Determination of Infused Epinephrine and Norepinephrine in Plasma Using Isolated Guinea Pig Heart Technique

Booker, Walter M.; Walton, Tracy; Linares, Rafael; Schaepdryver, A.F. De

doi:10.1161/01.res.11.5.820

Cited by 3 publications

(2 citation statements)

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“…This agent, a precursor of NOR and EPI successfully reversed the tachyphylaxis to ACh. With DOPAM, a longer incubation period was necessary (10 minutes; Booker, 1962). This change in the ACh schedule did not alter the development of tachyphylaxis to the drug, as established in control experiments ( 15-minute interval).…”

Section: ) Tachyphylaxis To Nicotinic Ach Effects and Its Reversalmentioning

confidence: 75%

The Cholinergic Receptor Systems of Atria*

Koppanyi

MacFarlane

1967

Annals of the New York Academy of Sciences

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The experiments involved in these studies have relevance only to the spontaneously beating, isolated rabbit atrial preparation. In view of the demonstrated species differences in the reaction of atrial tissue to drugs (Blinks, 1966), one must be cautious in making sweeping generalizations concerning mammalian atria in general and human atria in particular.Isolated spontaneously beating atria have long been employed in the study of autonomic drugs and may serve as suitable models for the elucidation of cholinergic and adrenergic mechanisms. These preparations have been used extensively in the study of both "muscarinic" and "nicotinic" effects of acetylcholine (ACh) .The atria are one of the few organs that can be used for studying both types of actions. This communication may further clarify these two distinct effects of ACh.There is little doubt that the vagotropic or the negative inotropic and chronotropic effects of exogenously administered ACh result from direct receptor interactions. On the other hand, the effects of relatively high concentrations of ACh in the atropine pretreated atria are indirect. These indirect actions, the positive inotropic and chronotropic responses, are commonly referred to as the nicotinic effects of ACh. These nicotinic effects of ACh do not result from the drug's action on the cholinergic receptor per se, but may be due to the release of catecholamines (CA) , probably norepinephrine (NOR), as could be shown by the presence of NOR in the coronary outflow of atropinized hearts. (Richardson & Woods, 1959).Since the stimulating effects of ACh are admittedly mediated through release of CA, we may regard ACh as an indirectly acting sympathomimetic agent. We should, therefore, expect that ACh and related agents possess actions similar to those of an indirectly acting sympathomimetic amine. In this series of experiments we have analyzed the responses to ACh by tests which are characteristic for indirectly acting sympathomimetic amines. These studies include the effects of ACh, a ) in the reserpinized preparation (Koppanyi & MacFarlane, 1964), b) in the presence of NOR release blockers and c ) following the oft repeated administration of the "nicotinic" doses of ACh which has been shown to result in tachyphylaxis (Koppanyi and Cowan, 1964). METHODSAll of the following experiments have been carried out on spontaneously beating rabbit atria. The atria were excised from male albino rabbits and suspended in a 40 ml organ bath, filled with oxygenated Locke solution (Crout et al., 1962). The force of contractions was recorded on a smoked drum kymograph with a Starling heart lever, and the rate with a Thorp impulse counter, set at ten-second intervals. Atria were also excised from rabbits, treated with reserpine (5.0 mg/kg, i.p.; reserpinized atria) 20 to 24 hours prior to sacrifice.All doses reported in this communication are expressed in terms of the respective salts.

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Section: ) Tachyphylaxis To Nicotinic Ach Effects and Its Reversalmentioning

confidence: 75%

The Cholinergic Receptor Systems of Atria*

Koppanyi

MacFarlane

1967

Annals of the New York Academy of Sciences

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“…The initial uptake into the binding sites or storage sites of normally innervated blood vessels is very rapid (Potter et , 1965). If these sites are saturated by a slow infusion of epinephrine or norepinephrine, these amines can still be detected 30 minutes after the end of Infusion (Booker et al,. 1962), The half-life of a 50 U8 per kg body weight Injection of epinephrine or norepinephrine in the rabbit is about 60 seconds.…”

Section: Regulation Of Coronary Blood Flowmentioning

confidence: 99%