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© 2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

In particular, cocaine induces acute hypertension due to increased vasoconstriction induced by increased endothelin-1 [16], impaired acetylcholine-induced vasorelaxation [17], inhibition of nitric oxide synthase [18], impaired intracellular calcium handling [19], and inhibition of sodium/potassium channels [20] as determined by cellular and molecular analytical approaches [11]. Cocaine also enhances coronary spasm/vasoconstriction and platelet adherence/thrombosis, leading to reduced myocardial oxygen supply [34]. [...]an imbalance between oxygen supply and demand results in MI [35]. According to previous studies, cocaine impairs nitric oxide release from endothelial cells [59,60]. [...]cocaine increases levels of cell adhesion molecules (e.g., intracellular adhesion molecule-1 (ICAM-1), cluster of differentiation 54 (CD54), vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1)), low-density lipoprotein migration, and leukocyte migration in blood vessels [61]. [...]intimal smooth muscle cells within the coronary artery wall increase [24,62], presumably leading to progression of atherosclerosis and potential sudden cardiac death [63].

Details

Title
Acute and Chronic Effects of Cocaine on Cardiovascular Health
Author
Kim, Sung Tae; Park, Taehwan
Publication year
2019
Publication date
2019
Publisher
MDPI AG
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2332021801
Copyright
© 2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.