-
Something wrong with this record ?
Early changes of brain perfusion after subarachnoid hemorrhage - the effect of sodium nitroprusside
M. Kolar, K. Nohejlova, J. Mares, J. Pachl
Language English Country Czech Republic
Document type Journal Article
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Antihypertensive Agents administration & dosage adverse effects MeSH
- Intracranial Hypotension chemically induced physiopathology MeSH
- Infusions, Intraventricular MeSH
- Rats MeSH
- Brain blood supply drug effects physiopathology MeSH
- Cerebrovascular Circulation drug effects physiology MeSH
- Nitroprusside administration & dosage adverse effects MeSH
- Rats, Wistar MeSH
- Subarachnoid Hemorrhage drug therapy physiopathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Causes of early hypoperfusion after subarachnoid hemorrhage (SAH) include intracranial hypertension as well as vasoconstriction. The aim of the study was to assess the effect of intracerebroventricular (ICV) administration of sodium nitroprusside (SNP) on early hypoperfusion after SAH. Male Wistar rats (220-240 g) were used, SAH group received 250 microl of fresh autologous arterial blood into the prechiasmatic cistern; sham-operated animals received 250 microl of isotonic solution. Therapeutic intervention: ICV administration of 10 microg SNP; 5 microl 5 % glucose (SNP vehicle) and untreated control. Brain perfusion and invasive blood pressure were monitored for 30 min during and after induction of SAH. Despite SNP caused increase of perfusion in sham-operated animals, no response was observed in half of SAH animals. The other half developed hypotension accompanied by brain hypoperfusion. There was no difference between brain perfusion in SNP-treated, glucose-treated and untreated SAH animals during the monitored period. We did not observe expected beneficial effect of ICV administration of SNP after SAH. Moreover, half of the SNP-treated animals developed serious hypotension which led to brain hypoperfusion. This is the important finding showing that this is not the option for early management in patient after SAH.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc17020927
- 003
- CZ-PrNML
- 005
- 20190814100158.0
- 007
- ta
- 008
- 170623s2016 xr d f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.933536 $2 doi
- 035 __
- $a (PubMed)28006941
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Kolář, Michal $u Department of Anesthesiology and Critical Care Medicine, Third Faculty of Medicine, Charles University, Prague, Czech Republic $7 xx0068615
- 245 10
- $a Early changes of brain perfusion after subarachnoid hemorrhage - the effect of sodium nitroprusside / $c M. Kolar, K. Nohejlova, J. Mares, J. Pachl
- 520 9_
- $a Causes of early hypoperfusion after subarachnoid hemorrhage (SAH) include intracranial hypertension as well as vasoconstriction. The aim of the study was to assess the effect of intracerebroventricular (ICV) administration of sodium nitroprusside (SNP) on early hypoperfusion after SAH. Male Wistar rats (220-240 g) were used, SAH group received 250 microl of fresh autologous arterial blood into the prechiasmatic cistern; sham-operated animals received 250 microl of isotonic solution. Therapeutic intervention: ICV administration of 10 microg SNP; 5 microl 5 % glucose (SNP vehicle) and untreated control. Brain perfusion and invasive blood pressure were monitored for 30 min during and after induction of SAH. Despite SNP caused increase of perfusion in sham-operated animals, no response was observed in half of SAH animals. The other half developed hypotension accompanied by brain hypoperfusion. There was no difference between brain perfusion in SNP-treated, glucose-treated and untreated SAH animals during the monitored period. We did not observe expected beneficial effect of ICV administration of SNP after SAH. Moreover, half of the SNP-treated animals developed serious hypotension which led to brain hypoperfusion. This is the important finding showing that this is not the option for early management in patient after SAH.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a antihypertenziva $x aplikace a dávkování $x škodlivé účinky $7 D000959
- 650 _2
- $a mozek $x krevní zásobení $x účinky léků $x patofyziologie $7 D001921
- 650 _2
- $a mozkový krevní oběh $x účinky léků $x fyziologie $7 D002560
- 650 _2
- $a intraventrikulární infuze $7 D057967
- 650 _2
- $a intrakraniální hypotenze $x chemicky indukované $x patofyziologie $7 D019585
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a nitroprusid $x aplikace a dávkování $x škodlivé účinky $7 D009599
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 _2
- $a potkani Wistar $7 D017208
- 650 _2
- $a subarachnoidální krvácení $x farmakoterapie $x patofyziologie $7 D013345
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Nohejlová, Kateryna $7 mzk2013788463 $u Department of Normal, Pathological and Clinical Physiology, Third Faculty of Medicine, Charles University, Prague, Czech Republic
- 700 1_
- $a Mareš, Jan, $d 1948-2021 $7 jn20000710436 $u Department of Normal, Pathological and Clinical Physiology, Third Faculty of Medicine, Charles University, Prague, Czech Republic
- 700 1_
- $a Pachl, Jan, $d 1949- $7 nlk19990073644 $u Department of Anesthesiology and Critical Care Medicine, Third Faculty of Medicine, Charles University, Prague, Czech Republic
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 65, Suppl. 5 (2016), s. S591-S599
- 773 0_
- $t Proceedings of the ... Physiological days : $x 1802-9973 $g Roč. 65, Suppl. 5 (2016), s. S591-S599 $w MED00183838
- 856 41
- $u http://www.biomed.cas.cz/physiolres/ $y domovská stránka časopisu
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 4 $z 0
- 990 __
- $a 20170623 $b ABA008
- 991 __
- $a 20190814100424 $b ABA008
- 999 __
- $a ok $b bmc $g 1236263 $s 981800
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2016 $b 65 $c Suppl. 5 $d S591-S599 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- BMC __
- $a 2016 $b 65 $c Suppl. 5 $d S591-S599 $i 1802-9973 $m Proceedings of the ... Physiological days $n Physiol. Res. (Print) $x MED00183838
- LZP __
- $b NLK118 $a Pubmed-20170623