Different Impacts of α- and β-Blockers in Neurogenic Hypertension Produced by Brainstem Lesions in Rat

Wen, Lijun; Hsieh, Kai‐Sheng; Lu, Pei Jung; Wu, Yu Chun; Ho, Wen Yu; Cheng, Pei; Lai, Chi Cheng; Hsiao, Michael; Tseng, Ching Jiunn

doi:10.1097/aln.0000000000000218

Cited by 20 publications

(16 citation statements)

References 31 publications

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“…7,8 Correlation with adrenergic receptor distribution fits with the widely accepted hypothesis that catecholamine-mediated direct myocardial injury underlies the pathophysiology of neurogenic stunned myocardium. Furthermore, basic science studies have revealed cardiopulmonary dysfunction after induced lesions throughout the brain and including the brainstem, 9 similar to the anatomic region of injury in our patient. Briefly, neurologic injury triggers a stress response that leads to elevated catecholamine levels both systemically via the hypothalamic-pituitary-adrenal axis and directly through norepinephrine release through nerve terminals at the myocardial endplate.…”

Section: Discussionsupporting

confidence: 71%

Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium

et al. 2016

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Cardiac dysfunction occurring secondary to neurologic disease, termed neurogenic stunned myocardium, is an incompletely understood phenomenon that has been described after several distinct neurologic processes. We present a case of neurogenic stunned myocardium, discovered intraoperatively after anesthetic induction, in a patient who presented to our operating room with a recent intraparenchymal hemorrhage. We discuss the longitudinal cardiac functional course after neurogenic stunned myocardium. Lastly, we discuss the pathophysiology of neurogenic stunned myocardium, as well as its implications for anesthesiologists caring for neurosurgical patients.

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Section: Discussionsupporting

confidence: 71%

Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium

et al. 2016

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“…18,19 However, there may be different mechanisms for the different forms of stress cardiomyopathy. 20 In subarachnoid hemorrhage, elevated plasma catecholamines may be secondary to hypothalamic and nucleus tractus solitarius damage 7,21 and correspond to elevated cardiac biomarkers. 22 Estrogen may play a protective role for cardiac myocytes against catecholamine toxicity.…”

Section: Discussionmentioning

confidence: 99%

Variant Neurogenic Stunned Myocardium in a Young Female After Subarachnoid Hemorrhage

Mahanna

Edwards

Tarante³

et al. 2016

A & A Case Reports

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Neurogenic stunned myocardium is a significant complication of subarachnoid hemorrhage. Diagnosis of neurogenic stunned myocardium is complicated by variable presentation. We present a case of a 23-year-old woman admitted with a subarachnoid hemorrhage from an arteriovenous malformation and associated aneurysm. Postoperatively, she developed pulmonary edema and mildly elevated cardiac biomarkers. Echocardiography showed hypokinesis of the basal left ventricular segments and normal contraction of the apical left ventricular segments consistent with a variant form of neurogenic stunned myocardium. We describe characteristics and outcomes of neurogenic stunned myocardium in this young patient with arteriovenous malformation-associated aneurysmal subarachnoid hemorrhage.

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“…Excessive catecholamines may induce PE, cause myocardial damage, and augment virus infection; therefore, WHO guidelines do not recommend the use of dopamine, epinephrine, or norepinephrine [13,16,31,32]. However, the adverse effects of catecholamines are mainly attributable to their α1-adrenergic effect [33] (which occurs after the use of norepinephrine and at high dopamine, epinephrine, and dobutamine infusion rates), and application of extracorporeal membrane oxygenation (ECMO) in infants and toddlers can cause severe complications [34].…”

Section: Cardiovascular Supportmentioning

confidence: 99%

Cardiopulmonary failure in children infected with Enterovirus A71

et al. 2020

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Enterovirus A71 (EV-A71) is one of the causative pathogens of hand, foot, and mouth disease (HFMD), which may cause severe neurological and cardiopulmonary complications in children. In this review, we discuss the pathogenesis, clinical manifestations, management strategy, and clinical outcomes of cardiopulmonary failure (CPF) in patients with EV-A71 infection. The pathogenesis of CPF involves both catecholamine-related cardiotoxicity following brainstem encephalitis and vasodilatory shock due to cytokine storm. Sympathetic hyperactivity, including tachycardia and hypertension, are the early clinical manifestations of cardiopulmonary involvement, which may progress to pulmonary edema/ hemorrhage and/or CPF. The management strategy comprises multidisciplinary supportive treatment, including fluid management, positive pressure ventilation support, and use of milrinone, vasopressors, and inotropes. Some patients may require extracorporeal membrane oxygenation. Major neurological sequelae are almost inevitable once a child develops life-threatening illness. Long-term care of these children is an important medico-social issue.

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Different Impacts of α- and β-Blockers in Neurogenic Hypertension Produced by Brainstem Lesions in Rat

Cited by 20 publications

References 31 publications

Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium

Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium

Variant Neurogenic Stunned Myocardium in a Young Female After Subarachnoid Hemorrhage

Cardiopulmonary failure in children infected with Enterovirus A71

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