Changes in the Subcellular Distribution of Cardiac Catecholamines in Dogs dying in Irreversible Hæmorrhagic Shock

Cardiac Norepinephrine Stores in Experimental Heart Failure in the Dog*

“…The findings of a decrease of norepinephrine not only in the failing right ventricle, but also in the left ventricle and in the atria support this hypothesis. The marked reductions of tissue norepinephrine stores, which have also been demonstrated to occur in hemorrhagic shock (29,30), a condition that is also accompanied by a greatly increased activity of the sympathetic nervous system (31), may be an analogous situation. The biochemical mechanism necessary for both synthesis and binding of the neurotransmitter in the terminations of sympathetic nerves within the myocardium might be -comprised in the failing ventricle, or actual deterioration of the nerve endings may occur.…”

Studies on the Interactions of Guanethidine and Bretylium With Noradrenaline Stores

“…This evidence would make the conclusion made by Cass & Spriggs (1961), Gaffney et al (1963) and Spriggs (1966) based on assay of the total tissue noradrenaline untenable. Since the transmitter amine available for release on-sympathetic nerve stimulation has been shown to reside in the particulate fraction of the vas deferens (Chang & Chang, 1965) as well as of the heart (Hift & Campos, 1962 ;Chang & Su, 1967) it is tempting to suggest that the adrenergic neurone-blocking effect of guanethidine may be due to a rapid depletion of the functional amine pool in the particulate fraction. This effect could be a displacement, since guanethidine is also retained by the particulate fraction, or could be due to an inhibition of the intracellular amine-concentrating mechanism (Shore & Giachetti, 1966).…”

Effect of cold stress on the subcellular distribution of noradrenaline in the rat heart

“…This might suggest that in the isolated perfused heart the ability of 'particles' to hold noradrenaline is impaired and such an existing impairement of storage or release mechanism in this preparation must be taken into consideration. It is interesting that Hift & Campos (1962) also found a greater decrease of noradrenaline from the particulate fraction in dogs under irreversible haemorrhagic shock, a condition in which sympathetic discharge is greatly increased (Millar, Keener & Benfey, 1959;Neil, 1962). It appears that sympathetic activities induced either by cold-exposure or by haemorrhagic hypotension tend to deplete particulate noradrenaline more than the supernatant noradrenaline from the heart.…”