Cardiac morphology in rats with growth hormone-producing tumours.
Cardiac enlargement and dysfunction are common in patients with acromegaly. Whether these changes are a direct consequence of growth hormone excess is obscured by the high frequency of hypertension, diabetes mellitus, or atherosclerosis in acromegalic patients. In this study, the effects of chronic elevations of growth hormone (GH) upon the heart were studied in rats with GH-producing tumours implanted subcutaneously for 4 weeks. Geometric measurements and histology were employed to detect the presence of cardiac changes. Increased mass was observed in the tumour-bearing animals. When compared with controls, in tumour-bearing rats there were significantly greater (P less than 0.05) right (0.17 +/- 0.03 v. 0.13 +/- 0.01 g) and left (0.62 +/- 0.05 v. 0.50 +/- 0.04 g) ventricular weights, external cardiac dimensions, and myocardial fibre diameters (9.4 +/- 0.6 v. 8.3 +/- 0.4 micron). However, these increases were linearly-related to increased body mass in the tumour-bearing group so that the ratios of ventricular weights to body weight were similar in both groups. Furthermore, no pathologic changes such as myocardial fibrosis or asymmetric septal hypertrophy were present in the tumour-bearing rats. Thus, under the conditions of this study, growth hormone excess induced cardiac growth, which appeared to represent a manifestation of generalized body growth rather than a distinct pathologic process.
Gilbert
P L
PL
Siegel
R J
RJ
Melmed
S
S
Sherman
C T
CT
Fishbein
M C
MC
D000818:Animals; D001835:Body Weight; D006332:Cardiomegaly / Q000209:etiology; D005260:Female; D013006:Growth Hormone / Q000378:metabolism*; D009206:Myocardium / Q000473:pathology*; D009374:Neoplasms, Experimental / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D009929:Organ Size; D051381:Rats; D011920:Rats, Inbred WF
D013006:Growth Hormone