Document Detail


Excretion of thromboxane A2 and prostacyclin metabolites during treadmill exercise in patients with intermittent claudication.
MedLine Citation:
PMID:  3402185     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Platelet activation, with subsequent formation of thromboxane A2 (TxA2), is thought to play a role in the development of arterial occlusion. In patients with severe atherosclerosis of the lower limbs, characterized by leg ulcers and rest pain, the basal formation of TxA2 and prostacyclin (PGI2) is increased. Corresponding data in patients with more moderate atherosclerosis of the lower limbs have not been reported. Since the capacity to physical exercise is not blunted in such patients proper evaluation of their TxA2-PGI2 synthesis should comprise not only assessment of the basal formation, but also TxA2/PGI2 biosynthesis during conditions of elevated cardiovascular activity. To address this, we analysed these eicosanoids in patients with a history of intermittent claudication. Urinary dinor-metabolites of TxB2 and PGI2 (Tx-M and PGI-M, respectively) were estimated by gas chromatography/negative ion-chemical ionization mass spectrometry in samples collected prior to, during and immediately after 20 min of severe treadmill exertion. The basal excretion of Tx-M was 105 +/- 26 pg/mg creatinine. It was not changed during exercise, but increased to 176 +/- 48 pg/mg creatinine (P less than 0.05) during the recovery. The basal excretion of PGI-M was 142 +/- 25 pg/mg creatinine. The PGI-M response to exercise varied from no change at all to a 30-fold increase, without any obvious correlation to experienced leg pain, walking distance or other recorded variables. During the recovery period the outflow of PGI-M was significantly higher than at rest (482 +/- 145 pg/mg creatinine; P less than 0.01). We conclude that in patients with intermittent claudication due to atherosclerosis (1) platelet activation does not occur during the course of the exercise, and (2) vascular prostacyclin formation can be dissociated from of TxA2 synthesis. The observed increase in PGI-M in some of the patients is suggested to reflect tissue ischaemia induced by the lack of adequate hyperaemia during exercise.
Authors:
A Wennmalm; A Edlund; B Sevastik; G A FitzGerald
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Clinical physiology (Oxford, England)     Volume:  8     ISSN:  0144-5979     ISO Abbreviation:  Clin Physiol     Publication Date:  1988 Jun 
Date Detail:
Created Date:  1988-09-13     Completed Date:  1988-09-13     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8309768     Medline TA:  Clin Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  243-53     Citation Subset:  IM    
Affiliation:
Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Sweden.
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MeSH Terms
Descriptor/Qualifier:
6-Ketoprostaglandin F1 alpha / analogs & derivatives*,  urine
Aged
Female
Humans
Intermittent Claudication / physiopathology*,  urine
Male
Middle Aged
Physical Exertion*
Thromboxane B2 / analogs & derivatives*,  urine
Grant Support
ID/Acronym/Agency:
HL 30400/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
54397-85-2/Thromboxane B2; 58962-34-8/6-Ketoprostaglandin F1 alpha; 63250-09-9/2,3-dinor-thromboxane B2; 64700-71-6/2,3-dinor-6-ketoprostaglandin F1alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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