Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2005-9-26
pubmed:abstractText
Conventional peritoneal dialysis solutions (PDS) are vasoactive. This study was conducted to identify vasoactive components of PDS and to describe quantitatively such vasoactivity. Anesthetized nonheparinized rats were monitored continuously for hemodynamics while the microvasculature of the jejunum was studied with in vivo intravital microscopy. In separate experiments, vascular reactivity of rat endothelium-intact and -denuded aortic rings (2 mm) was studied ex vivo in a standard tissue bath. In both studies, suffusion of the vessels was performed with filter-sterilized isotonic and hypertonic solutions that contained glucose or mannitol as osmotic agents. PDS served as a control (Delflex 2.25%). Hypertonic glucose and mannitol solutions produced a significant vascular reactivity in aortic rings and instantaneous and sustained vascular relaxation at all levels of the intestinal microvasculature. Similarly, lactate that was dissolved in a low-pH isotonic physiologic salt solution produced significant force generation in aortic rings. Whereas isotonic glucose and mannitol solutions had no vasoactivity in aortic rings, isotonic glucose produced a selective, insidious, and time-dependent vasodilation in the intestinal premucosal arterioles (18 +/- 0.2% of baseline), which was not observed in the larger inflow arterioles (100 mum). This isotonic glucose-mediated vascular relaxation can be attenuated by approximately 50% with combined adenosine A(2a) and A(2b) receptor antagonists and completely abolished by adenosine A(1) receptor inhibition. By using two different experimental techniques, this study demonstrates that hyperosmolality and lactate are the major vasoactive components of clinical peritoneal dialysis solutions. The pattern and the magnitude of such reactivity are dependent on vessel size and on the solutes' metabolic activity. Low pH of conventional PDS is not a vasoactive component by itself but renders lactate vasoactive. Energy-dependent transport of glucose into cells mediates vasodilation of small visceral arterioles by an adenosine receptor-mediated mechanism and constitutes a significant fraction of PDS-mediated vascular reactivity in the visceral microvasculature.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-10329946, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-10821789, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-11015083, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-11090572, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-11274242, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-11805178, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-12455570, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-12462567, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-1263858, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-1263862, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-14527368, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-1951740, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-2411604, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-3425755, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-37363, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-3898870, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-482297, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-487831, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-5540886, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-637909, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-7300129, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-7631754, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-7996841, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-8119058, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-8342649, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9068026, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9105711, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9186879, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9249480, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9316861, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9605578, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9681159, http://linkedlifedata.com/resource/pubmed/commentcorrection/16079269-9927404
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2931-40
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Disparity in osmolarity-induced vascular reactivity.
pubmed:affiliation
Department of Physiology and Biophysics, Health Sciences Center A-1115, University of Louisville, Louisville, KY 40292, USA. erzaka01@louisville.edu
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, N.I.H., Extramural