Source:http://linkedlifedata.com/resource/pubmed/id/16695943
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| Predicate | Object |
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| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2010-6-29
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| pubmed:abstractText |
The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time was studied in 11 normal male subjects. Methoxamine, a pressor amine of predominantly vasoconstrictor activity but lacking significant inotropic effect, was administered intravenously resulting in an average increase in mean arterial pressure of 27 mm Hg. Heart rate was held constant by high right atrial pacing, and there was no significant change in cardiac output. During methoxamine infusion, when stroke volume, heart rate, and inotropic state were held constant, left ventricular ejection time increased as mean arterial pressure increased. There was a highly significant correlation between the increase in mean systolic blood pressure and the prolongation of left ventricular ejection time (r = 0.870). In one subject, an increase in mean systolic pressure of 75 mm Hg prolonged left ventricular ejection time 55 msec, producing paradoxical splitting of the second heart sound. The prolongation of left ventricular ejection time during infusion was not blocked by the prior intravenous administration of atropine sulfate or propranolol hydrochloride, thus ruling out both vagal inhibition of the left ventricle and reflex withdrawal of sympathetic tone as its cause. In three subjects, left ventricular end diastolic pressure was measured and found to be significantly increased. This finding suggests that the normal left ventricle maintains a constant stroke volume in the presence of an increased pressure load by the Frank Starling mechanism. This study concludes that arterial pressure must be included as a prime determinant of left ventricular ejection time along with stroke volume, heart rate, and inotropic state in intact man.
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| pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13062088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13284181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13417065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13513779,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13523814,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13617659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13706460,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13746559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13784135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-13998538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-14120103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-14338695,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16695943-5911057
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0021-9738
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
47
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
217-30
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| pubmed:dateRevised |
2010-9-14
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| pubmed:year |
1968
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| pubmed:articleTitle |
The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time.
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| pubmed:affiliation |
University of Pittsburgh School of Medicine, Department of Medicine, Pittsburgh, Pennsylvania.
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| pubmed:publicationType |
Journal Article
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