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H 1 AND H 2 HISTAMINE ACTIONS ON LUNG VESSELS; THEIR RELEVANCE TO HYPOXIC VASOCONSTRICTION
Author(s) -
Barer Gwenda R.,
Emery Celia J.,
Mohammed F. H.,
Mungall I. P. F.
Publication year - 1978
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1978.sp002428
Subject(s) - histamine , vasoconstriction , hypoxic pulmonary vasoconstriction , cats , constriction , medicine , vasodilation , endocrinology , pharmacology , antagonist , chemistry , anesthesia , receptor
Pulmonary vasomotor actions of histamine and the possible relationship of histamine to hypoxic pulmonary vasconstriction were studied in anaesthetized cats with one lobe of lung perfused at constant flow and in isolated perfused rat and ferret lungs. In the cat histamine caused dilatation, biphasic responses and constriction with increasing doses. Histamine induced dilatation was better demonstrated during hypoxic vasoconstriction and was reduced by an H 2 histamine antagonist; constriction with histamine was abolished by an H 1 antagonist. Histamine also caused both vasodilatation and vasoconstriction in ferret lungs. A mast cell stabilizing agent had no effect on hypoxic pulmonary vasoconstriction in cats or rats. This response was unaffected in cats but greatly reduced in rats and ferrets by cyproheptadine, a combined histamine and 5‐ hydroxytryptamine inhibitor. It was unaffected in cats but abolished in ferrets by an H 1 histamine inhibitor. It was again unaffected in cats but greatly reduced in rats and ferrets by an H 2 histamine inhibitor. These species differences may reflect differences in mechanism but more probably reflect non‐specific effects of the inhibitors in certain circumstances. However, when drugs nearly abolished hypoxic vasoconstriction, ATP still caused vasoconstriction.

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