時序性研究以超音波逆散射總成度量心肌內收縮力及組織都卜勒超音波度量心室機械表現闡明高血脂及藥物治療於兔心肌之影響
Other Title
Alterations of contractile synchronism and myocardial mechanical
performance of rabbit heart byhypercholesterolemia and intervened with
atorvastatin or rosiglitazone
performance of rabbit heart byhypercholesterolemia and intervened with
atorvastatin or rosiglitazone
Date Issued
2005
Date
2005
Author(s)
林隆君
DOI
932314B002205
Abstract
The effects of hypercholesterolemia on the myocardium per se include electrophysiological and
mechanical alterations. Because gap junctions are essential in electromechanical coupling
throughout the heart, we examined the correlation between the temporal expression of cardiac
connexin43 (Cx43), contractile function, and conduction velocity in cholesterol-fed rabbits.
Along the feeding protocol for 12 weeks, serum cholesterol level gradually increased (P<0.001).
In contrast, expression of cardiomyocyte Cx43 protein progressively decreased (60% reduction at
12 weeks, P<0.001). Such a reduction was also demonstrated by immunoconfocal microscopy,
which further showed redistribution of Cx43 gap junctions at the lateral cell membrane. The
down-regulation of Cx43 protein was associated with increased levels of Cx43 mRNA (3.5 times
at 12 weeks, P<0.001) and phosphorylated c-Jun N-terminal kinase (three times at 12 weeks,
P=0.001). Functionally, although fractional shortening of the left ventricle remained unchanged
throughout the feeding protocol, the cholesterol-fed rabbits had a reduced cardiac
cycle-dependent variation of integrated backscatters, a decreased mitral ring systolic velocity, and
an increased modified Tei index (all P<0.001), all of which indicated impaired intrinsic
myocardial contractility and attenuated ventricular systolic performance. In Langendorff-perfused
hearts of the cholesterol-fed rabbits, decreased conduction velocity was found (P<0.005).
Withdrawing a cholesterol-enriched diet for 18 weeks restored the contractile parameters and
Cx43 protein expression. These findings suggest that Cx43 is highly involved in the molecular
mechanism of hypercholesterolemia-induced cardiac contractile dysfunction and dysrhythmias.
Subjects
connexin
contractility
echocardiography
gap junction
hypercholesterolemia
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
File(s)![Thumbnail Image]()
Loading...
Name
932314B002205.pdf
Size
1.13 MB
Format
Adobe PDF
Checksum
(MD5):a37c38c849ae61f6679dbd590b1e8417