Circulatory effects of sympathomimetic amines

Eckstein, John W.; Abboud, François M.

doi:10.1016/0002-8703(62)90230-2

Cited by 74 publications

(32 citation statements)

References 144 publications

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“…Results of these studies have largely focused on two particular features: histological evidence of myocarditis (catecholamine cardiomyopathy) 28 " 31 and demonstration of hypertension and bradycardia. 20 -2I -32~34 To determine threshold levels for its metabolic effects, Silverberg et al 35 infused NE in stepwise fashion in doses from 0.1 to 5 ^.g/min over 60 minutes. At the highest dose in these short-term studies (plasma levels of 2150 ± 66 pg/ml), systolic and diastolic arterial blood pressures rose while HR fell.…”

Section: Discussionmentioning

confidence: 99%

“…2 ' 8> l5 Patients with chronic myocardial failure, regardless of etiology, have elevated plasma norepinephrine (NE) levels. 16 In addition, defects in baroreceptor reflex-mediated vasoconstrictor responses have been noted in dogs 17 and in patients 18 -19 with marked myocardial dysfunction.Several studies, summarized by Eckstein and Abboud, 20 have evaluated the general effects of changes in plasma NE concentrations on cardiovascular function; few, however, have examined systematically the effects of altered regulatory mechanisms operating during chronic elevations in plasma NE. …”

mentioning

confidence: 99%

“…Several studies, summarized by Eckstein and Abboud, 20 have evaluated the general effects of changes in plasma NE concentrations on cardiovascular function; few, however, have examined systematically the effects of altered regulatory mechanisms operating during chronic elevations in plasma NE.…”

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confidence: 99%

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Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

King¹,

Sack²,

Kichuk³

et al. 1987

Hypertension

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SUMMARY To better define the mechanisms of blood pressure control in states of catecholamine excess, we infused norepinephrine for 28 days using subcutaneously implanted osmotic pumps in dogs previously instrumented for monitoring left ventricular dynamics and cardiac output. Plasma norepinephrine rose from 238 ± 27 to 4346 ± 952 pg/ml at 21 days, while epinephrine and dopamine levels did not change. Heart rate fell from 85 ± 4 to 63 ± 6 beats/min, while arterial pressure was unchanged from baseline. Total peripheral resistance rose 0.011 ± 0.003 mm Hg/ml/min from a control value of 0.029 ± 0.002 mm Hg/ml/min, and cardiac output decreased 1093 ± 292 ml/min from a baseline level of 3575 ± 156 ml/min. Since stroke volume did not change, the maintenance of arterial pressure is related to decreases in cardiac output secondary to bradycardia. Buffering mechanisms are responsible for maintenance of systemic arterial pressure because hexamethonium and atropine caused hypertension. Although left ventricular end-diastolic pressure, end-diastolic diameter, shortening, rate of change of pressure, velocity of myocardial shortening, cardiac work, stroke work, and the double product did not change significantly during the study, postmortem examination demonstrated biventricular hypertrophy. Thus, despite markedly elevated catecholamine levels and no elevation of systemic arterial pressure, myocardial hypertrophy developed. These studies lend support to the hypothesis that norepinephrine may be a direct myocardial tropic hormone and suggest that intense activation of reflex buffering mechanisms maintains blood pressure in the normal range during chronic catecholamine infusion. (Hypertension 9: 582-590, 1987) KEY WORDS • bradycardia • hypertension • hypertrophy • catecholamines • total peripheral resistance • atropine E LEVATIONS in catecholamine levels may be associated with a number of disease states, including mitral valve prolapse (MVP), 1 -2 chronic myocardial failure, 3 " 6 and pheochromocytoma. 7 These disease states may be characterized by sustained or episodic hypertension, myocardial dysfunction, and cardiomyopathy.Recently, it has been noted that certain patients with MVP, chronic myocardial failure, or pheochromocytoma have dysautonomia, manifested by abnormalities in heart rate or blood pressure response (or both) to orthostatic change or exercise. 8 " 12 Some investigations of patients with MVP having dysautonomia are consistent with evidence of hyperadrenergic states and some with simultaneous hypervagatonia. 9 -13 Significant elevations in serum catecholamine levels have been observed in a group of symptomatic patients with MVP 1 ' l4 ; these results have been confirmed by other workers. 2 ' 8> l5 Patients with chronic myocardial failure, regardless of etiology, have elevated plasma norepinephrine (NE) levels. 16 In addition, defects in baroreceptor reflex-mediated vasoconstrictor responses have been noted in dogs 17 and in patients 18 -19 with marked myocardial dysfunction.Several studies, summarized by Ec...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

