The Cardiovascular Effects of Air Pollution: the Role of Nitric Oxide

Status

Completed

Phases

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT00845767

Enrollment

Registered

2009-02-18

Start date

2009-04-30

Completion date

2009-07-31

Last updated

2009-10-09

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Endothelial Dysfunction

Keywords

Nitric Oxide, Nitric Oxide Synthase, Air Pollution, Endothelial Dysfunction, Diesel Exhaust

Brief summary

Exposure to air pollution has been linked to increased cardiorespiratory morbidity and mortality. The exact component of air pollution that mediates this effect is unknown, but the link is strongest for fine combustion derived particulate matter derived from traffic sources. Recently, it has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. The mechanism underlying these detrimental vascular is unclear, but is thought to be via oxidative stress and altered bioavailability of endogenous nitric oxide. In these studies we plan to elucidate the role of endogenous nitric oxide (NO) in the adverse vascular responses observed following exposure to diesel exhaust.

Interventions

PROCEDUREForearm Vascular Study

Forearm venous occlusion plethysmography during intraarterial infusion of L-NMMA (2-8 µmol/min) followed by co-infusion of sodium nitroprusside (90-900 ng/min) as a nitric oxide clamp. Forearm blood flow then measured during the clamp in response to infused vasodilators acetylcholine (5-20 mg/min), bradykinin (100-1000 pmol/min), verapamil (10-100 µg/min) and sodium nitroprusside (2-8 µg/min).

Study design

Allocation

RANDOMIZED

Intervention model

CROSSOVER

Primary purpose

BASIC_SCIENCE

Masking

TRIPLE (Subject, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender

ALL

Age

18 Years to 40 Years

Healthy volunteers

Yes

Inclusion criteria

* Healthy volunteers

Exclusion criteria

* Use of regular medication (except oral contraceptive pill) * Current smokers * Significant occupational exposure to air pollution * Intercurrent illness

Design outcomes

Primary

Measure	Time frame
Forearm blood flow as measured by venous occlusion plethysmography during infusion of NOS inhibitors and vasodilators	2-4 hours after exposure

Secondary

Measure	Time frame
Plasma nitrite concentrations	During forearm study
Plasma concentrations of t-PA and PAI	After infusion of bradykinin during forearm study

Countries

Sweden

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Mar 24, 2026