» Articles » PMID: 7645194

Altered Adenosine Triphosphatase Activities in Pigs with Naturally Occurring Hypertrophic Cardiomyopathy

Overview
Journal Vet Res Commun
Publisher Springer
Date 1995 Jan 1
PMID 7645194
Citations 2
Authors
Affiliations
Soon will be listed here.
Abstract

The purpose of this study was to determine whether myocardial adenosine triphosphatase (ATPase) activities were reduced in pigs with naturally occurring hypertrophic cardiomyopathy (HCM). The selection of hearts for the HCM and the normal control groups depended on histological examination. Specific ATPase activity and 5'-nucleotidase activity were measured in left ventricular myocardium obtained from HCM (n = 7) and normal control (n = 7) animals. The histological features of HCM included marked disorientation of muscle cells, thickening of the intramural coronary arterial wall with a narrowed lumen, endocardial fibrosis and myocardial fibrosis. The HCM group showed significant increases in both heart weight (32%) and heart weight to body weight ratio (46%). The total ATPase activity in crude homogenates from the HCM group was significantly decreased by 16%. Azide-sensitive ATPase (mitochondrial ATPase) activity, ouabain-sensitive ATPase (Na+, K+-ATPase) activity, basal Mg(2+)-ATPase activity and Ca(2+)-ATPase activity were all significantly decreased by 18%, 30%, 20% and 50%, respectively. In contrast, no significant decrease was found in the mean values for 5'-nucleotidase activity. These results suggest that myocardial ATPase activities are suppressed in pigs with naturally occurring HCM.

Citing Articles

A One Health Approach to Hypertrophic Cardiomyopathy.

Ueda Y, Stern J Yale J Biol Med. 2017; 90(3):433-448.

PMID: 28955182 PMC: 5612186.


Spontaneous Dilated Cardiomyopathy and Right-Sided Heart Failure as a Differential Diagnosis for Hepatosis Dietetica in a Production Pig.

Collins D, Eaton K, Hoenerhoff M Comp Med. 2015; 65(4):327-32.

PMID: 26310462 PMC: 4549678.

References
1.
Maron B, Bonow R, Cannon 3rd R, Leon M, Epstein S . Hypertrophic cardiomyopathy. Interrelations of clinical manifestations, pathophysiology, and therapy (1). N Engl J Med. 1987; 316(13):780-9. DOI: 10.1056/NEJM198703263161305. View

2.
Maron B, MCINTOSH C, Klues H, Cannon 3rd R, Roberts W . Morphologic basis for obstruction to right ventricular outflow in hypertrophic cardiomyopathy. Am J Cardiol. 1993; 71(12):1089-94. DOI: 10.1016/0002-9149(93)90578-z. View

3.
Gwathmey J, Morgan J . Altered calcium handling in experimental pressure-overload hypertrophy in the ferret. Circ Res. 1985; 57(6):836-43. DOI: 10.1161/01.res.57.6.836. View

4.
Liu S, Roberts W, Maron B . Comparison of morphologic findings in spontaneously occurring hypertrophic cardiomyopathy in humans, cats and dogs. Am J Cardiol. 1993; 72(12):944-51. DOI: 10.1016/0002-9149(93)91112-u. View

5.
Panagia V, Heyliger C, Singal P, Dhalla N . Subcellular distribution of cardiac 5'-nucleotidase: alteration of microsomal pool in hypertrophied pig heart. J Mol Cell Cardiol. 1986; 18(8):815-26. DOI: 10.1016/s0022-2828(86)80956-7. View