The effect of a selective 5‐HT<sub>2</sub> antagonist, ketanserin, on the pulmonary responses to <i>Escherichia coli</i> endotoxin

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‐HT2 blocking drug. Ketanserin (0.2 mg kg−1) itself lowered arterial pressure (by 30–40 mmHg) but this systemic hypotension was relatively transient. 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. The reductions in arterial (mixed venous) pH and in P that resulted from endotoxin administration were not affected by pretreatment with ketanserin.

The effect of a selective 5‐HT₂ antagonist, ketanserin, on the pulmonary responses to Escherichia coli endotoxin Journal Articles