King¹,

Sack²,

Kichuk³

et al. 1987

Hypertension

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“…Adrenergic mechanisms in the heart are generally considered purely excitatory and classified as the beta receptor type (13)(14)(15). Recently, several workers (16)(17)(18)(19) have reported the existence of both alpha and beta receptors in the hearts of mammals.…”

Section: Discussionmentioning

confidence: 99%

Effect of Hypothyroid Status on Myocardial Responses to Sympathomimetic Drugs

et al. 1971

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The physiological relationship between thyroid hormone and the catecholamines has been investigated for many years (1, 2). In spite of numerous studies it is still not clear whether thyroid status alters the sensitivity of the heart to catecholamines. Coville (3) has reported that thyroid hormone increased the magnitude of the response to catecholamines, while some authors have failed to show that altering the thyroid status affects the response to catecholarnines (4, 5). Recently, it was tried to explore some effects of thyroidectomy on the response of alpha and beta adrenergic receptor mechanisms to catecholamines (6). A few workers have reported the existence of both alpha and beta receptors in the hearts of mammals (7,8).
Present studies reported here were made in an attempt to clarify some of the discrepancies in many reports by seeking a quantitative difference between different types of cardiac adrenergic receptor mechanisms after 6-propyl-2-thiouracil (PTU) treatment. METHODSMale Wistar strain rats (170 to 200 g) were used for experiments. The rats were divided into two groups. Group A was served as control. Group B -,vas in a hypothyroid state produced by feeding on 0.15 % PTU diet for 6 to 8 weeks. This group developed dryness of fur, slow heart rate and a great retardation in growth.Each rat was killed by a blow on the head and the heart was rapidly removed and the left atrium dissected free. Isolated left atria were suspended in a 25-m1 tissue bath containing Ringer solution of the following composition (mM); NaCl, 158; KCI, 5.6; CaCl2, 3.6; Na HCO2, 3.6; and glucose, 15.6. The solution was maintained at a temperature of 30 -:---0.5 C and saturated with pure oxygen. The preparations were driven at a rate of 180 beats/min.through an electrode by a square wave pulse of 6 msec duration and voltage of approximately twice threshold delivered by a stimulator (Nihon Kohden MSE-3). A force displacement transducer (Nihon Kohden SB-IT) was used for measurement of isometric contractile force which was recorded by an ink writing oscillograph. A resting tension of 0.5 g was placed on each atrium. The preparations were allowed to equilibrate in Ringer solution for about 60 min. before exposing them to drugs. Drugs were dissolved before use in 0.9;V saline.The drugs used in these experiments were 1-phenylephrine hydrochloride , 1-isoproterenol

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“…Methods for evaluating antagonism at ca-adrenoceptor sites are less commonly used but this can be achieved by using a-adrenoceptor agonists such as noradrenaline or phenylephrine (Eckstein & Abboud, 1962). Although noradrenaline is the naturally occurring transmitter substance utilized by the sympathetic autonomic nervous system, we preferred phenylephrine because it was used in the original animal studies (Farmer et al, 1972; Kennedy & Levy, 1975), is not taken up by adrenergic neurones as is noradrenaline and in particular this agonist had previously been used in assessing the antagonist properties of intravenously administered labetalol (Boakes et al, 1971 and the blood pressure recording which corresponded to the heart rate measurement taken as the end point was derived from a mean of two readings taken at 3.5 min and at 4 min of each dose level for each subject.…”

Section: Introductionmentioning

confidence: 99%

Assessment of alpha‐ and beta‐adrenoceptor blocking actions of labetalol.

Richards¹,

Tuckman²,

Prichard³

1976

Brit J Clinical Pharma

107

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Isoprenaline dose‐response curves plotting increases in heart rate before and after labetalol are suggestive of competitive antagonism at beta‐adrenoceptor sites. Phenylephrine dose‐response curves using increases in systolic pressure before and after labetalol are suggestive of competitive antagonism at alpha‐adrenoceptor sites. The ratio of alpha:beta‐adrenoceptor antagonism induced by labetalol is approximately 1:3. Peak pharmacological responses after a single oral dose of labetalol (400 mg) occurred between 90‐120 min after administration.

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Circulatory effects of sympathomimetic amines

Cited by 74 publications

References 144 publications

Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

Effect of Hypothyroid Status on Myocardial Responses to Sympathomimetic Drugs

Assessment of alpha‐ and beta‐adrenoceptor blocking actions of labetalol.

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