title: Role of nitric oxide in the regulation of blood flow in the rat submandibular gland during carotid artery occlusion.
abstract: The possible involvement of nitric oxide in the preservation of blood flow to the rat submandibular gland after uni- or bilateral occlusion of the common carotid was studied. Glandular blood flow and mean blood pressure were monitored before, during and after carotid occlusion in the presence and absence of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine-methyl-ester (L-NAME). To calculate vascular resistance, the local perfusion pressure distal to the point of occlusion was also measured. In normal rats, uni- or bilateral carotid occlusion resulted in an immediate decrease in ipsilateral glandular blood flow. After the cessation of carotid occlusion, hyperaemia was observed in the submandibular gland. Both local perfusion pressure and vascular resistance decreased during carotid occlusion. In the group pretreated with L-NAME, trends in blood-flow responses to uni- or bilateral occlusion were identical to those registered in the control groups, though the magnitude of the alterations was significantly less. The well-maintained glandular blood flow was due to functioning vascular anastomoses and compensating dilatation of glandular blood vessels. Nitric oxide had only a restrained effect on this compensatory mechanism.
authors.affiliation: Clinic of Conservative Dentistry, Semmelweis University, P.O. Box 124, 1088 Mikszáth K. tér 5, H-1431, Budapest, Hungary. vag@konfog.sote.hu
authors.forename: J
authors.initials: J
authors.lastname: Vág
authors.forename: C
authors.initials: C
authors.lastname: Hably
authors.forename: B
authors.initials: B
authors.lastname: Kerémi
authors.forename: E
authors.initials: E
authors.lastname: Kovács
authors.forename: J
authors.initials: J
authors.lastname: Bartha
authors.forename: A
authors.initials: A
authors.lastname: Fazekas
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D001163:Arteriovenous Anastomosis / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002340:Carotid Artery Diseases / Q000503:physiopathology*; D017536:Carotid Artery, Common / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006940:Hyperemia / Q000503:physiopathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013363:Submandibular Gland / Q000098:blood supply* / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester