Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-3-11
pubmed:abstractText
The smooth muscle-constricting, platelet amine, serotonin (5-hydroxytryptamine; 5-HT) is theorized to play an important role in the cardiopulmonary dysfunction that accompanies embolization. The present study was designed to examine this hypothesis. Autologous clot, 0.75 g/kg, was injected IV into 14 dogs. After 30 minutes, one half of the animals were randomly assigned to the treatment group and received a bolus infusion of 0.15 mg/kg ketanserin, a quinazoline derivative known to be a selective 5-HT receptor antagonist. Five minutes after embolization there were increases in mean pulmonary arterial pressure (MPAP) from 12 mm to 48 mmHg (p less than 0.001); pulmonary vascular resistance (PVR) from 2.2 mm to 12.2 mmHg X min/L (p less than 0.001); physiologic shunt (QS/QT) from 12% to 44% (p less than 0.01); and physiologic dead space (VD/VT), calculated from end tidal and arterial PCO2, from 8% to 39% (p less than 0.001). Within 15 minutes platelet counts decreased from 186,000/mm3 to 134,800/mm3 (p less than 0.05); 5-HT contained in circulating platelets fell from 1.71 micrograms/ to 1.44 micrograms/10(9) platelets (p less than 0.05). Five minutes after ketanserin, MPAP declined to 27 mmHg and was lower than the control value of 41 mmHg (p less than 0.05); PVR decreased to 6.2 mmHg X min/L, lower than 12 mmHg X min/L in controls (p less than 0.01); QS/QT fell to 26% in contrast to 47% in controls (p less than 0.05); and VD/VT declined moderately to 32% (p less than 0.05), although this value was not different from 38% in control animals. Cardiopulmonary function continued to improve in treated animals until termination of the experiment at four hours when pulmonary angiograms and perfusion scans demonstrated vascular recruitment compared with untreated embolized control dogs. These data demonstrate that the cardiopulmonary consequences of experimental embolization are primarily determined by the vasoconstrictive and bronchoconstrictive actions of 5-HT.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-13065459, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-13233134, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-398987, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-4326431, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-4690104, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-4730069, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-564466, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-5904533, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-622690, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-6261070, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-6284801, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-6461081, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-6778964, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-6992319, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-7009520, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-7017981, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-7030086, http://linkedlifedata.com/resource/pubmed/commentcorrection/6824376-738122
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0003-4932
pubmed:author
pubmed:issnType
Print
pubmed:volume
197
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-5
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Therapeutic benefits of 5-hydroxytryptamine inhibition following pulmonary embolism.
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, Non-U.S. Gov't