title: Increased pressure in venous sinusoids during decongestion of rat nasal mucosa induced by adrenergic agonists.
abstract: The haemodynamic effects of sympathetic agonists causing decongestion of the nasal mucosa have been investigated in rats. Access to mucosa was obtained from the dorsal side through a small cavity drilled in the nasal bone. The pressures in the venous sinusoids and in the interstitial fluid of nasal mucosa were recorded by micropuncture technique. The local red cell flux (LDF) was monitored by laser Doppler flowmetry, and the blood volume in the mucosa was measured by radio-labelled erythrocytes and albumin. In control rats the tissue blood volume was 0.25 +/- 0.03 g (g wet wt)-1. The interstitial fluid pressure (IFP) was 2.4 +/- 0.6 mmHg and the average blood pressure in venous sinusoids (Ps) was 12.8 +/- 2.7 mmHg. After topical application of noradrenaline (NA) the local blood volume was reduced to 0.12 +/- 0.03 g g-1. Ps was increased to 18.0 +/- 4.0 mmHg, whereas IFP was maintained and LDF was reduced to 40.4% of control, indicating a greater rise in post than in presinusoid vascular resistance. Blocking of both alpha 1 and alpha 2-receptors by phentolamine caused a rise in mucosa blood volume and in LDF by 16 and 20% of control, respectively. Ps increased significantly to 15.2 +/- 3.3 mmHg. Specific stimulation or blocking of alpha 1-receptors by phenylephrine or prazosin induced similar or slightly smaller vascular responses than NA or phentolamine. The effects of the specific alpha 2-agonist (clonidine) or antagonist (yohimbine) on rat mucosa were small, indicating a domination of the alpha 1-receptors. Thus, application of NA caused a rise in blood pressure in the venous sinusoids of nasal mucosa. As LDF fell simultaneously, the reduced blood volume must be due to an increased tone in the muscular wall of venous sinusoids.
authors.affiliation: Department of Physiology, University of Bergen, Norway.
authors.forename: A B
authors.initials: AB
authors.lastname: Kristiansen
authors.forename: K J
authors.initials: KJ
authors.lastname: Heyeraas
authors.forename: A
authors.initials: A
authors.lastname: Kirkebø
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume; D003000:Clonidine / Q000494:pharmacology; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007834:Lasers; D014663:Nasal Decongestants / Q000494:pharmacology*; D009297:Nasal Mucosa / Q000098:blood supply*; D009638:Norepinephrine / Q000494:pharmacology; D010256:Paranasal Sinuses / Q000098:blood supply / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects; D014680:Veins; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D014663:Nasal Decongestants; D010656:Phenylephrine; D015016:Yohimbine; D003000:Clonidine; D009638:Norepinephrine; D011224:Prazosin; D010646:Phentolamine