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The effect of a selective 5‐HT 2 antagonist, ketanserin, on the pulmonary responses to Escherichia coli endotoxin
Author(s) -
Ball H.A.,
Parratt J.R.,
Rodger I.W.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb10033.x
Subject(s) - ketanserin , medicine , anesthesia , vascular resistance , pharmacology , blood pressure , bradycardia , fissipedia , hemodynamics , serotonin , heart rate , 5 ht receptor , receptor
1 5‐Hydroxytryptamine (5‐HT, 5–160 μg kg −1 ) injected intravenously in pentobarbitone‐anaesthetized, open‐chest cats caused dose‐dependent increases in pulmonary arterial and intratracheal pressures. There was also a marked systemic hypotension and bradycardia. The pulmonary effects were completely prevented by ketanserin (0.2 mg kg −1 ), a selective 5‐HT 2 blocking drug. 2 Ketanserin (0.2 mg kg −1 ) itself lowered arterial pressure (by 30–40 mmHg) but this systemic hypotension was relatively transient. 3 Endotoxin ( E. coli ) administration resulted in pulmonary hypertension, increases in intratracheal pressure and airways resistance and reductions in lung compliance and in arterial P . Only the airways resistance response was modified by ketanserin (0.2 mg kg −1 ), suggesting a relatively unimportant role for 5‐HT in mediating the acute, pulmonary effects of endotoxin in this species. 4 The reductions in arterial (mixed venous) pH and in P that resulted from endotoxin administration were not affected by pretreatment with ketanserin.