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Early to late sparing of radiation damage to the parotid gland by adrenergic and muscarinic receptor agonists
Authors
A W T Konings
Budford-Mason AP
+43 more
Chang TT
Coppes RP
Coppes RP
Dardick I
Denny PC
Eisbruch A
El Mofty SK
Fleming N
Franzé
Funegard U
Gerstin EH
Gomperts BD
Gustafsson H
H H Kampinga
Henricksson R
Jensen AB
Johnson JT
L J W Zeilstra
Leslie MD
Leveque FG
Martinez JR
Nagler RM
Nagler RM
Paardekooper GMRM
Peter B
Peter B
Peter B
Phillips RM
Pierre KJ
R P Coppes
Redman RS
Roesink JM
Sawaki K
Shannon IL
Sodicoff M
Valdez IH
Valdez IH
Vissink A
Vissink A
Vissink A
Vissink A
Wolff A
Zimmerman RP
Publication date
28 September 2001
Publisher
Nature Publishing Group
Doi
Cite
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on
PubMed
Abstract
Damage to salivary glands after radiotherapeutic treatment of head and neck tumours can severely impair the quality of life of the patients. In the current study we have investigated the early-to-late pathogenesis of the parotid gland after radiation. Also the ability to ameliorate the damage using pretreatment with adrenergic or muscarinic receptor agonists is studied. Rats were locally irradiated with or without i.p. pretreatment with phenylephrine (α-adrenoceptor agonist, 5 mg kg−1), isoproterenol (β-adrenoceptor agonist, 5 mg kg−1), pilocarpine (4 mg kg−1), methacholine (3.75 mg kg−1) (muscarinic receptor agonists) or methacholine plus phenylephrine. Parotid salivary flow rate, amylase secretion, the number of cells and gland histology were monitored sequentially up to 240 days postirradiation. The effects were described in 4 distinct phases. The first phase (0–10 days) was characterised by a rapid decline in flow rate without changes in amylase secretion or acinar cell number. The second phase (10–60 days) consists of a decrease in amylase secretion and is paralleled by acinar cell loss. Flow rate, amylase secretion and acinar cell numbers do not change in the third phase (60–120 days). The fourth phase (120–240 days) is determined by a further deterioration of gland function but an increase in acinar cell number, albeit with poor tissue morphology. All drug pretreatments used could reduce radiation effects in phase I and II. The protective effects were lost during phase IV, with the exception of methacholine plus phenylephrine pretreatment. The latter combination of drugs ameliorated radiation-damage throughout the entire follow-up time. The data show that combined pre-irradiation stimulation of muscarinic acetylcholine receptors with methacholine plus α-adrenoceptors with phenylephrine can reduce both early and late damage, possibly involving the PLC/PIP2 second messenger pathways. This opens perspectives for the development of clinical applicable methods for long-term sparing of parotid glands subjected to radiotherapy of head and neck cancer patients. © 2001 Cancer Research Campaignhttp://www.bjcancer.co
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