| pubmed-article:9560262 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9560262 | lifeskim:mentions | umls-concept:C0080309 | lld:lifeskim |
| pubmed-article:9560262 | lifeskim:mentions | umls-concept:C1547239 | lld:lifeskim |
| pubmed-article:9560262 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:9560262 | lifeskim:mentions | umls-concept:C1517499 | lld:lifeskim |
| pubmed-article:9560262 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:9560262 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:9560262 | pubmed:dateCreated | 1998-6-4 | lld:pubmed |
| pubmed-article:9560262 | pubmed:abstractText | We used a catheter-based technique to achieve generalized cardiac gene transfer in vivo and to alter cardiac function by overexpressing phospholamban (PL) which regulates the activity of the sarcoplasmic reticulum Ca2+ ATPase (SERCA2a). By using this approach, rat hearts were transduced in vivo with 5 x 10(9) pfu of recombinant adenoviral vectors carrying cDNA for either PL, beta-galactosidase (beta-gal), or modified green fluorescent protein (EGFP). Western blot analysis of ventricles obtained from rats transduced by Ad.PL showed a 2.8-fold increase in PL compared with hearts transduced by Ad.betagal. Two days after infection, rat hearts transduced with Ad.PL had lower peak left ventricular pressure (58.3 +/- 12.9 mmHg, n = 8) compared with uninfected hearts (92.5 +/- 3.5 mmHg, n = 6) or hearts infected with Ad.betagal (92.6 +/- 5.9 mmHg, n = 6). Both peak rate of pressure rise and pressure fall (+3, 210 +/- 298 mmHg/s, -2, 117 +/- 178 mmHg/s, n = 8) were decreased in hearts overexpressing PL compared with uninfected hearts (+5, 225 +/- 136 mmHg/s, -3, 805 +/- 97 mmHg/s, n = 6) or hearts infected with Ad.betagal (+5, 108 +/- 167 mmHg/s, -3, 765 +/- 121 mmHg/s, n = 6). The time constant of left ventricular relaxation increased significantly in hearts overexpressing PL (33.4 +/- 3.2 ms, n = 8) compared with uninfected hearts (18.5 +/- 1.0 ms, n = 6) or hearts infected with Ad.betagal (20.8 +/- 2.1 ms, n = 6). These differences in ventricular function were maintained 7 days after infection. These studies open the prospect of using somatic gene transfer to modulate overall cardiac function in vivo for either experimental or therapeutic applications. | lld:pubmed |
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| pubmed-article:9560262 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9560262 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9560262 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9560262 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9560262 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:SchmidtUU | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:LeeK HKH | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:MatsuiTT | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:RosenzweigAA | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:GwathmeyJ KJK | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:DecG WGW | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:SemigranM JMJ | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:HajjarR JRJ | lld:pubmed |
| pubmed-article:9560262 | pubmed:author | pubmed-author:GuerreroJ LJL | lld:pubmed |
| pubmed-article:9560262 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9560262 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:9560262 | pubmed:volume | 95 | lld:pubmed |
| pubmed-article:9560262 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9560262 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9560262 | pubmed:pagination | 5251-6 | lld:pubmed |
| pubmed-article:9560262 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9560262 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9560262 | pubmed:articleTitle | Modulation of ventricular function through gene transfer in vivo. | lld:pubmed |
| pubmed-article:9560262 | pubmed:affiliation | Cardiovascular Research Center and Heart Failure and Cardiac Transplantation Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA. | lld:pubmed |
| pubmed-article:9560262 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9560262 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9560262 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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