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Ziqiu Ming

Publications and source records attributed to Ziqiu Ming.

2 recordsLinked to original sources
PubMed2006

Transgenic alpha1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival.

OBJECTIVE: Myocardial contractility is enhanced in transgenic (TG) mice with cardiac-restricted overexpression of the alpha1A-adrenergic receptors (alpha1A-AR). We tested the hypothesis that this enhanced inotropy protects against dysfunction and remodeling after myocardial infarction (MI). METHODS: We subjected alpha1A-TG and non-TG mice (NTG) to MI and determined changes in left ventricular (LV) function and diastolic dimension (LVDd) by echocardiography prior to and at 1, 3, 7, 12 and 15 weeks thereafter. RESULTS: Although infarct size was similar in the NTG and alpha1A-TG groups (32+/-2 vs. 29+/-2% of LV, P=NS), mortality due to heart failure was lower after MI in the alpha1A-TG (37%, n=39) than that in the NTG animals (63%, n=56, P=0.026). NTG and alpha1A-TG mice showed similar reductions in LV fractional shortening (FS) and increases in LVDd at week-1 after MI. However, whereas NTG mice showed continuous deterioration over a 15-week period after MI in FS (fell by 40%, from 30+/-2 to 18+/-1%, P<0.01) and LVDd (increased by 24%, from 4.2+/-0.1 to 5.2+/-0.1 mm, P<0.01), the changes in both FS (fell by 14%, from 42+/-2 to 36+/-2%) and LVDd (increased by 8%, from 3.8+/-0.1 to 4.1+/-0.1 mm, both changes P<0.01 vs. NTG) were significantly less severe in the alpha1A-TG mice and did not progress after 3 weeks. At 15 weeks after MI, LV catheterization revealed better preservation of dP/dtmax in the alpha1A-TG vs. NTG mice (7270+/-324, vs. 5938+/-372 mmHg/s, P<0.05). CONCLUSION: Enhanced inotropy resulting from transgenic overexpression of alpha1A-AR is well maintained chronically after MI and limits echocardiography-determined LV remodeling, preserves function, and reduces acute heart failure death.

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PubMed2005

The immunoquantification of caveolin-1 and eNOS in human and rabbit diseased blood vessels.

In this study, caveolin-1 (cav-1), an inhibitor of endothelial nitric oxide synthase (eNOS), was semi-quantified in diseased human and rabbit blood vessels. New Zealand White rabbits were fed, for 12 weeks, a high methionine diet (to induce intimal hyperplasia), 0.5% cholesterol diet, a normal diet, or the combination of both experimental diets. Excess segments of human internal mammary arteries (IMA) and radial arteries (RA) were obtained from patients undergoing coronary artery bypass surgery. eNOS and cav-1 were localized throughout both human and rabbit vessels. In rabbit arteries, eNOS was significantly increased in the endothelium overlying intimal thickening and atherosclerotic plaques compared with the adjacent endothelium overlying normal media. Interestingly, the endothelial cav-1:eNOS ratio increased 5-fold only in endothelium overlying plaques but decreased in endothelium overlying vessels with neo-intimal thickening. In human tissue, there was no difference between RA and IMA eNOS immunoreactivity in endothelium, intima, or media; however, RA endothelial, intimal, and medial cav-1 immunoreactivity increased 4-fold (p<0.02), 8-fold (p<0.001), and 4-fold (p<0.004), respectively, compared with IMA. Furthermore, the cav-1:eNOS immunostaining ratio in the media correlated with intimal thickening (r2 = 0.5). Our results suggest a close relationship between increased cav-1 and diseased blood vessels.

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