Study on the Cardiac Toxicity of Different Concentrations of Ethanol

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The study by Tsai and Kass was referenced to support the effects of low level ethanol, but was not a similar to my investigation. A study by Danziger et. al investigated the effects of ethanol on ECC coupling in cardiac myocytes as a whole, looking at the direct effects on calcium-myofilament interactions and sarcoplasmic reticulum Ca2+ content. The study also investigated contractility, but used EtOH concentrations similar to that of extreme intoxication. Therefore, this study was chosen as the primary reference.

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I had become interested in depressed contractility at the cellular level after pondering on the alarming rates of HF and obesity in Michigan and all of America as well. Health literacy, or the ability to understand basic health information to make appropriate health decisions, is extremely low in America; only 12 percent of U.S. adults had proficient health literacy (America’s Health Literacy: Why We Need Accessible Health Information). By investigating the effect of ethanol on contractility at the cellular level, I hoped that the results would contribute to improving the America’s health literacy of CVD and HF, and would in turn promote a regulation of alcohol consumption.

Furthermore, I hope that by using low- level concentrations of ethanol, the results will showcase that even moderate intoxication can have harmful effects on the heart. I hypothesize that as the concentrations of ethanol increase, the maximum extent of cell shortening in the myocytes will decrease, depressing myocardial contractility over an exposure of 7 minutes. A higher concentration of ethanol will have a greater negative inotropic effect per minute. It will decrease contractility through actions at the myofilaments, as the myocytes will not be loaded with Ca2+ probes (Danziger et al. 1991).

The independent variable is the ethanol concentrations (vol/vol) in each culture of myocytes. The concentrations, 0 %, .05%, .1%, .15%, .2% (vol/vol), were chosen based off of previous studies. In the primary reference study by Danziger et al., concentrations of .15%, 1%, 2%, and 3% (vol/vol) were used. However, this is representative of extreme intoxication, and my interest of study is in investigating moderate intoxication levels of ethanol. Therefore, it was more suitable to choose the study’s lowest concentration as one of my higher concentrations. A solution of 0% ethanol, or water, was used as a control. Water is abundant in blood, and has no negligible effect on contractility. Therefore, water will not have a significant effect on cardiac myocyte contractility.

The dependent variable is the maximum extent of cell shortening of the cardiac myocytes in each culture. I chose this variable to be examined over the contraction duration, for example, as the percentage change of ES (from the baseline) directly correlates to contractility. The contraction duration is a suitable variable for further research, such as identifying arrhythmias. It would not make sense to examine contraction duration for this investigation as arrhythmias have complex underlying mechanisms in the heart, which cardiac myocytes alone cannot effectively portray. Since ES percentage directly correlates to contractility, a shorter percentage indicates lower and depressed contractility (Joulin et. al 2006).

The cardiac myocytes used in this experiment are from rats. Myocytes from different species may respond differently to the same ethanol concentration, reducing the validity and reliability of the multiple trials taken with respect to the ES. The environment in which the cardiac myocytes were exposed to ethanol in was kept constant. The environment was sterile to avoid extraneous variables that could affect the contractility of the cells, which would ultimately affect the ES percentage after EtOH exposure. The time in which each culture was exposed to EtOH was kept constant.

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