Mesenteric vascular reactivity to histamine receptor agonists and antagonists

• Published in: Digestive diseases and sciences Vol. 26; no. 5; pp. 438 - 443
• Main Authors: Walus, K M, Fondacaro, J D, Jacobson, E D
• Format: Journal Article
• Language: English
• Published: United States 01-05-1981
• Subjects: Adrenergic Agonists - pharmacology; Animals; Blood Flow Velocity; Dimaprit; Dogs; Dose-Response Relationship, Drug; Female; Furans - pharmacology; Hemodynamics - drug effects; Histamine - administration & dosage; Histamine H1 Antagonists - pharmacology; Histamine H2 Antagonists - pharmacology; Infusions, Intra-Arterial; Male; Mesentery - blood supply; Oxygen Consumption - drug effects; Ranitidine; Receptors, Histamine - drug effects; Receptors, Histamine H1 - drug effects; Regional Blood Flow - drug effects; Thiourea - pharmacology; Tripelennamine - pharmacology
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/BF01313587

Response patterns of intestinal blood flow, oxygen extraction and consumption, blood flow distribution, and motility were assessed during intraarterial infusions of histamine, histamine after H1 or H2 blockade, dimaprit or dimaprit after H2 blockade. Histamine produced an initial peak response of blood flow with a slow decrease thereafter. Oxygen extraction was evenly depressed throughout the infusion, and oxygen consumption increased at the beginning. All initial responses were blocked by tripelennamine. Ranitidine, a new H2 antagonist, accelerated the decay of all responses. Dimaprit produced effects identical to those of histamine after tripelennamine. Distribution of blood flow was unchanged at the beginning of histamine infusion, but subsequently showed a shift to muscularis which was blocked by tripelennamine. Histamine usually stimulated intestinal contractions and this effect was abolished by tripelennamine. Thus, H1 stimulation, besides producing an initial vasodilation, increases oxygen uptake and redistributes flow to the muscularis.