To print: Select File and then Print from your browser's menu --------------------------------------------------------------------------------------- Title: Research Shows Second-hand Smoke and High Cholesterol Damage Heart URL: http://www.pslgroup.com/dg/6FA2.htm Doctor's Guide March 26, 1996
SAN FRANCISCO March 26, 1996 -- The heart attacks that often kill non-smokers who are chronically exposed to second-hand tobacco smoke may result from a long disease process caused by smoke and high cholesterol acting together to damage cells lining artery walls, new experiments by UC San Francisco cardiologists suggest. Damage done to these cells by smoke and fat may be offset somewhat by massive doses of a precursor of a molecule used by cells to send signals, or by vitamin E, the researchers found. They also determined that the damage may be made worse by the sex hormone testosterone. The researchers presented their preliminary findings today (March 25) at the annual meeting of the American College of Cardiology in Orlando, Fla. Epidemiological studies comparing deaths among populations with differing lifestyles indicate that each year 50,000 or more non-smokers die from heart attacks attributable to second-hand smoke. Heart disease greatly outstrips lung cancer or other cancers as the most prominent, deadly health risk faced by non-smokers thus exposed. The new UCSF findings shed light on the biological reasons why second-hand smoke is harmful to heart health. "Our experiments demonstrate that smoking and diet can affect the health of cells that are vital in preventing the clogging and hardening of arteries," says Stuart Hutchison, MD, a clinical instructor in cardiology at UCSF who presented some of the group's findings. The UCSF group focuses on gaining a better understanding of how diet, smoking and hormones affect a microscopically thin layer of cells, called endothelial cells, which lines the inner surface of blood vessels. By preventing blood-borne molecules from attaching to blood vessel walls, healthy endothelial cells prevent the build-up of plaque, Hutchison explains. The cells also release and respond to chemicals that cause blood vessels to widen and narrow as the physiological situation demands. If these cells are lost or damaged, blood vessels are more likely to accumulate plaque, and the blood vessels become less capable of adjusting their diameters to meet the body's oxygen needs. Plaque accumulation and its possible role in heart disease has been appreciated for centuries, Hutchison points out. In comparison, the loss of the ability to regulate blood vessel diameter has been known for less than two decades, and research into its contributions to heart disease has intensified and become more fruitful in recent years, according to Hutchison. The researchers used rabbits to perform controlled experiments that would be difficult or impossible to conduct in humans. On a small scale, the heart and blood vessel anatomy of rabbits mimics that of humans, and the circulatory systems of the two mammals are believed to respond similarly to life's insults. The UCSF scientists exposed male rabbits to smoke and a high cholesterol diet for ten weeks. To conduct detailed investigations of endothelial cell performance and of affects on blood vessels, the researchers studied the responses of living slices of aorta bathed in a saline solution similar to blood, bubbling oxygen into solution to keep cells alive. The UCSF group measured plaque build-up, as well as the ability of aortic slices from treated animals to contract and relax in response to pharmacological substances. Both measures of heart disease were adversely affected when rabbits were fed a high cholesterol diet and exposed to tobacco smoke. The purpose of using L-arginine in the studies, Hutchison says, is that it is a building block used by endothelial cells to make nitric oxide, a signaling molecule in the cells. The cells produce nitric oxide to control the diameter of blood vessel cells. The researchers found that nitric oxide production dropped in endothelial cells exposed to smoke. Supplementing the diet with L-arginine helped the aortic slices to remain flexible. This suggests that L-arginine leads to increased production of nitric oxide, causing the vessel to relax, Hutchison said. The UCSF team also bathed some of the aortic slices from the rabbits in a solution containing physiologic concentrations of various sex hormones, including testosterone and estrogen. "In these male rabbits, estrogen did not improve the impaired response, and testosterone actually worsened it," Hutchison says. "This suggests that in male animals testosterone may participate in some aspects of atherosclerosis. "This work raises questions about a possible role of sex hormones as protective or contributing factors in heart disease," Hutchison adds. "With more women trying to weigh the risks and benefits of post-menopausal estrogen therapy, and with many adolescent boys and men abusing male sex hormones in an effort to better compete athletically, understanding these connections becomes increasingly important." In comparison to men, women are believed to be somewhat protected from heart disease by estrogen until production of the hormone drops at menopause. The researchers used vitamin E, an anti-oxidant, to investigate the possible role of oxidation in damaging blood vessels and endothelial cells. They wanted to know if oxidation is implicated in causing a blood vessel to become less flexible. Vitamin E restored the ability of blood vessels to relax in response to pharmacological agents in the smoke-exposed, high cholesterol rabbits, but research on aortic slices in this group has thus far been inconclusive, Hutchison says. "These preliminary studies are helpful in understanding how cellular changes contribute to heart disease," Hutchison says. "However, we used massive doses of supplements to help us examine very specific aspects of blood vessel behavior and our results do not lead us to recommend dietary supplements for human heart disease at this time. "Ultimately," Hutchison adds, "We hope similar studies will help us learn how to better detect and prevent these harmful biological events before a heart attack occurs." Other UCSF Division of Cardiology physicians who participated in the research presented today include William Parmley, MD, professor and chief; Kanu Chatterjee, MD, professor; Stanton Glanz, MD, professor; Khrishna Sudhir, MD, assistant professor; Tony Chou, MD, assistant professor; and Prakash Deedwania, MD, a clinical professor of medicine at UCSF who is also the chief of cardiology at the Veterans Administration Hospital in Fresno. --------------------------------------------------------------------------------------------- Copyright © 1999 P\S\L Consulting Group Inc. All rights reserved. Republication or redistribution of P\S\L content is expressly prohibited without the prior written consent of P\S\L. P\S\L shall not be liable for any errors, omissions or delays in this content or any other content on its sites, newsletters or other publications, nor for any decisions or actions taken in reliance on such content. --------------------------------------------------------------------------------------------- This news story was printed from *Doctor's Guide to the Internet* located at http://www.docguide.com --------------------------------------------------------------------------------------- Return to News Story Page This site is maintained by webmaster@pslgroup.com Please contact us with any comments, problems or bugs. All contents Copyright (c) 1998 P\S\L Consulting Group Inc. All rights reserved.