January 1, 1982 Experimental Physiology, 67, 7-15.
Correspondingly the acini were loaded with secretory granules at 12 and 48 hours but were extensively depleted of granules at 24 hours. This loss of granules is considered to be due to sympathetic "degeneration secretion" caused by the release of noradrenaline from the degenerating adrenergic nerves between 12 and 24 hours after ganglionectomy. This is thought to be the first example of morphological change resulting from "degeneration activation" to be recorded microscopically.
Cell Tissue Res. 1975 Sep 16;162(1):1-12.
Degeneration Secretion and Supersensitivity in Salivary Glands following Denervations, and the Effects on Choline Acetyltransferase Activity.
Garrett JR, Ekstr�m J, Anderson LC (eds): Neural Mechanisms of Salivary Gland Secretion.Front Oral Biol. Basel, Karger, 1999, vol 11, pp 166-184
(DOI: 10.1159/000061117)
Circulating catecholamines, however, influence the amount of amylase and peroxidase secreted by the rat parotid gland in response to parasympathetic nerve stimulation and account for most of the increased secretion of these enzymes following chronic sympathectomy.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1193204
There was a reduction in all proline-rich proteins (PRP) in the saliva following sympathectomy.
http://www.find-health-articles.com/rec_pub_2450385-influences-short-term-sympathectomy-composition-proteins-rat-parotid.htm
Chronically low blood pressure is accompanied by a variety of complaints including fatigue, reduced drive, faintness, dizziness, headaches, palpitations, and increased pain sensitivity [1–4]. In addition, hypotensive individuals report cognitive impairment, above all deficits in attention and memory. Nevertheless, it is generally the case that in research, as well as in clinical practice, relatively little importance is ascribed to hypotension. One reason for this is that, despite mental symptoms, cerebral dysfunction generally is not taken into account [1]. This is a consequence of the current doctrine that low systemic blood pressure is compensated by autoregulatory processes which prevent reduced blood perfusion of the brain [5, 6].
Some recent findings challenge this doctrine: reduced cognitive performance in hypotension has been demonstrated by neuropsychological testing, and EEG studies have revealed diminished cortical activity. Moreover, the assumption of unimpaired brain perfusion in hypotension no longer holds. In the present review the necessity of a reappraisal concerning hypotension is discussed in light of the relationship between blood pressure and cerebral functioning.
Clin Auton Res. 2007 April; 17(2): 69–76. Published online 2006 November 14. doi: 10.1007/s10286-006-0379-7. | PMCID: PMC1858602 |
and Rainer SchandryStefan Duschek, Phone: +49-89/2180-5297, Fax: +49-89/2180-5233, Email: duschek@psy.uni-muenchen.de