Zeitschrift für klinische Toxikologie
Offener Zugang

Abstrakt

Could Concurrent Use of Herbal Medicinal Products and Prescription Drugs Raise Older Adults Risk of Vascular Dementia?

Samantha Bodine, Logan Sneed, Zia Shariat-Madar

While the role of chemical insults or the buildup of chemical insults in cardiovascular pathogenesis continuously draws attention, the potential interference of a variety of currently used or investigational drugs on the ability of endothelial cells (ECs) which are responsible for providing a unique surface to allow the cellular elements of blood to flow without adhering to the vessel lining has been much less appreciated in drug discovery research. Activated ECs are more sensitive to long-term, continuous drug exposure than normal cells. Prolonged activation of ECs predisposes the blood vessel wall to vasoconstriction, leukocyte adherence, platelet activation, thrombosis, impaired coagulation, vascular inflammation, pro-oxidation, and atherosclerosis. The studies of hypercholesterolemia, homocystinemia, hyperglycemia, hypertension, smoking, inflammation, aging, diabetes mellitus, and heart rhythm abnormalities further lend credence for the contribution of perturbed EC structure and function in the development of heart attacks. These risk factors are often established in elders living with one or more chronic diseases and to some extent hold true across all adult age groups. Evidence indicates that vascular reactivity is an independent risk factor for dementia. Most people who have exhibited vascular dementia following a stroke had a high blood pressure or diabetes prior to the occurrence. Often adults with chronic diseases are treated with long-term, continuous, prescription drug(s) and self-administration of traditional medicines. Thus, an assessment of a combination of traditional medicines with widely used prescription drugs on activated ECs should be tested in experimental animal models of these diseases to demonstrate whether the long-term exposure of this combination therapy exacerbates vascular reactivity and worsens ischemic perfusion defect.