Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-1-24
pubmed:abstractText
Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion, and that ET-1 was increased during reperfusion. This study was aimed to verify if captopril was able to reduce plasma ET-1 during thrombolysis in AMI. Seventy-three patients, hospitalized for suspected AMI within 4 h from the onset of symptoms suitable for thrombolysis (1st episode), Killip class 1-2, were randomized (double blind) into two groups: group 1 (37 pts), 8 F/29 M, received captopril, 6.25 mg, orally 15 min before thrombolysis. Group 2: (36 pts) 8 F/28 M, received placebo before thrombolysis. All patients met the reperfusion criteria. Plasma ET-1 were checked on admission, at 1 h and at 2 h, after starting thrombolysis. Group 1 contained ten unstable angina, 17 anterior and ten inferior AMIs. Group 2 contained ten unstable angina, 16 anterior and ten inferior AMIs. Mean concentrations of ET-1: Unstable angina: group 1, basal--4.56, at 1 h--4.47, 2 h--5.89 pg/ml; group 2: basal--4.17, at 1 h--4.59, 2 h--5.24 pg/ml. Inferior AMI: group 1: basal--6.87, 1 h--7.75, 2 h--8.47; group 2: basal--6.34, 1 h--6.68, 2 h--7.98 pg/ml. Anterior AMI: group 1: basal--7.17, 1 h--7.93, 2 h--10.76 pg/ml (between basal and 2-h samples P < 0.05); group 2: basal--7.46, 1 h--7.51, 2 h--10.74 pg/ml. Differences between the two groups were not significant. Our data suggest that captopril does not affect plasma ET-1 during thrombolysis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0167-5273
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
131-5
pubmed:dateRevised
2006-7-12
pubmed:meshHeading
pubmed-meshheading:8522408-Administration, Oral, pubmed-meshheading:8522408-Angina, Unstable, pubmed-meshheading:8522408-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:8522408-Blood Pressure, pubmed-meshheading:8522408-Captopril, pubmed-meshheading:8522408-Creatine Kinase, pubmed-meshheading:8522408-Double-Blind Method, pubmed-meshheading:8522408-Electrocardiography, pubmed-meshheading:8522408-Endothelins, pubmed-meshheading:8522408-Female, pubmed-meshheading:8522408-Heart Rate, pubmed-meshheading:8522408-Humans, pubmed-meshheading:8522408-Isoenzymes, pubmed-meshheading:8522408-Male, pubmed-meshheading:8522408-Myocardial Infarction, pubmed-meshheading:8522408-Myocardial Reperfusion, pubmed-meshheading:8522408-Placebos, pubmed-meshheading:8522408-Recombinant Proteins, pubmed-meshheading:8522408-Thrombolytic Therapy, pubmed-meshheading:8522408-Time Factors, pubmed-meshheading:8522408-Tissue Plasminogen Activator
pubmed:year
1995
pubmed:articleTitle
Captopril does not affect plasma endothelin-1 during thrombolysis and reperfusion.
pubmed:affiliation
Division of Cardiology, G.F. Ingrassia Hospital, Palermo, Italy.
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial