| ▌ 素材简介 |
高血压与心衰。解说词：
One of the best-recognized consequences of sustained hypertension is the development of dilated cardiomyopathy
that is characterized by progressive dilation of the left ventricle and decreased systolic performance of the left
ventricle. One of the hallmarks of dilated cardiomyopathy is the progressive thinning of the left ventricular wall, as
well as an overall increase in left ventricular cavity dimensions.
There are also a number of characteristic abnormalities of myocardial ultrastructure that occur in dilated
cardiomyopathy. As shown, there is progressive disarray of the myofilaments, accompanied by excessive
myocardial fibrosis. Both of these abnormalities are believed to contribute to the depressed systolic performance of
the left ventricle.
As in cardiac hypertrophy, there are a number of significant abnormalities in excitation contraction coupling that
occur in the failing cardiac myocyte. As shown, calcium influx through the L-type calcium channel results in
decreased release of calcium from the sarcoplasmic reticulum, which in the failing heart is believed to arise
secondary to hyperphosphorylation of the ryanondine receptor. The decrease in calcium that is available to activate
the cross-bridges leads to decreased sarcomere shortening and to myocyte dysfunction. In addition, there is also
decreased function of the calcium pump of the sarcoplasmic reticulum that removes calcium from the cytosol back
to the sarcoplasmic reticulum. These latter abnormalities also contribute to the decrease in calcium that is available
to activate the cross-bridges as the myocyte contracts.
In the preceding sequence we have reviewed some of the abnormalities of excitation contraction coupling in the
failing heart. The net result of these abnormalities is that there is a decrease of speed and extent of shortening of the
actin and myosin cross-bridges, as shown in the lower panel of this sequence. These abnormalities in myocyte
shortening are believed to contribute importantly to the development of left ventricular systolic dysfunction in the
failing heart. |
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