Source:http://linkedlifedata.com/resource/pubmed/id/11693271
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
16
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| pubmed:dateCreated |
2001-11-5
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| pubmed:abstractText |
Acute effects of triiodothyronine (T3) on postischemic myocardial stunning and intracellular Ca2+ contents were studied in the isolated working hearts of streptozotocin-induced diabetic rats and age-matched controls. After two weeks of diabetes, serum T3 and T4 levels were decreased to 62.5% and 33.9% of control values. Basal preischemic cardiac performance did not differ between diabetic and control rats. In contrast, during reperfusion after 20-min ischemia, diabetic rats exhibited an impaired recovery of heart rate (at 30-min reperfusion 57.5% of baseline vs. control 88.5%), left ventricular (LV) systolic pressure (44.1% vs. 89.5%), and cardiac work (23.1% vs. 66.0%). When 1 and 100 nM T3 was added before ischemia, heart rate was recovered to 77.2% and 81.8% of baseline, LV systolic pressure to 68.3% and 81.9%, and cardiac work to 50.8% and 59.0%, respectively. Diabetic rat hearts showed a higher Ca2+ content in the basal state and a further increase after reperfusion (4.96+/-1.17 vs. control 3.78+/-0.48 micromol/g, p<0.01). In diabetic hearts, H+ release was decreased after reperfusion (5.24+/-2.21 vs. 8.70+/-1.41 mmol/min/g, p<0.05). T3 administration caused a decrease in the postischemic Ca2+ accumulation (lnM T3 4.66+/-0.41 and 100 nM T3 3.58+/-0.36) and recovered the H+ release (lnM T3 16.2+/-3.9 and 100 nM T3 11.6+/-0.9). T3 did not alter myocardial O2 consumption. Results suggest that diabetic rat hearts are vulnerable to postischemic stunning, and T3 protects the myocardial stunning possibly via inhibiting Ca2+ overload.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0024-3205
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
7
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| pubmed:volume |
69
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1907-18
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11693271-Animals,
pubmed-meshheading:11693271-Calcium,
pubmed-meshheading:11693271-Diabetes Mellitus, Experimental,
pubmed-meshheading:11693271-Dose-Response Relationship, Drug,
pubmed-meshheading:11693271-Heart,
pubmed-meshheading:11693271-Hemodynamics,
pubmed-meshheading:11693271-Male,
pubmed-meshheading:11693271-Myocardial Reperfusion Injury,
pubmed-meshheading:11693271-Myocardial Stunning,
pubmed-meshheading:11693271-Myocardium,
pubmed-meshheading:11693271-Oxygen Consumption,
pubmed-meshheading:11693271-Perfusion,
pubmed-meshheading:11693271-Random Allocation,
pubmed-meshheading:11693271-Rats,
pubmed-meshheading:11693271-Rats, Sprague-Dawley,
pubmed-meshheading:11693271-Streptozocin,
pubmed-meshheading:11693271-Thyroxine,
pubmed-meshheading:11693271-Triiodothyronine,
pubmed-meshheading:11693271-Ventricular Function, Left
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| pubmed:year |
2001
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| pubmed:articleTitle |
Triiodothyronine concomitantly inhibits calcium overload and postischemic myocardial stunning in diabetic rats.
|
| pubmed:affiliation |
Second Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan.
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| pubmed:publicationType |
Journal Article,
In Vitro
|