Show simple item record

dc.contributor.authorBoink ABTJ
dc.contributor.authorde Wildt DJ
dc.contributor.authorde Jong Y
dc.contributor.authorde Groot G
dc.contributor.authorVaessen HAMG
dc.contributor.authorMeulenbelt J
dc.contributor.authorvan Dijk A
dc.contributor.authorVosmeer H
dc.date.accessioned2012-12-12T13:41:34Z
dc.date.available2012-12-12T13:41:34Z
dc.date.issued1990-08-31
dc.identifier318802002
dc.identifier.urihttp://hdl.handle.net/10029/256229
dc.description.abstractFrom a previous study it was concluded that intravenous infusion of sodium fluoride (NaF) in rats is a suitable model to study the toxicity of hydrofluoric acid. In this supplementary study we investigated the effect of intravenous infusion of a high and low dose of NaF (120 and 25 mg.kg -1.hr -1) on the plasma concentration of lactate, magnesium, potassium and inorganic phosphate. As compared to the control groups an increase of the lactate concentration in plasma was found, mainly in the terminal phase of the NaF infusion period. This indicates that the decrease of base excess which is frequently found in fluoride intoxications, is caused by tissue hypoxia following impaired circulation. The magnesium concentration in plasma decreased steadily during both NaF infusions. Because magnesium ions have an essential role in many enzymatic processes and because changes of the magnesium concentration in plasma exert hemodynamical effects further studies into the consequences of these finding seem justified. In the terminal stage of NaF infusion hyperkalemia was observed. From our experiments it is unclear whether this rise of the potassium concentration is due to fluoride itself, the treatment-induced acidosis, or that cell necrosis due to hypoperfusion is responsible for this increase.<br>
dc.description.sponsorshipRIVM
dc.format.extent39 p
dc.language.isoen
dc.publisherRijksinstituut voor Volksgezondheid en Milieu RIVM
dc.relation.ispartofRIVM Rapport 318802002
dc.relation.urlhttp://www.rivm.nl/bibliotheek/rapporten/318802002.html
dc.subject07nl
dc.subjectfluoridenl
dc.subjectfluorwaterstofnl
dc.subjecttoxiciteitnl
dc.subjectlactaatnl
dc.subjectmagnesiumnl
dc.subjectkalium; anorganisch fosfaatnl
dc.subjectgeioniseerd calciumnl
dc.subjecthartfunctienl
dc.subjecthemodynamiek; zuur-base evenwichtnl
dc.subjectbloedgassen.nl
dc.titleAn investigation of the pathophysiological mechanisms of hydrofluoric acid intoxication in rats and pigs. Interim report concerning the results of phase 2.1: The effect of sodium fluoride infusion on the plasma concentrations of lactate and magnesiumen
dc.title.alternativeOnderzoek naar pathofysiologische mechanismen van fluorwaterstof intoxicaties in ratten en varkens. Interim rapport betreffende de resultaten van fase 2.1: De effecten van natriumfluoride op de plasma concentratie van lactaat en magnesium.nl
dc.typeReport
dc.date.updated2012-12-12T13:41:35Z
html.description.abstractFrom a previous study it was concluded that intravenous infusion of sodium fluoride (NaF) in rats is a suitable model to study the toxicity of hydrofluoric acid. In this supplementary study we investigated the effect of intravenous infusion of a high and low dose of NaF (120 and 25 mg.kg -1.hr -1) on the plasma concentration of lactate, magnesium, potassium and inorganic phosphate. As compared to the control groups an increase of the lactate concentration in plasma was found, mainly in the terminal phase of the NaF infusion period. This indicates that the decrease of base excess which is frequently found in fluoride intoxications, is caused by tissue hypoxia following impaired circulation. The magnesium concentration in plasma decreased steadily during both NaF infusions. Because magnesium ions have an essential role in many enzymatic processes and because changes of the magnesium concentration in plasma exert hemodynamical effects further studies into the consequences of these finding seem justified. In the terminal stage of NaF infusion hyperkalemia was observed. From our experiments it is unclear whether this rise of the potassium concentration is due to fluoride itself, the treatment-induced acidosis, or that cell necrosis due to hypoperfusion is responsible for this increase.&lt;br&gt;


This item appears in the following Collection(s)

Show simple item record