CELLULAR MECHANISMS OF IMPAIRED CARDIAC E NERGETICS IN PATIENTS WITH DILATED CARDIOMYOPATHY - A DECREASE IN MITOCHONDRIAL RESPIRATION AND CREATINE-KINASE EXPRESSION

Citation
Ta. Branishte et al., CELLULAR MECHANISMS OF IMPAIRED CARDIAC E NERGETICS IN PATIENTS WITH DILATED CARDIOMYOPATHY - A DECREASE IN MITOCHONDRIAL RESPIRATION AND CREATINE-KINASE EXPRESSION, Kardiologia, 32(5), 1992, pp. 13-16
Citations number
14
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00229040
Volume
32
Issue
5
Year of publication
1992
Pages
13 - 16
Database
ISI
SICI code
0022-9040(1992)32:5<13:CMOICE>2.0.ZU;2-K
Abstract
The mitochondrial functional characteristics were assessed in the biop sy specimens from patients with various Functional Classes dilated car diomyopathy (DCMP). The assessment was made by using endomyocardial bi opsy specimens weighing 2-4 mg which had been taken from 39 patients a ged 19-64 years during coronary ventriculography and cardiac transplan tation. The status of mitochondria and the efficiency of mitochondrial creatine kinase functioning were evaluated by recording the respirati on of saponin-skinned muscular fibers. The maximum mitochondrial respi ration rate calculated on a dry weight basis was not substantially dif ferent in all functional classes of DCMP, while the acceptor control i ndex (V(max)/V0) and the level of creatine-activated respiration decre ased with an increase in the functional class of DCMP. The findings sh ow a good positive correlation between ejection fraction and creatine- stimulated respiration values and a linear negative correlation betwee n this parameter and end-diastolic pressures. Thus, the respiratory pa rameters of mitochondria in the endomyocardial biopsy specimens may be used to assess the severity of cardias lesions.