Biology 202: Sample Research Paper: Follow this Format
Effect of Ethanol on Respiratory Rate of Goldfish
Chris Horner
Biology 202
February 28, 2011
Introduction
Alcohol is a known central nervous system depressant and thus effects change on various aspects of physiological functions. Ethanol has long been thought to be a respiratory depressant in animals. However, large doses are usually required to induce noticeable effects on respiration. Deaths from acute alcohol intoxication have long been believed to be due to respiratory failure in humans (Johnstone and Witt 1972). Several studies have documented this. Loomis (1952), Klingman and Haag (1958), and Malt and Baue (1971) found that dogs intoxicated with ethyl alcohol will invariably die of respiratory failure. These effects occur at rather high doses and similar effects are expected to occur with humans (Kaye and Haag 1947). Studies on human alcohol consumption indicate that the effects associated with ethanol ingestion depend on many variables. Whether that person is a chronic user contributes to tolerance to ethyl alcohol. However, an overwhelming amount of evidence supports the hypothesis that alcohol does indeed slow bodily functions. With that in mind we set out to determine if alcohol is, indeed, a depressant then it would effect some sort of change in respiratory rates of goldfish. Specifically, we hypothesized that the alcohol would slow the respiratory rates of our test subjects and that the effects would be dose dependent.
In our experiment our sample fish population would be subjected to different levels of alcohol concentration and opercular beats would be measured. The inebriation vehicle chosen is that of direct addition of the ethanol to the subject’s aqueous environment with the assumption that ethanol freely diffuses across the gills (Johnston and Bernard 1983). Thus, blood ethanol concentrations of the fish would be approximately equivalent to that of their surroundings.
Methods and Materials
In preparation for this experiment 10 goldfish were obtained from a local pet store. These fish were placed into 10 separate, 1-liter containers with 1 liter of deionized water (temperature 22 C) in each. An aerator was placed into each container and attached to a laboratory air supply in order to "oxygenate" the water and exclude the possibility of error due to anoxia. The fish were given 15 minutes to acclimate themselves to their new environment. Then the respiratory rate, as measured by beats of operculi, for each fish were counted for one-minute intervals. This count was repeated three times for each fish and the average number of beats taken.
To each container ethanol was added in the form of 80 proof vodka, so as to adjust the alcohol concentration to .05 percent. The fish were allowed 5 minutes to acclimate to this "new" environment and to allow time for the alcohol to take affect. Again, the beats of the operculi were counted for 1 minute. This process was repeated and each time the alcohol concentration was doubled. The experiment was discontinued after observing respiratory rate at a final concentration of .8 percent. The fish were then removed from the test containers and returned to a container of fresh water in order to "detoxify" their blood.
A chi- square analysis was performed using the recorded beats of operculi for each concentration of alcohol as compared with normal rates.
Results
The results of our experiment were not consistent with previous studies. We did not observe any depressive effects of the ethanol on fish gill beats. There were some changes in rates (Figure 1) but chi- square analysis showed these changes were not significant. Even at the .8 percent level the rates held and were comparable to gill beat counts for pure water.
We did notice some effects of alcohol on the fish. At the close of the experiment, at the .8 percent level, the fish were very docile. Meaning, the fish were slow to react and were moving slowly. This observation told us that the alcohol was being taken up by the fish and was having some effects on their central nervous system.
Figure 1. Observed respiratory changes in goldfish in response to ethanol.
Discussion
Upon examination of the data we can see that our hypothesis was not supported. Despite all of the evidence from previous studies on the depressive effects of ethanol on the respiration of animals, we did not find this to be true in our experiment. The rates did not change significantly even though the blood ethanol levels our fish were exposed to would have been approximately 1.5 times the lethal amount for a human (Kaye and Haag 1947). As stated previously, the depressive effects are usually found at higher blood concentrations. The goldfish, evidently, has a much higher tolerance for ethanol than do humans. O’Connor, et al. (1988). exposed goldfish to ethanol concentrations up to 1.7 percent. Although effects on respiratory rates were not examined in this study one could surmise that since the fish were able to survive this level of blood alcohol concentration that they may have some tolerance. This could be because goldfish and other cyprinid fish sometimes produce ethanol as an end metabolic product during anoxic conditions. When conditions are anoxic goldfish convert lactate to ethanol (Crawshaw et al. (1989). This anaerobic respiration enables the fish to survive for extended periods of time in low oxygen environments. It may be that these fish have developed tolerance to the effects of ethanol as a result of recurrent exposure to this ethanol pathway.
Some studies suggest that autonomic responses such as heart and respiration rate actually increase with ethanol consumption and are not necessarily related to blood alcohol concentrations (Johnstone and Witt 1972, Zilm 1981). In either case we observed no significant changes for these fish.
Literature Cited
Crawshaw, L. I., L. P. Wollmuth, and C. S. O’Connor. 1989. Intracranial ethanol and
ambient anoxia elicit selection of cooler water by goldfish. American Journal of Physiology 256: R133-137
Johnston, I. A., and L.M. Bernard. 1983. Utilization of the ethanol pathway in carp
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Johnstone, R. E. and R. L. Witt. 1972. Respiratory effects of ethyl alcohol intoxication.
Journal of the American Medical Association 222: 486
Kaye, S. and H. B. Haag. 1947. Terminal blood alcohol concentrations in 94 fatal cases
of acute alcoholism. Journal of the American Medical Association 165: 451- 452
Klingman, G. I. and H. B. Haag. 1958. Studies on severe alcohol intoxication in dogs.
Quarterly Journal for the Studies of Alcohol 19: 203- 225
Loomis, T. A. 1952. The effect of alcohol on myocardial and respiratory function.
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Malt, S. H. and A. E. Baue. 1971. The effects of ethanol as related to trauma in the awake
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O’Connor, C. S., L. I. Crawshaw, R. C. Bedichek, and J. C. Crabbe. 1988. The effect of
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Zilm, D. H., 1981. Ethanol- induced spontaneous and evoked EEG, heart rate, and
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