Ignite Creation Date:
2024-05-06 @ 3:20 PM
Last Modification Date:
2024-10-26 @ 1:47 PM
Study NCT ID:
NCT04597879
Status:
UNKNOWN
Last Update Posted:
2022-11-03
First Post:
2020-10-09
Brief Title:
Impact of Severe Brain Injury on Neuro-vascular and Endothelial Regulation of Peripheral Microcirculation
Sponsor:
University Hospital Grenoble
Organization:
University Hospital Grenoble
Study Overview
Official Title:
Study of the Impact of Severe Brain Injury on the Neuro-vascular and Endothelial Regulation of Peripheral Microcirculation
Status:
UNKNOWN
Status Verified Date:
2022-10
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
MicroTC
Brief Summary:
Severe brain injury SBI is one of the worlds leading causes of death and disability in young adults but its peripheral vascular consequences in humans are poorly understood
This prospective monocentric pathophysiological study aims to investigate differences in vasoreactivity in the anterior aspect of the contralateral forearm at the most injured cerebral hemisphere between patients with severe head trauma and patients with severe trauma without associated brain injury matched on sex and age - 5 years
This prospective monocentric pathophysiological study aims to investigate differences in vasoreactivity in the anterior aspect of the contralateral forearm at the most injured cerebral hemisphere between patients with severe head trauma and patients with severe trauma without associated brain injury matched on sex and age - 5 years
Detailed Description:
Severe brain injury SBI is one of the worlds leading causes of death and disability in young adults
Its impact on cerebral vascularization is well known At the systemic level it induces transient dysfunctions that can develop into severe failures even in cases of isolated SBI Studies on a mouse model of SBI show alterations in peripheral vascular reactivity that persist over time and are linked to endothelial dysfunction the mechanism of which is a decoupling of endothelial NO synthase in a context of systemic inflammation However no data are available regarding the peripheral vascular consequences of SBI in humans
The main objective of this prospective monocentric pathophysiological study is to determine whether the postocclusive hyperaemic response at the anterior surface of the contralateral forearm to the most injured cerebral hemisphere differs between patients with severe brain injury and patients with severe trauma without associated head injury matched on sex and age - 5 years by studying the amplitude of post-occlusive hyperaemia maximum amplitude expressed as percentage of vasodilatation and area under the curve AUC as a function of the group
Its impact on cerebral vascularization is well known At the systemic level it induces transient dysfunctions that can develop into severe failures even in cases of isolated SBI Studies on a mouse model of SBI show alterations in peripheral vascular reactivity that persist over time and are linked to endothelial dysfunction the mechanism of which is a decoupling of endothelial NO synthase in a context of systemic inflammation However no data are available regarding the peripheral vascular consequences of SBI in humans
The main objective of this prospective monocentric pathophysiological study is to determine whether the postocclusive hyperaemic response at the anterior surface of the contralateral forearm to the most injured cerebral hemisphere differs between patients with severe brain injury and patients with severe trauma without associated head injury matched on sex and age - 5 years by studying the amplitude of post-occlusive hyperaemia maximum amplitude expressed as percentage of vasodilatation and area under the curve AUC as a function of the group
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 38RC20014 | OTHER | Promotor | None |