Linked Life Data

8356471

Source:http://linkedlifedata.com/resource/pubmed/id/8356471

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-9-21
pubmed:abstractText
On the isolated perfused heart model of septic rats, the present study showed that: (1) Calcium content and 45Ca-influx of myocardium increased 190%, 208% (P < 0.01) and that of mitochondria elevated 332%, 178% (P < 0.01) respectively with no change of myocardial 45Ca-release during sepsis. (2) 10(-8) mol/L calcitonin gene-related peptide (CGRP) or 10(-7) mol/L atriopeptin (ANP) added into the Krebs-Henseleit solution could effectively reduce 45Ca-influx to myocardium and mitochondria with no effect on myocardial 45Ca-release. (3) The calcium uptake reserve of mitochondria evaluated in vitro showed that the maximal calcium uptake and uptake velocity of mitochondria during sepsis were reduced 34.6%, 33.3% (P < 0.01) respectively. The data suggested that the net increase of myocardial Ca2+ content resulted from increase of 45Ca-influx with no change of 45Ca-efflux and the reduction of mitochondrial Ca2+ buffering capacity during sepsis were key events in the pathogenesis of intracellular Ca(2+)-overload. CGRP and ANP could effectively alleviate Ca(2+)-overload of myocardium and mitochondria. This may have some cellular protection action during sepsis.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0371-0874
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
158-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
[Changes of calcium transport capacity of myocardium and myocardial mitochondria during sepsis].
pubmed:affiliation
Department of Pathophysiology, Beijing Medical University.
pubmed:publicationType
Journal Article, In Vitro, English Abstract