Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-3-9
pubmed:abstractText
The role of nitric oxide (NO) in the mechanism of hemodilution-induced cerebral hyperemia is unclear. Based on findings in hypoxemia, the authors hypothesize that NO of neuronal origin contributes to an increase in velocity of erythrocytes in the cerebral microcirculation during anemia produced by isovolemic hemodilution. The change in erythrocyte velocity in cerebrocortical capillaries was assessed by intravital fluorescence video microscopy. A closed cranial window was implanted over the frontoparietal cortex of barbiturate-anesthetized, ventilated adult rats. Erythrocytes were labeled in vitro with fluorescein isothiocyanate and infused intravenously, and their velocity in subsurface capillaries was measured by frame-to-frame image tracking. Arterial blood was withdrawn in increments of 2 mL and replaced by serum albumin; arterial blood pressure was maintained at control level with an infusion of methoxamine. Erythrocyte velocity increased progressively, reaching 215% of baseline, as arterial hematocrit was reduced from 45% to 17%. Pretreatment of a separate group of rats with 7-nitroindazole (20 mg/kg intraperitoneally), a relatively selective inhibitor of neuronal NO synthase, abolished the increase in velocity at hematocrits greater than 20%, but the maximum velocity attained at the lowest hematocrit was similar to that in the control group. The results suggest that NO from neuronal source may contribute to the increase in capillary erythrocyte flow during moderate isovolemic hemodilution.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-4
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10698058-Anemia, pubmed-meshheading:10698058-Animals, pubmed-meshheading:10698058-Blood Flow Velocity, pubmed-meshheading:10698058-Blood Pressure, pubmed-meshheading:10698058-Capillaries, pubmed-meshheading:10698058-Cerebrovascular Circulation, pubmed-meshheading:10698058-Enzyme Inhibitors, pubmed-meshheading:10698058-Erythrocytes, pubmed-meshheading:10698058-Hematocrit, pubmed-meshheading:10698058-Hemodilution, pubmed-meshheading:10698058-Hyperemia, pubmed-meshheading:10698058-Hypoxia, Brain, pubmed-meshheading:10698058-Indazoles, pubmed-meshheading:10698058-Male, pubmed-meshheading:10698058-Microscopy, Video, pubmed-meshheading:10698058-Nitric Oxide, pubmed-meshheading:10698058-Nitric Oxide Synthase, pubmed-meshheading:10698058-Nitric Oxide Synthase Type I, pubmed-meshheading:10698058-Rats, pubmed-meshheading:10698058-Rats, Sprague-Dawley
pubmed:year
2000
pubmed:articleTitle
7-Nitroindazole impedes erythrocyte flow response to isovolemic hemodilution in the cerebral capillary circulation.
pubmed:affiliation
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't