The urinary catecholamine and plasma cortisol levels in patients with subarachnoid haemorrhage

Neil‐Dwyer, G.; Cruickshank, J. M.; Stott, A.W.; Brice, Jason

doi:10.1016/0022-510x(74)90008-2

Cited by 76 publications

(17 citation statements)

References 17 publications

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“…Meyer et al 19 and Neil-Dwyer et al 20 demonstrated an increase in urinary excretion of free catecholamines and their metabolites in patients after SAH. Furthermore, NeilDwyer et al 20 suggested that high urinary concentrations were associated with the presence of vasospasm. An increase in sympathetic nervous system and adrenal medullary activity results in increases in plasma norepinephrine and epinephrine concentrations.…”

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confidence: 99%

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Benedict¹,

Loach²

1978

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SUMMARYIn patients with subarachnoid hemorrhage there were increased concentrations of plasma epinephrine and norepinephrine when compared with those concentrations in a group of patients admitted to hospital with other illness.Reassessment after a variable period showed that in patients whose eventual clinical result was poor the plasma epinephrine and norepinephrine concentrations increased further while in those with a good result those concentrations showed a decline. No such changes were evident in plasma dopamine-,8-hy droxylase activities which were within normal range.In a sub-group of patients who had neurosurgery after admission for clipping an aneurysm, the post-operative changes of plasma epinephrine and norepinephrine concentrations were related to the clinical condition of the patients.

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confidence: 99%

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Benedict¹,

Loach²

1978

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“…We ask paediatricians, infectious-disease physicians, and neurosurgeons throughout England, Scotland, and Wales to notify cases of encephalitis and certain other specified neurological conditions in children aged 2 Community physicians and general practitioners are asked to provide immunisation histories for cases and controls, and in both groups the mother is interviewed at home to ascertain factors in the medical histories of the child and the family and in the social environment that might predispose to serious neurological illnesses.…”

Section: Study Methodsmentioning

confidence: 99%

National Childhood Encephalopathy Study: an interim report.

Miller¹,

Ross²

1978

BMJ

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Discussion.~~~~~~~S imulated SAH,4 hypothalamic stimulation,1' and parenteral administration of catecholamines5 in animals produce necrotic myocardial lesions, which may be prevented by severing the cord at C2 level or by administering reserpine or propranolol.4 A possible effect of the hypothalamic lesions after a SAH12 is to produce an abnormal reaction of the autonomic nervous system resulting in persistantly high excretion rates of urinary catecholamines.2 The close association between the hypothalamus and the autonomic nervous system, coupled with the high correlation between hypothalamic and myocardial lesions after SAH,13 points to a catecholamine-linked origin of the myocardial necrosis.The pathological results of this study should be interpreted in the light of results (unpublished) of a recent survey, which showed that out of 54 patients who died of SAH at the Southeast Thames regional neurosurgical unit, 49 had hypothalamic lesions similar to those found in this study and 42 of these patients (78% of the whole) had necrotic myocardial lesions. Thus the fact that in our study all six patients who died in the drug-treated group had "clean hearts" (with normal ECGs) while all six in the placebo-treated group had focal necrotic myocardial lesions (and abnormal ECGs) becomes important. Due to the probable absence of alpha-receptors in the myocardium"4 we presume that propranolol rather than phentolamine was the agent responsible.What are the clinical implications of these results ? Excessive amounts of catecholamines may induce heart failure, as in the cardiomyopathy associated with phaeochromocytomas."5 Some other types of congestive cardiomyopathy may well result from an abnormal interaction between catecholamines and the myocardium and benefit from beta-blockade.16 A recent report'7 described such a cardiomyopathy, which was cured by stopping treatment with ephedrine. Some authors consider that catecholamines play a crucial part in the onset of myocardial infarction,'8 thus suggesting an explanation for the protective effect of beta-blockade on the ischaemic myocardium. Despite its "cardioprotective effect," propranolol did not influence mortality in cases of SAH and accompanying myocardial damage. This is because lethal secondary events such as a second SAH are not critically influenced by propranolol or phentolamine, though the results of this preliminary study suggest a possible protective action of these two drugs with regard to cerebrovascular spasm. In other "stress areas" with associated myocardial necrotic lesions and unstable cardiac rhythms, such as head injuries,7 beta-blockade may have an important role. The source of hearts for cardiac transplantation is another important, though perhaps more remote, factor to be considered. If, as is often the case, the donor has died after a cerebrovascular accident or head injury then early administration of a beta-blocker to the potential donor might be wise.We would like to thank Dr D M Burley of Ciba Laboratories for supplying the phentolamine for the...

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“…46 Whether it is due to a direct effect of blood irritating the brain, 47 ' 48 to the sudden increase of ICP, 48> 50 or to both is not clear. In any case, one may postulate that the severe arterial hypertension caused by a sympathetic discharge overwhelms an already partially compromised autoregulatory mechanism.…”

Section: Response Of Icp and Mabp To Hypertensive Sah In A Monkey Of mentioning

confidence: 99%

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

Martins

Doyle

Newby

et al. 1975

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The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.

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The urinary catecholamine and plasma cortisol levels in patients with subarachnoid haemorrhage

Cited by 76 publications

References 17 publications

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

National Childhood Encephalopathy Study: an interim report.

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

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