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MYOCARDIAL SYNTHESIS OF PROSTAGLANDIN‐LIKE SUBSTANCES AND CORONARY REACTIONS TO CARDIOSTIMULATION AND TO HYPOXIA
Author(s) -
SUNAHARA F.A.,
TALESNIK J.
Publication year - 1979
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.1476-5381.1979.tb17335.x
Subject(s) - medicine , hypoxia (environmental) , arachidonic acid , prostaglandin , endocrinology , coronary vasodilator , vasodilation , chemistry , oxygen , biochemistry , organic chemistry , enzyme
1 Continuous recording of cardiac contractions and coronary flow from isolated perfused hearts of rats permitted the study of coronary reactions to: (a) cardiostimulation induced by single doses or slow infusions of noradrenaline, CaCl 2 , glucagon or electrically induced tachycardia; (b) short interruptions of coronary inflow (hypoxia). 2 Except during tachycardia the heart rate was kept constant at 210 beats/min by electrical pacing. 3 Metabolic coronary vasodilatation (MCD) resulting from cardiac hyperactivity induced by noradrenaline, Ca 2+ , tachycardia or glucagon was inhibited by administration of prostaglandin E 2 . Reactive hyperaemia response to hypoxia was unaffected by prostaglandin administration. 4 Inhibition of MCD could also be obtained by prolonged infusion with arachidonic acid (1.6 × 10 −7 m ), presumably by its conversion into prostaglandin‐like substance since arachidonic acid failed to block MCD in hearts from rats pretreated with non‐steroidal anti‐inflammatory drugs (indomethacin, naproxen, phenylbutazone). 5 Reactive hyperaemia was unaffected either by arachidonic acid or by blockade of the synthesis of prostaglandin‐like substances by anti‐inflammatory drugs. 6 Since prostaglandin synthetase inhibition does not prevent but may enhance MCD, we do not advocate prostaglandin‐like substances as agents directly responsible for the coronary vasodilatation that follows cardiac hyperactivity. 7 We postulate that cardiac overproduction of prostaglandins may lead to a failure in the adaptive coronary flow response to cardiac hyperactivity (coronary insufficiency?).