Abstract

1 The time from the injection of sodium cromoglycate 10 to 50 mug/kg into a saphenous vein, the cervical carotid arteries, the left ventricle and the aortic arch, to the onset of reflex hypotension has been measured in anaesthetized dogs. The shortest latency was 16.9 s on injection of sodium cromoglycate into the left ventricle.2 Instillation of 2% lignocaine into the pericardium of an anaesthetized dog blocked the reflex hypotensive response to sodium cromoglycate (10 to 50 mug/kg i.v.), and also prevented sodium cromoglycate (100 mug/kg) from reversing reflex bronchoconstriction induced by inhalation of an aerosol of histamine.3 The effect of sodium cromoglycate (100 mug/kg i.v.) on resting discharge and histamine-induced discharge (20 mug/kg i.v.) of five lung irritant receptors in five anaesthetized dogs has been studied. Sodium cromoglycate (100 mug/kg i.v.) did not affect the resting discharge of these receptors or their ability to respond to histamine.4 Sodium cromoglycate (100 mug/kg i.v.) increased the rate of discharge of three receptors found in the endocardium of the left ventricle of the canine heart. A solution of sodium cromoglycate (0.1%) was applied topically to one receptor and its rate of discharge was increased.5 It is suggested that in the dog, sodium cromoglycate produces reflex hypotension and reverses histamine-induced reflex bronchoconstriction by activating receptors in the left ventricle of the heart.

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