Impact of NOS, COX, and ROS Inhibition on Cerebral Blood Flow Regulation
Public ClinicalTrials.gov record NCT03066115. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.
Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.
Official title
Contributions of Nitric Oxide Synthase, Cyclooxygenase, and Reactive Oxygen Species to Regional Cerebrovascular Control During Hypoxia and Hypercapnia
Brief summary
Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.
Elucidating cerebrovascular control mechanisms during physiologic stress may help identify novel therapeutic targets aimed at preventing or reducing the impact of cerebrovascular disease. The physiological stressors of hypoxia and hypercapnia will be utilized to elicit increases in cerebral blood flow (CBF), and intravenously infused drugs will allow for the testing of potential mechanisms of cerebrovascular control. Specifically, the contributions of nitric oxide synthase (NOS), cyclooxygenase (COX), and reactive oxygen species (ROS) to hypoxic and hypercapnic increases in CBF will be examined. The concept that these mechanisms interact in a compensatory fashion to ensure adequate CBF during both hypoxia and hypercapnia will also be tested. \~25 young, healthy men and women will be tested at rest and during hypoxia and hypercapnia. Subjects will participate in two randomized, counterbalanced study visits under the following conditions: inhibition of NOS, NOS-COX, and NOS-COX-ROS or inhibition of COX, COX-NOS, COX-NOS-ROS. During hypoxia, arterial oxygen saturation will be lowered to 80% and end-tidal carbon dioxide will be maintained at basal levels. During hypercapnia arterial carbon dioxide will be increased \~10 mmHg above basal levels and arterial oxygen saturation will be maintained. Blood flow velocity will be measured with transcranial Doppler ultrasound in the anterior (middle cerebral artery; MCA) and posterior (basilar artery; BA) circulations as a surrogate for CBF. It is hypothesized that both NOS and COX independently contribute to hypoxic and hypercapnic vasodilation in the MCA and BA, combined NOS-COX contribute to hypoxic and hypercapnic vasodilation in MCA and BA to a greater extent than either NOS or COX alone, and NOS-COX-ROS contribute to hypoxic and hypercapnic vasodilation in the MCA and BA to a greater extent than NOS-COX.
Study identification
- NCT ID
- NCT03066115
- Recruitment status
- Withdrawn
- Study type
- Interventional
- Phase
- Phase 1
- Enrollment
- Not listed
Conditions and interventions
Conditions
Interventions
- L-NMMA Drug
- Ketorolac Drug
- Ascorbic Acid Drug
- Intravenous Catheter Procedure
- Transcranial Doppler Ultrasound Procedure
Drug · Procedure
Eligibility (public fields only)
- Age range
- 18 Years to 45 Years
- Sex
- All
- Healthy volunteers
- Accepts healthy volunteers
This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.
Study timeline
- Start date
- Nov 30, 2020
- Primary completion
- Nov 30, 2021
- Completion
- Nov 30, 2021
- Last update posted
- Jan 9, 2019
2020 – 2021
United States locations
- U.S. sites
- 1
- U.S. states
- 1
- U.S. cities
- 1
| Facility | City | State | ZIP | Site status |
|---|---|---|---|---|
| University of Wisconsin, Madison | Madison | Wisconsin | 53706 | — |
Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.
About this trial record page
- What this page shows
- Public field values for ClinicalTrials.gov record NCT03066115, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
- What this page does not do
- No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
- Where the data comes from
- Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
- Last refresh
- Last update posted Jan 9, 2019 · Synced Sep 2, 2026
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Open the official record
The complete protocol, eligibility criteria, and contact information for NCT03066115 live on ClinicalTrials.gov.