| pubmed-article:9530212 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0006901 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0600138 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C1159441 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C1518425 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C0806140 | lld:lifeskim |
| pubmed-article:9530212 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:9530212 | pubmed:issue | 3 Pt 2 | lld:pubmed |
| pubmed-article:9530212 | pubmed:dateCreated | 1998-4-14 | lld:pubmed |
| pubmed-article:9530212 | pubmed:abstractText | We investigated, using a direct, intravital microscopic technique, whether nitric oxide (NO) from neuronal nitric oxide synthase (nNOS) plays a role in the cerebral capillary flow response to acute hypoxia. Erythrocyte flow in subsurface capillaries of the frontoparietal cortex of adult Sprague-Dawley rats was visualized using epifluorescence videomicroscopy after fluorescent labeling of red blood cells (RBC) in tracer concentrations. The velocity of labeled RBC in individual capillaries was measured off-line using an image analysis system. Hypoxia was produced by lowering the inspired O2 concentration to 15% for 5 min in control animals and in those pretreated with the selective nNOS inhibitor 7-nitroindazole (7-NI; 20 mg/kg ip). In the control group, hypoxia increased RBC velocity by 34 +/- 8%. In the group treated with 7-NI, this response was reversed to a statistically significant 8 +/- 3% decrease. This paradoxical response to hypoxia after 7-NI was observed in nearly all capillaries. 7-NI itself decreased the baseline RBC velocity by 12 +/- 4%. The cerebral hyperemic response to hypoxia was also assessed with the laser Doppler flow (LDF) technique. In control animals, hypoxia produced a 33 +/- 6% increase in LDF, similar to the increase in RBC velocity. After 7-NI treatment, the response to hypoxia was moderately attenuated but still significant at a 19 +/- 2% increase in LDF. These results support the role of NO from nNOS in the cerebral hyperemic response to hypoxia. They imply that 7-NI interfered with a physiological mechanism that was fundamental to cerebral capillary flow regulation and provide direct evidence that cerebral capillary perfusion may be dissociated from a concurrent change in regional tissue perfusion as reflected by LDF. In conclusion, NO from nNOS contributes to the maintenance of RBC flow in cerebral capillaries and plays a critically important role in the selective regulation of cerebral capillary flow during hypoxia. | lld:pubmed |
| pubmed-article:9530212 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9530212 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9530212 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9530212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9530212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9530212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9530212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9530212 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9530212 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9530212 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:9530212 | pubmed:author | pubmed-author:KampineJ PJP | lld:pubmed |
| pubmed-article:9530212 | pubmed:author | pubmed-author:ShenHH | lld:pubmed |
| pubmed-article:9530212 | pubmed:author | pubmed-author:HudetzA GAG | lld:pubmed |
| pubmed-article:9530212 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9530212 | pubmed:volume | 274 | lld:pubmed |
| pubmed-article:9530212 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9530212 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9530212 | pubmed:pagination | H982-9 | lld:pubmed |
| pubmed-article:9530212 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9530212 | pubmed:meshHeading | pubmed-meshheading:9530212-... | lld:pubmed |
| pubmed-article:9530212 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9530212 | pubmed:articleTitle | Nitric oxide from neuronal NOS plays critical role in cerebral capillary flow response to hypoxia. | lld:pubmed |
| pubmed-article:9530212 | pubmed:affiliation | Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA. | lld:pubmed |
| pubmed-article:9530212 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9530212 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:9530212 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9530212 | lld:pubmed |
