Abstract
The reports that amine-depleted cat papillary muscles have impaired contractile properties have suggested the possibility that an intramyocardial mechanism may regulate cardiac contractility through the release of stored norepinephrine (NE). We have tested this hypothesis by comparing the performance of control and reserpinepretreated dog heart-lung preparations during the stress of graded increase in flow work, pressure work and dose of pentobarbital. The performance of control and amine-depleted hearts was indistinguishable during each of these three types of severe stress. These observations together with other reports in the literature suggest that, whatever impairment of cardiac performance may be associated with myocardial NE depletion in the intact animal or man, it is not due to the loss of an intramyocardial mechanism which regulates contractility through NE release.
Footnotes
- Received August 15, 1966.
- Accepted November 3, 1966.
- © 1967 by The Williams & Wilkins Company
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