Effects of glucocorticoids upon the glycosaminoglycans in salivary glands in the rat

The glycosaminoglycans of the salivary glands were studied in male rats after adrenalectomy and after the daily administration of either 100 or 300 μg of cortisol acetate to adrenalectomized rats during one month. Total uronic acid concentration was determined in the salivary glands. Chromatographic separation of the uronic acid fractions was performed on cellulose microcolumns. Adrenalectomy decreased the uronic acid concentration in the submaxillary and retrolingual glands, while the administration of cortisol acetate increased its concentration in these glands. No changes were detected in the uronic acid concentration in the parotid glands. Adrenalectomy affected the glycoprotein, hyaluronic acid and dermatan sulphate fractions, while cortisol acetate affected the hyaluronic acid, chondroitin-4-sulphate and chondroitin-6-sulphate fractions.     

Nitric oxide-dependent mitotic activity in salivary glands of the rat upon sympathetic stimulation

Incorporation of [3H]thymidine into trichloroacetic acid (TCA)-insoluble material of the parotid and submandibular glands was used as an index of mitotic activity following unilateral electrical stimulation of the sympathetic innervation (20 Hz, 4 min every fifth minute over 34 min). Stimulation under beta-adrenoceptor blockade (propranolol 2 mg/kg, intravenous) alone or combined with alpha-adrenoceptor blockade (phentolamine 2 mg/kg, intravenous) did not increase the rate of [3H]thymidine incorporation into the two types of glands. However, under alpha-adrenoceptor blockade the [3H]thymidine incorporation increased into the parotid glands, by 122% (compared to the glands on the contralateral side), but not into the submandibular glands. In the presence of the neuronal type NO-synthase (nNOS) blocker N-PLA (30 mg/kg, intravenous) or the unselective NO-synthase blocker L-NAME (30 mg/kg, intravenous), this increase was reduced to 49 and 47%, respectively. Thus, the major part of the sympathetically nerve-evoked beta-adrenoceptor-mediated mitotic response was found to depend on the activity of neuronal type NO-synthase to generate NO. Since the sympathetic nerve fibres of the parotid gland lack NO-synthase, the neuronal type NO-synthase subjected to the inhibitors is likely to be of parenchymal origin.     

Radioautography of Ca in rat salivary glands

Radioautographic visualization of Ca⁴⁵ in rat salivary glands indicated marked storage in submaxillary gland acinar cells. Acinar cells of the sublingual gland stored somewhat less, while acinar cells of the parotid and granular tubule cells of the submaxillary gland contained only slightly more Ca⁴⁵ than connective tissue. The uptake of Ca⁴⁵ in submaxillary and parotid gland acinar cells was greatly reduced 2 hr after isoproterenol. After chronic administration of isoproterenol, radioautographic visualization of Ca⁴⁵ localization indicated that the great increase in storage of calcium in the submaxillary gland produced by this drug probably resulted from an increase in the proportion of the gland made up by acinar cells.     

Characterization of cGMP-related phosphodiesterase isoenzymes in rat salivary glands

 Isolation and characterization of the cGMP-related phosphodiesterase (PDE) isoenzymes in rat salivary glands were investigated. Both cGMP- and cAMP-PDE activities were mainly present in the 100 000 g supernatant fractions from the parotid, submandibular, and sublingual glands. The results of inhibition studies and ion-exchange chromatography suggest that Ca²⁺/calmodulin markedly stimulates PDE1 in the parotid and sublingual glands, and slightly in the submandibular gland. PDE2 was detected only in the parotid gland. PDE3 was identified in the parotid and submandibular glands. PDE5 was detected in the submandibular and sublingual glands by using inhibition studies, ion-exchange chromatography, and Western blotting. Received: August 21, 2001 / Accepted: May 28, 2002     

Histochemical identification of plasminogen activator in rat salivary glands

Plasminogen activator was demonstrated in sublingual, submaxillary and parotid glands. The lytic areas in the fibrin clot, induced by activation of plasminogen into the specific fibrinolytic enzyme plasmin, were evident microscopically as well defined areas of liquefaction. The fibrinolytic activity was directly related to time of incubation of the tissue with the plasminogen-rich fibrin clot. No activity was found in the plasminogen-free fibrin clot. This indicated that the lysis was due to specific activation of plasminogen by the tissue's activator, and not due to non-specific proteolysis. The gland activator was always related to blood vessels, and found to be effective in activating human and bovine plasminogen.     

The pathology of salivary glands. Tumors of the salivary glands

The management of benign and malignant neoplasms of the salivary glands requires precise knowledge of tumor histogenesis and classification as well as surgical skills. Pleomorphic adenoma and Whartin's tumor are the most frequent tumors in parotid glands while the probability for malignant tumors is higher in other glands, especially in sublingual and minor salivary glands. Those malignant salivary glands tumors are rare and necessitate multidisciplinar staging and management in close collaboration with the pathologist and the radiation oncologist.     

The effects of cigarette exposure on rat salivary proteins and salivary glands

Objective:  Passive smoking is the involuntary inhalation of cigarette smoke (CS) and has an adverse impact on oral health. We examined the effect of CS exposure on saliva and salivary glands (SGs).
Methods:  Cigarette smoke-exposed rats were intermittently housed in an animal chamber with whole-body exposure to CS until killed. Whole saliva was collected before CS exposure (0 day), and 15 and 30 days after the start of CS exposure. Saliva secretion was stimulated by administration of isoproterenol and pilocarpine after anesthesia. SGs were collected on 31 days.
Results:  The increase in body weight of the CS-exposed rats was less than that of the control rats. Salivary flow rates did not differ at 0, 15 or 30 days after the start of CS exposure. However, the amylase and peroxidase activities and total protein content in the saliva were significantly lower in 15-day CS-exposed rats than in 15-day control rats. Histological examination of the SGs of CS-exposed rats showed vacuolar degeneration, vasodilation and hyperemia.
Conclusion:  These results suggest that CS exposure has adverse impacts on salivary composition and SGs, which could aggravate the oral environment.     

Impairment by ethanol of prostaglandin production in rat salivary glands

Sublingual salivary acini and submandibular tissue were incubated in DMEM medium in the presence of various concentrations (0-5%) of ethanol and the content of the three major prostaglandins, PGE2, PGF2 alpha and 6-keto-PGF1 alpha, were determined by radioimmunoassay. In In the sublingual gland, ethanol caused a decrease in PGE2 and PGF2 alpha levels, but had no effect on 6-keto-PGF1 alpha, while all three prostaglandins were affected in the submandibular gland. At 2.5% ethanol, the production of PGF2 alpha and PGE2 in sublingual gland decreased by 10% and reached maximum inhibition at 5% ethanol, at which concentration there was a 20 and 30% decrease in their levels. In submandibular gland, 2.5% ethanol caused a 20% decrease in PGE2, 30% in PGF2 alpha and 50% in 6-keto-PGF1 alpha; 40% inhibition in PGE2, 57% in 6-keto-PGF1 alpha and 65% in PGF2 alpha occurred in the presence of 5% ethanol. These findings suggest that alcohol impairs the function of salivary glands by inhibiting prostaglandin production.