Effect of epinephrine and norepinephrine on the electrocardiogram of 100 normal subjects∗

Lepeschkin, E.; Marchet, H.; Schroeder, G.; Wagner, Richard; Silva, P. de Paula e; Raab, W.

doi:10.1016/0002-9149(60)90124-7

Cited by 79 publications

(24 citation statements)

References 17 publications

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“…In 1960, Lepeschkin et al infused adrenaline into normal human subjects and recorded the electrocardiogram changes of a reduction in T wave height and an increase in U wave amplitude [18]. Subsequently, infused adrenaline, at very high dose, was found to cause hypokalaemia in man [ll].…”

Section: Discussionmentioning

confidence: 99%

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

et al. 1983

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Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the beta-adrenoceptor antagonists, atenolol or timolol. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (-8 beats/min). Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 +/- 0.02 s to 0.41 +/- 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a beta 2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.

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Section: Discussionmentioning

confidence: 99%

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

et al. 1983

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“…While subarachnoid hemorrhage is a most common cause, other central lesions that lead to enhanced sympathetic nerve activity also predispose an individual to the fatal outcome (30). In fact, sympathetic nerve activity and excessive circulating catecholamines alone may lead to cardiac arrhythmias and death (12,33). Sudden death in humans with central lesions correlates with cardiac arrhythmias, but the lesions also may lead to cardiac damage (9,25,34) even in the absence of arrhythmias.…”

mentioning

confidence: 99%

Cardiac damage after lesions of the nucleus tractus solitarii

Nayate

Moore²,

Weiss³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Nayate A, Moore SA, Weiss R, Taktakishvili OM, Lin L.-H., Talman WT. Cardiac damage after lesions of the nucleus tractus solitarii. Am J Physiol Regul Integr Comp Physiol 296: R272-R279, 2009. First published November 19, 2008 doi:10.1152/ajpregu.00080.2008.-Humans with central lesions that augment sympathetic nerve activity are predisposed to cardiac arrhythmias, myocardial lesions, and sudden death. Previously, we showed that selectively killing neurons with neurokinin-1 receptors in the nucleus tractus solitarii (NTS) of rats attenuated the baroreflex and, in some animals, led to sudden unexplained death within ϳ2 wk. Interruption of arterial baroreflexes is known to increase sympathetic activity. Here we tested the hypothesis that lesions in the NTS lead to fatal cardiac arrhythmias and myocardial lesions. We studied electrocardiograms, echocardiograms, blood pressure, and heart rate in 14 adult male rats after bilateral microinjection into the NTS of stabilized substance P conjugated to the toxin saporin and compared the variables in five sham control rats and in five animals with toxin injected outside the NTS. Only injection of toxin into the NTS led to increased lability of arterial blood pressure, a sign of baroreflex interruption. Two animals treated with toxin died suddenly. All animals engaged in normal activity until, in two, rapid development of asystole and death over 6 -8 min. Cardiac function when examined by echocardiography was normal, but pathologic examination of the heart revealed diffuse microscopic areas of acute coagulation necrosis in the myocardium in five animals, focal subacute necrosis in two animals, and both changes in one animal. This study supports the hypothesis that NTS lesions interrupting the baroreflex may induce cardiac arrhythmias and myocardial changes similar to those seen in humans with central lesions and may lead to sudden cardiac death. baroreflex; cardiac arrhythmia; heart injuries; sudden death; sympathetic nervous system PREVIOUS STUDIES HAVE SUGGESTED that substance P, acting at neurons that express neurokinin-1 (NK1) receptors, may participate in transmission of arterial baroreflexes at the level of the nucleus tractus solitarii (NTS) (17,23,26). In an earlier study, we injected into NTS a toxin that selectively targeted neurons with NK1 receptors (24), and we showed that the ensuing lesion attenuated baroreflex responses (24). The altered baroreflex transmission was associated with sudden, unexpected, death in 33% of the experimental animals. Death in these animals was reminiscent of that seen in humans who have sustained central lesions (30). While subarachnoid hemorrhage is a most common cause, other central lesions that lead to enhanced sympathetic nerve activity also predispose an individual to the fatal outcome (30). In fact, sympathetic nerve activity and excessive circulating catecholamines alone may lead to cardiac arrhythmias and death (12,33). Sudden death in humans with central lesions correlates with cardiac arrhythmias, but the lesions also may l...

