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BENZYL CARBAMYL ANALOGUE OF LIGNOCAINE: VASODEPRESSOR MECHANISM OF ACTION
Author(s) -
Chiang Y. L.,
Freeman J. J.,
Sowell J. W.,
Kosh J. W.
Publication year - 1982
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1982.tb00836.x
Subject(s) - action (physics) , mechanism (biology) , chemistry , mechanism of action , anesthesia , medicine , pharmacology , philosophy , biochemistry , physics , epistemology , quantum mechanics , in vitro
SUMMARY 1. The benzyl carbamyl analogue of lignocaine [2‐(diethylaminoacet‐amido)‐3‐carbamyl‐4‐methyl‐5‐benzylpyrrole] at an intravenous dose of 4 mg/kg caused a blood pressure decrease of 54 mmHg. 2. A greater hypotensive effect was observed in hypertensive compared to nor‐motensive animals. Anaesthesia magnified the vasodepressor effect in both groups. 3. The analogue did not possess centrally‐mediated effects on blood pressure but exerted its hypotensive effect via a peripheral mechanism. 4. The analogue produced a relaxant effect on intestinal and vascular smooth muscle while exerting minimal effects on muscarinic, sympathetic, or ganglionic nicotinic receptors. 5. The analogue exhibited less cardiac depressant action on left ventricular rate (d p /d t and force of contraction than lignocaine. 6. Lethal effects for the analogue were first observed at 16 mg/kg following intravenous administration and at 500 mg/kg following intraperitoneal administration. 7. In conclusion, the benzyl carbamyl analogue exhibited direct vascular smooth muscle relaxant activity with less cardiac or CNS side effects than lignocaine.