Intrinsic cardiac adrenergic (ICA) cell density and MAO-A activity in failing rat hearts

• Published in: Journal of muscle research and cell motility Vol. 35; no. 1; pp. 47 - 53
• Main Authors: van Eif, Vincent W. W., Bogaards, Sylvia J. P., van der Laarse, Willem J.
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.02.2014; Springer Nature B.V
• Subjects: Animal Anatomy; Animals; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell Count; Clorgyline - pharmacology; Disease Models, Animal; Heart Failure - enzymology; Heart Failure - metabolism; Heart Failure - pathology; Histology; Life Sciences; Male; Monoamine Oxidase - metabolism; Monoamine Oxidase Inhibitors - pharmacology; Morphology; Myocytes, Cardiac - enzymology; Myocytes, Cardiac - pathology; Norepinephrine - metabolism; Original Paper; Oxygen Consumption; Proteomics; Rats; Rats, Wistar; Monoamine oxidase A; Pulmonary hypertension; Intrinsic cardiac adrenergic (ICA) cells; Basal oxygen consumption
• ISSN: 0142-4319; 1573-2657
• DOI: 10.1007/s10974-013-9373-6

The efficiency (work/oxygen consumption) of isolated papillary muscles from failing hearts is reduced. We investigated whether this can be due to an increase of intrinsic cardiac adrenergic (ICA) cell density. The number of ICA cells in the septum and both ventricular walls was determined by tyrosine hydroxylase immunohistochemistry in rats with monocrotaline-induced pulmonary hypertension. We found that the number of ICA cells is about 200,000 per rat heart. ICA cell density was significantly lower in right ventricular myocardium of hypertrophied hearts ( P  < 0.01). MAO-A enzyme histochemistry and inhibition experiments with clorgyline in papillary muscles were performed to localize the enzyme and to determine its oxygen consumption. Upregulation of MAO-A was found in the right ventricular wall and papillary muscles of failing hearts ( P  = 0.018). A positive correlation between ICA cell density and MAO-A activity was absent. Clorgyline (2 μM) decreased the basal rate of oxygen consumption of right ventricular papillary muscles by 65 μM O 2 /s ( P  = 0.027). This rate can only be maintained for several seconds judging from the catecholamine content of the preparations reported previously. High ICA cell activity rather than density and/or recycling of oxidized catecholamines are discussed as alternative explanations for the low myocardial efficiency in experimental pulmonary hypertension.