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“…All the above ECG changes have been described in association with administration of catecholamines (Lepeschkin et al, 1960;Damato et al, 1969;Sparks et al, 1970;Haft et al, 1972), where both transient and more permanent changes, associated with endocardial necrotic lesions, may occur. Also, a correlation between endogenous catecholamine excretion in subarachnoid haemorrhage and peaked P waves, a short P-R interval, S-T and T wave changes a long Q-Tc, a tall U wave and pathological Q waves, has been demonstrated (Cruickshank et al, 1974).…”

Section: Rfsultsmentioning

confidence: 99%

Electrocardiographic changes and their prognostic significance in subarachnoid haemorrhage

Cruickshank

Neil‐Dwyer

Brice

1974

Journal of Neurology, Neurosurgery & Psychiatry

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SYNOPSIS In a study on the prognostic significance of catecholamine-linked ECG changes in 40 cases of subarachnoid haemorrhage, there were 16 men of mean age 41 years (range 13-56) and 24 women of mean age 42 years (range 11-65). There were six deaths, and five of these patients had consistently abnormal ECGs. Analysis of the abnormal components of ECGs revealed that the presence of either a pathological Q wave or a raised S-T segment indicated a poor prognosis. The two patients with pathological Q waves both died, and the three patients with raised S-T segments all developed cerebral arterial spasm, one of whom died. A high incidence of peaked P waves, short P-R intervals, a long Q-Tc, and tall U waves occurred in the ECGs of six patients who died, the 15 patients with cerebral arterial spasm, and the seven patients who were later to develop cerebral arterial spasm. Three of the latter eventually died, in contrast with the single death in the 22 patients who did not develop cerebral arterial spasm and had a low incidence of P wave peaking, short P-R intervals, a long Q-Tc, and tall U waves. Various combinations of these four ECG changes, in addition to peaking of the T wave, indicated a bad prognosis irrespective of the type of treatment. The criteria for prognosis on the role of catecholamines in causing the ECG abnormalities are discussed.The mechanism by which changes in the electrocardiogram (ECG) associated with subarachnoid haemorrhage are brought about has been a matter for speculation. Possible explanations have included hypokalaemia (Hersch, 1964) (Iliynski and Astrakhantseva, 1967) and by Cruickshank and his colleagues (1974). In the latter study a strong correlation was shown between urinary catecholamine levels and certain ECG changes-namely, peaking of the P wave, a short P-R interval, and peaking of the T wave; a weaker relationship was also demonstrated between urinary catecholamine levels and T wave inversion, a long Q-Tc, tall U waves, and pathological Q-waves. Hypokalaemia as a possible cause of the ECG changes was ruled out.If catecholamines are a common factor between ECG changes and cerebral arterial spasm in subarachnoid haemorrhage, then the above catecholamine-linked ECG changes might serve as prognostic indicators. The present study was designed to investigate this possibility. METHODSForty cases of subarachnoid haemorrhage, proved by lumbar puncture, comprised 16 men of mean age 41 years (range 13-56) and 24 women of mean age 42 years (range 11-65). There were no cases with a history of hypertension or ischaemic heart disease. Thirty-seven cases had carotid angiography, and most had additional vertebral angiograms. Angiograms were reported on without knowledge of results of other investigations. Cases were classed into three angiographic groups: (1) cases with no cerebral angiographic spasm, termed the non-spasm group, (2) cases with cerebral angiographic spasm, 755

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Effect of epinephrine and norepinephrine on the electrocardiogram of 100 normal subjects∗

Cited by 79 publications

References 17 publications

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

Cardiac damage after lesions of the nucleus tractus solitarii

Electrocardiographic changes and their prognostic significance in subarachnoid haemorrhage

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