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Myocardial and haemodynamic effects of the beta‐adrenoceptor blocking drug alprenolol (H56/28) in anaesthetized cats
Author(s) -
PARRATT J. R.,
WADSWORTH R. M.
Publication year - 1969
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.1476-5381.1969.tb10572.x
Subject(s) - alprenolol , heart rate , medicine , vascular resistance , hemodynamics , cardiology , blood pressure , angina , diastole , myocardial infarction , propranolol , anesthesia
1 . The effects of the beta‐adrenoceptor blocking drug alprenolol (H56/28) on myocardial and general haemodynamics were studied in anaesthetized cats. 2 . Alprenolol (0·5 mg/kg and 1·0 mg/kg) reduced femoral systolic and diastolic pressures, heart rate and left ventricular systolic pressure. The rate of rise of the left ventricular pressure pulse (d p /d t ) was reduced despite a significant elevation of left ventricular end‐diastolic pressure. This is evidence for decreased myocardial contractility. On some occasions there was a transient initial increase in +ve d p /d t max. possibly indicative of moderate β‐adrenoceptor stimulant activity. 3 . Myocardial and liver blood flows were measured using a heated thermocouple technique. Alprenolol slightly decreased both myocardial and liver blood flows (mean of 17% and 15% respectively with a dose of 1·0 mg/kg). Myocardial and liver vascular resistances were only very slightly increased. 4 . Alprenolol had no direct effect on calculated myocardial and liver metabolic heat production. 5 . In doses up to 1·0 mg/kg alprenolol had no effect on airway resistance but occasionally decreased ( in vivo ) intestinal muscle movement. 6 . Since alprenolol (although reducing calculated myocardial oxygen consumption and the myocardial and metabolic heat stimulant effects of catecholamines) has no significant effect on myocardial vascular resistance, it is suggested that it would be a useful adjunct in the therapy of angina pectoris.