Inhaled nitric oxide reduces brain damage by collateral recruitment in a neonatal stroke model
BACKGROUND AND PURPOSE: We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model in rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage in adults. Our objective was to examine whether iNO could modify cerebral blood flow during ischemia-reperfusion and reduce lesions in the developing brain.
METHODS: In vivo variations in cortical NO concentrations occurring after 20-ppm iNO exposure were analyzed using the voltammetric method in P7 rat pups. Inhaled NO-mediated blood flow velocities were measured by ultrasound imaging with sequential Doppler recordings in both internal carotid arteries and the basilar trunk under basal conditions and in a neonatal model of ischemia-reperfusion. The hemodynamic effects of iNO (5 to 80 ppm) were correlated with brain injury 48 hours after reperfusion.
RESULTS: Inhaled NO (20 ppm) significantly increased NO concentrations in the P7 rat cortex and compensated for the blockade of endogenous NO synthesis under normal conditions. Inhaled NO (20 ppm) during ischemia increased blood flow velocities and significantly reduced lesion volumes by 43% and cellular damage. In contrast, both 80 ppm iNO given during ischemia and 5 or 20 ppm iNO given 30 minutes after reperfusion were detrimental.
CONCLUSIONS: Our findings strongly indicate that, with the appropriate timing, 20 ppm iNO can be transported into the P7 rat brain and mediated blood flow redistribution during ischemia leading to reduced infarct volume and cell injury.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2012 |
|---|---|
| Erschienen: |
2012 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:43 |
|---|---|
| Enthalten in: |
Stroke - 43(2012), 11 vom: 05. Nov., Seite 3078-84 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Charriaut-Marlangue, Christiane [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
|---|
| Anmerkungen: |
Date Completed 03.01.2013 Date Revised 22.11.2016 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1161/STROKEAHA.112.664243 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM220757682 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM220757682 | ||
| 003 | DE-627 | ||
| 005 | 20231224050220.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231224s2012 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1161/STROKEAHA.112.664243 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0736.xml |
| 035 | |a (DE-627)NLM220757682 | ||
| 035 | |a (NLM)22949477 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Charriaut-Marlangue, Christiane |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Inhaled nitric oxide reduces brain damage by collateral recruitment in a neonatal stroke model |
| 264 | 1 | |c 2012 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 03.01.2013 | ||
| 500 | |a Date Revised 22.11.2016 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND AND PURPOSE: We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model in rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage in adults. Our objective was to examine whether iNO could modify cerebral blood flow during ischemia-reperfusion and reduce lesions in the developing brain | ||
| 520 | |a METHODS: In vivo variations in cortical NO concentrations occurring after 20-ppm iNO exposure were analyzed using the voltammetric method in P7 rat pups. Inhaled NO-mediated blood flow velocities were measured by ultrasound imaging with sequential Doppler recordings in both internal carotid arteries and the basilar trunk under basal conditions and in a neonatal model of ischemia-reperfusion. The hemodynamic effects of iNO (5 to 80 ppm) were correlated with brain injury 48 hours after reperfusion | ||
| 520 | |a RESULTS: Inhaled NO (20 ppm) significantly increased NO concentrations in the P7 rat cortex and compensated for the blockade of endogenous NO synthesis under normal conditions. Inhaled NO (20 ppm) during ischemia increased blood flow velocities and significantly reduced lesion volumes by 43% and cellular damage. In contrast, both 80 ppm iNO given during ischemia and 5 or 20 ppm iNO given 30 minutes after reperfusion were detrimental | ||
| 520 | |a CONCLUSIONS: Our findings strongly indicate that, with the appropriate timing, 20 ppm iNO can be transported into the P7 rat brain and mediated blood flow redistribution during ischemia leading to reduced infarct volume and cell injury | ||
| 650 | 4 | |a Journal Article | |
| 650 | 7 | |a Neuroprotective Agents |2 NLM | |
| 650 | 7 | |a Nitric Oxide |2 NLM | |
| 650 | 7 | |a 31C4KY9ESH |2 NLM | |
| 700 | 1 | |a Bonnin, Philippe |e verfasserin |4 aut | |
| 700 | 1 | |a Gharib, Abdallah |e verfasserin |4 aut | |
| 700 | 1 | |a Leger, Pierre-Louis |e verfasserin |4 aut | |
| 700 | 1 | |a Villapol, Sonia |e verfasserin |4 aut | |
| 700 | 1 | |a Pocard, Marc |e verfasserin |4 aut | |
| 700 | 1 | |a Gressens, Pierre |e verfasserin |4 aut | |
| 700 | 1 | |a Renolleau, Sylvain |e verfasserin |4 aut | |
| 700 | 1 | |a Baud, Olivier |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Stroke |d 1970 |g 43(2012), 11 vom: 05. Nov., Seite 3078-84 |w (DE-627)NLM000010995 |x 1524-4628 |7 nnns |
| 773 | 1 | 8 | |g volume:43 |g year:2012 |g number:11 |g day:05 |g month:11 |g pages:3078-84 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1161/STROKEAHA.112.664243 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 43 |j 2012 |e 11 |b 05 |c 11 |h 3078-84 | ||