Norman Brachfeld, M.D., F.A.C.P.; Peter Kuehn, M.D.; Masaka Kawade, M.D.; Erdogan Oran, M.D.
This content is PDF only. Please click on the PDF icon to access.
Mechanisms responsible for the documented cardiotoxicity of nicotine are unknown and are complicated by the diverse effects of this complex agent. It has been shown to release catecholamines from ganglia and from stores and to stimulate release of antidiuretic hormone. In the brain, nicotine toxicity may be expressed as an interference with cellular respiratory metabolism. Experiments were designed to dissect its diffuse activity and to evaluate its primary hemodynamic and cardiometabolic actions at low and elevated dose levels on the isolated, perfused, beating rat heart. Effects on lysosomal, mitochondrial, and supernatant enzyme systems of the myocardium were studied. There was
Brachfeld N, Kuehn P, Kawade M, et al. Nicotine Mediated Release of Myocardial Cell and Lysosomal Enzymes.. Ann Intern Med. 1967;66:1034. doi: https://doi.org/10.7326/0003-4819-66-5-1034_1
Download citation file:
Published: Ann Intern Med. 1967;66(5):1034.
Results provided by:
Copyright © 2020 American College of Physicians. All Rights Reserved.
Print ISSN: 0003-4819 | Online ISSN: 1539-3704
Conditions of Use