Spin-spin relaxation times in myocardial hypertrophy induced by endocrine agents in rat.
Magnetic resonance techniques afford a significant advantage for noninvasive diagnosis of cardiovascular pathology. The purpose of our present study was to assay the proton nuclear magnetic resonance (1H-NMR) sensitivity in the differential diagnosis of certain endocrine cardiovascular complications. In this context, we investigated the water state and content in the hypertrophied myocardium. Male and female Wistar rats were treated with different hormones (hydrocortisone acetate, testosterone, estradiol, thyroid hormones) in combination with isoproterenol (a synthetic catecholamine that induces myocardial ischemia and hypertrophy). The animals were sacrificed after 20 days of treatment and samples of integral myocardium and left ventricular myocardium were analyzed on a 1H-NMR AREMI spectrometer (0.6 T; proton resonance at 25 MHz). The estimation of T2 was made by Carr Purcell-Meiboom-Gill pulse sequence. The data were fitted to a bi-exponential curve, yielding short (T21) values for bound water and long (T22) values for free water. In order to evaluate the myocardial hypertrophy, the following ratios were calculated: integral myocardium to body weight; left ventricle to body weight; left ventricle to integral myocardium. The first two ratios were also calculated for dried tissue, in order to estimate its contribution to myocardial hypertrophy. Our findings demonstrate that myocardial hypertrophy is associated with a decrease of T22, as a consequence of the increase in the dried component (i.e. proteins) of the tissue, while the total tissue water (H2Ot%), measured by gravimetry) was not significantly modified. Nevertheless, it is reasonable that the increase in the protein content would be proportional with the increase in H2Ot%. The decrease of T21 seems to be proportional with the level of left ventricle hypertrophy in female groups. The 1H-NMR measurements were much sensitive for the differential diagnosis of myocardial hypertrophy in the case of left ventricle.
Burtea
C
C
Institute of Pathology and Medical Genetics 'Victor Babes', Bucharest, Romania.
Gatina
R
R
Stoian
G
G
Mardare
M
M
Dumitru
I F
IF
Dragomir
C T
CT
D000318:Adrenergic beta-Agonists / Q000633:toxicity; D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced* / Q000175:diagnosis* / Q000378:metabolism; D004958:Estradiol / Q000633:toxicity; D005260:Female; D006728:Hormones / Q000633:toxicity*; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000633:toxicity; D007545:Isoproterenol / Q000633:toxicity; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D008432:Mathematical Computing; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011522:Protons; D051381:Rats; D017208:Rats, Wistar; D013739:Testosterone / Q000633:toxicity; D013963:Thyroid Hormones / Q000633:toxicity; D014867:Water / Q000378:metabolism
D000318:Adrenergic beta-Agonists; D006728:Hormones; D011522:Protons; D013963:Thyroid Hormones; D014867:Water; C021650:hydrocortisone acetate; D013739:Testosterone; D004958:Estradiol; D007545:Isoproterenol; D006854:Hydrocortisone