Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

Wachter, C; Heinemann, A; Jocic, M; Holzer, P.
Visceral vasodilatation and somatic vasoconstriction evoked by acid challenge of the rat gastric mucosa: diversity of mechanisms.
J PHYSIOL, LONDON 1995 486: 505-516. [OPEN ACCESS]
Web of Science PubMed PUBMED Central Google Scholar


Autor/innen der Med Uni Graz:
Heinemann Akos
Holzer Peter

Dimensions Citations:

Plum Analytics:
1. Acid back-diffusion through a disrupted gastric mucosal barrier increases blood flow to the stomach without any change in systemic blood pressure. This study was undertaken to examine the gastric acid-evoked changes in blood flow in a number of visceral and somatic arterial beds and to elucidate the mechanisms which lead to the regionally diverse haemodynamic responses. 2. The gastric mucosa of urethane-anaesthetized rats was challenged with acid by perfusing the stomach with ethanol (15%, to disrupt the gastric mucosal barrier) in 0.15 M HCl. Blood flow was estimated by laser Doppler flowmetry, the hydrogen clearance method or the ultrasonic transit time shift technique. 3. Gastric acid challenge increased blood flow in the gastric mucosa and left gastric artery while blood flow in the femoral artery and skin declined. 4. Afferent nerve stimulation by intragastric administration of capsaicin enhanced blood flow in the left gastric artery but did not diminish blood flow in the femoral artery when compared with the vehicle. 5. The gastric acid-evoked dilatation of the left gastric artery was depressed by acute extrinsic denervation of the stomach, capsaicin-induced ablation of afferent neurones or hexamethonium-induced blockade of autonomic ganglionic transmission. 6. The gastric acid-induced constriction of the femoral artery was attenuated by acute extrinsic denervation of the stomach but left unaltered by capsaicin, hexamethonium, guanethidine, indomethacin, telmisartan (an angiotensin II antagonist), [d(CH2)5(1), Tyr(Me)2, Arg8]-vasopressin (a vasopressin antagonist), bosentan (an endothelin antagonist) and acute ligation of the blood vessels to the adrenal glands. 7. These data show that acid challenge of the gastric mucosa elicits visceral vasodilatation and somatic vasoconstriction via divergent mechanisms. The gastric hyperaemia is brought about by extrinsic vasodilator nerves, whereas the reduction of somatic blood flow seems to be mediated by non-neural, probably humoral, vasoconstrictor messengers that remain to be identified.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Capsaicin - administration and dosage
Denervation - administration and dosage
Female - administration and dosage
Femoral Artery - drug effects
Gastric Mucosa - drug effects
Hemodynamic Processes - drug effects
Hexamethonium - pharmacology
Hydrochloric Acid - pharmacology
Perfusion - pharmacology
Rats - pharmacology
Rats, Sprague-Dawley - pharmacology
Regional Blood Flow - drug effects
Research Support, Non-U.S. Gov't - drug effects
Stomach - innervation
Vasoconstriction - innervation
Vasodilation - innervation
Viscera - blood supply

© Meduni Graz Impressum