-arginine prevents endothelial dysfunction secondary to environmental tobacco smoke in normocholesterolemic rabbits
Hypertension
Changes in the structure and mechanical properties of pulmonary arteries of rats exposed to cigarette smoke
Am Rev Respir Dis
Hemodynamic and gas exchange responses to infusion of acetylcholine and inhalation of nitric oxide in patients with chronic obstructive lung disease and pulmonary hypertension
Am Rev Respir Dis
Short-term pulmonary vasodilation with L-arginine in pulmonary hypertension
Circulation
Cited by (39)
Fraction of Exhaled Nitric Oxide Is Elevated in Patients With Stable Chronic Obstructive Pulmonary Disease: A Meta-analysis
2020, American Journal of the Medical SciencesCitation Excerpt :FeNO has not been well characterized in COPD because there are many factors that affect it. Studies have shown that smoking can inhibit the expression of eNOS and iNOS and reduce the production of NO.41,42 However, many oxides in smoke will react with NO and increase the consumption of NO. The influence of smoking on FeNO persists for at least 24 hours; however, FeNO levels can gradually recover after an individual quits smoking.43,44 Therefore, FeNO in smokers is lower than that in nonsmokers.45
Benfotiamine attenuates nicotine and uric acid-induced vascular endothelial dysfunction in the rat
2008, Pharmacological ResearchParental smoking and lung function in healthy children and adolescents
2007, Archivos de BronconeumologiaGenetic polymorphisms in arginase I and II and childhood asthma and atopy
2006, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Environmental tobacco smoke is a stimulus for airway inflammation41 that might magnify genetic effects that influence this pathway. In addition to effects on inflammatory cells, smoking can decrease endothelial NOS activity in smooth muscle,42 which, if occurring in the airway, would result in decreased bronchodilatory NO. Because arginase activity depletes arginine, leading to decreased substrate for endothelial NOS, there could be a synergistic decrease in NO production. There may also be synergism on the basis of airway remodeling, which both smoking and arginase activity can promote.43
Impairment of Endothelial Function by Aerosol From Marijuana Leaf Vaporizers
2023, Journal of the American Heart Association
Dr. Hutchison was supported in part by a fellowship from the R.
Samuel McLaughlin Foundation, Toronto, Ontario, Canada.