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Norepinephrine release from the isolated rabbit heart by stimulation of sympathetic nerves and their pharmacological effect



Norepinephrine release from the isolated rabbit heart by stimulation of sympathetic nerves and their pharmacological effect



Arch Exptl Pathol U Pharmakol 244(1): 31-96



Rabbit hearts were isolated with the nervous supply from the right stellate ganglion intact, and perfused with Tyrode solution. The catechol amines released were adsorbed onto Al2O3 and measured biologically. The rate and force of contraction of the heart increased during stimulation of the postganglionic sympathetic fibres, the coronary flow decreased and the output of catecholamines increased by a factor of 32 times compared to the resting output. Fluorimetric analysis showed that the catechol amine released was mainly norepinephrine during the period of stimulation, only 3.6% being epinephrine. In a series of experiments the sympathetic stimulation was repeated on the same preparation 4 times at intervals of 30 minutes. With every subsequent period of stimulation the norepinephrine output decreased equally by 44%. The effect of drugs was studied by infusing them before and during sympathetic stimulation, and the norepinephrine output was compared to the corresponding output of control hearts. Guanethidine decreased the norepinephrine output irreversibly by 77% and blocked the response to sympathetic stimulation. Cocaine increased the norepinephrine output by 127% and potentiated the chronotropic response to stimulation. Psicaine increased the norepinephrine output by 76%. Tetracaine decreased the norepinephrine output by 79% and blocked the response to sympathetic stimulation; this effect was fully reversible after withdrawing the tetracaine infusion. Harmaline reduced the norepinephrine output by 48% but did not significantly alter the response to stimulation. Dichloroisoproterenol (DCI) increased the norepinephrine output by 148% and blocked the response to stimulation. Hexamethonium did not alter the norepinephrine output or the response to stimulation. Lowering the Ca concentration of the perfusion fluid from 3.6 meq/l to 0.9 or 0.45 meq/l decreased the norepinephrine output by 55 and 68%, respectively. There was a proportional smaller increment of the force of contraction during stimulation. It is suggested that a certain amount of the norepinephrine liberated at the nerve ending is taken up by the amine stores of the tissue. Drugs which have previously been shown to block norepinephrine uptake such as cocaine and DCI consequently elevate noradrenaline output of the heart during sympathetic stimulation. Concentrations of cocaine which potentiate the effect of sympathetic stimulation do not inhibit the release of transmitter from the nerve endings. The release of sympathetic transmitter depends on the presence of Ca ions.

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Accession: 025089356

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