Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1-2
|
| pubmed:dateCreated |
1997-5-6
|
| pubmed:abstractText |
We examined the effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), on mortality, morbidity, and cardiovascular parameters following traumatic brain injury (TBI) in the rat. Rats were anesthetized with 2% isoflurane prior to moderate (2.0 atmosphere), central fluid percussion TBI. Temporalis muscle temperature was maintained at 37 +/- 0.5 degrees C. L-NAME (10 mg/kg iv) was administered once at either 5 min before, 5 min after, or 15 min after TBI. Sensorimotor deficits and spatial learning/ memory deficits were assessed after injury. Separate groups of rats were monitored for cardiovascular parameters. Preinjury administration of L-NAME significantly increased mortality from 13 (vehicle) to 70% (associated with pulmonary edema), whereas postinjury, L-NAME had no effect on mortality (14 and 25%). L-NAME administered at 5 or 15 min after injury had no significant effect on motor performance or cognitive performance deficits associated with TBI. L-NAME in uninjured rats increased arterial blood pressure by 25 mmHg within 2 min. L-NAME injected 5 min before TBI greatly prolonged the hypertensive episode associated with TBI (1 min in vehicle vs 60 min in L-NAME). L-NAME injected 5 min after TBI caused a sustained 35 mmHg increase in blood pressure. These findings suggest that acute inhibition of NOS has detrimental consequences on mortality that may be owing to its cardiovascular effects.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:issn |
1044-7393
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
30
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
125-37
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9138424-Analysis of Variance,
pubmed-meshheading:9138424-Animals,
pubmed-meshheading:9138424-Blood Pressure,
pubmed-meshheading:9138424-Body Temperature,
pubmed-meshheading:9138424-Brain,
pubmed-meshheading:9138424-Brain Injuries,
pubmed-meshheading:9138424-Carbon Dioxide,
pubmed-meshheading:9138424-Chi-Square Distribution,
pubmed-meshheading:9138424-Cognition,
pubmed-meshheading:9138424-Hypertension,
pubmed-meshheading:9138424-Male,
pubmed-meshheading:9138424-Maze Learning,
pubmed-meshheading:9138424-Morbidity,
pubmed-meshheading:9138424-Motor Activity,
pubmed-meshheading:9138424-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:9138424-Nitric Oxide Synthase,
pubmed-meshheading:9138424-Oxygen,
pubmed-meshheading:9138424-Pulmonary Edema,
pubmed-meshheading:9138424-Rats,
pubmed-meshheading:9138424-Rats, Sprague-Dawley,
pubmed-meshheading:9138424-Time Factors
|
| pubmed:articleTitle |
Inhibition of nitric oxide synthase potentiates hypertension and increases mortality in traumatically brain-injured rats.
|
| pubmed:affiliation |
Department of Surgery, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|