POLYAMINES IN CYSTIC FIBROSIS 72 1 gainscores (before or after treatment), however, there was a significantly higher variance in the pyritinol group in four parameters. The latter findings suggest medication effects for a not as yet specifiable subpopulation. The problem of how to.define objective indications for a psychoactive drug was therefore considered to be the most difficult task for such a study.
We present controlled laboratory studies of the spontaneously hypertensive rat which indicate that hypertension is an important pathophysiological risk factor in age-related hearing loss. Our results are in concert with previous retrospective clinical studies that pointed to this possibility in man. Hypertension as a risk factor for hearing loss is within the bounds of known measures ofdiagnosis, treatment, and even prevention, with monitoring early in life. Because hypertension is such a major public health problem in the United States, in view of our results it is possible that its treatment and early diagnosis will benefit a significant number of people who would otherwise lose their hearing with advancing age. We compared the round window ac cochlear potential-sensitivity and -intensity functions in 10 female spontaneously hypertensive rats and 10 female normotensive Wistar-Kyoto control rats. The animals were all 12 months old and weighed between 170 and 250 g. The normotensives had higher maximum cochlear potential-intensity values compared with the hypertensives: 1,000 Hz (P < 0.005), 5,000 Hz (P < 0.005), and 10,000 Hz (P < 0.01). One-microvolt isopotential cochlear potentials for the low frequencies of the normotensives showed greater sensitivity than those of the hypertensives: 100 Hz (P < 0.05), 200 Hz (P < 0.10), 290 Hz (P < 0.05), 500 Hz (P < 0.005), 700 Hz (P < 0.12), 1,000 Hz (P < 0.025), and 2,000 Hz (P < 0.10). Blood pressure of the hypertensive group was significantly greater than that of the normotensive rats (P < 0.001). The hearts and aortas of the hypertensive group were hypertrophied. Autonomic imbalance, platelet aggregation, decreased arterioles, and natriuretic hormone were discussed as possible etiologies for the measured sensory hearing loss.An important frontier for clinical otologists and scientists in physiological acoustics is the study ofthe etiology ofpresbycusis (1). This paper represents a new approach to the problem, and our results could have far-reaching significance for the potential amelioration ofprogressive loss of hearing with old age. We focused our attention on hypertension, which is a major pathophysiological process associated with aging. We found a striking correlation between hypertension and hearing loss in a controlled laboratory experiment. Thus, we identified a risk factor for hearing loss that is within the bounds of known measures of diagnosis, treatment, and even prevention, with monitoring early in life.Previous work on presbycusis-although not defining its pathophysiology-has served to document the histopathological nature of inner ear degeneration with age (2, 3). Other important studies have delineated the contributions ofnoise and ototoxic drugs to loss of hearing with age (4). Even earlier laboratory experiments have explained in detail the principles behind the otologist's operations for conductive deafness in people (5).Our experiments were motivated in part by conflicting retrospective clinical studies in the literature. Some reports have...
We have discovered an animal model, the white carneau pigeon, which for the first time, through its use in laboratory experiments, has demonstrated significant correlations between the magnitude of inner ear electric potentials and standard measures of blood pressure, blood cholesterol, and blood coagulation. Also, we have found that a new blood coagulation research tool—the sonoclot machine—can demonstrate blood coagulation physiology parameters which correlate highly with cochlear potentials in our animal model. The above results will be discussed in relation to our previous findings of relationships of atherosclerosis to hearing in the same animal model. [Work supported by NIH Grant Number NS-12013.]
Previously we reported [J. G. McCormick, R. M. Clayton, and I. L. Holleman, J. Acoust. Soc. Am. 52, 193 (1972)] that round window cochlear potentials of old pigeons that developed spontaneous carotid atherosclerotic plaques were poorer in sensitivity than younger birds of the same breed with little or no evidence of plaques. We also noted that a high cholesterol diet fed to these birds was correlated with a reduction of cochlear potentials. This initial work, which included studies on birds genetically resistant to atherosclerosis was a pilot project on 75 birds. In our present paper we will report further findings from a one year study of over 220 additional atheroselerotic pigeons. The age relationship to cochlear potential loss is substantiated, and correlative sophisticated blood coagulation tests will be discussed. [Work supported by NIH Grant No. NS-12013 and Bowman Gray School of Medicine, Venture Capital Grant No. 2-156-801-2507.]
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