Catecholamines, infection, and death in acute ischemic stroke

Chamorro, Ángel; Vargas, Martha; Obach, Vı́ctor; Cervera, Álvaro; Gómez-Choco, Manuel; Torres, Ferrán; Planas, Anna M.

doi:10.1016/j.jns.2006.10.001

Cited by 173 publications

(153 citation statements)

References 47 publications

(47 reference statements)

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“…In good agreement with previous observations by us and by others, 7,11,25 granulocytes were increased in patients with SAIs (median, SAI+ d0,1,3,5,7 =53.3%, 84.3%, 76.0%, 79.0%, 82.2%; median, SAI− d0,1,3,5,7 =56.8%, 70.3%, 67.5%, 55.7%, 64.1%; P=0.0004); whereas monocytes remained unaltered. Metanephrine serum concentrations did not differ significantly between patients with and without SAI ( Table I in the online-only Data Supplement).…”

Section: March 2014supporting

confidence: 93%

“…Stress hormones have been suggested to act as central regulators of SIIAs 6,25,26 ; some characteristics of SIIAs can be mimicked in cell culture by adding catecholamines. 7 Here we investigated, whether the alterations observed in patients with stroke derived phagocytes could be induced in samples from healthy individuals by in vitro exposure to the catecholamines epinephrine and norepinephrine, the glucocorticoid dexamethasone or acetylcholine.…”

Section: In Vitro Effects Of Stress Hormones and Acetylcholine On Phamentioning

confidence: 99%

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Stroke Alters Respiratory Burst in Neutrophils and Monocytes

Ruhnau

Schulze

Gaida

et al. 2014

Stroke

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Background and Purpose— Stroke-induced immune alterations predispose patients to infections. Although the relationship between stroke and the adaptive immune system has been investigated in detail, to date it is unknown whether the innate immune system, which forms the first line of antibacterial defense, is also impaired in patients with stroke. Therefore, we investigated whether chemotaxis, phagocytosis, oxidative burst, degranulation of defensins, and NETosis in monocytes and in neutrophil granulocytes are altered in patients with stroke compared with controls. Methods— Sixty-three patients having acute ischemic stroke were recruited within 12 hours of symptom onset; blood was sampled on admission and on days 1, 3, 5, and 7. Thirty-seven age-matched controls were also recruited. Cell migration, phagocytosis, and oxidative burst of phagocytes were determined in vitro. Human neutrophil peptides 1 to 3 and serum metanephrine levels were measured by enzyme-linked immunosorbent assay, and NETosis was quantified by immunohistochemistry. Results— The key mechanisms required for bacterial killing, oxidative burst, and NETosis were significantly reduced in samples taken from patients with stroke compared with controls, whereas migration, phagocytic function, and defensin production remained unimpaired in monocytes and granulocytes from patients with stroke. Conclusions— Stroke-induced immune alterations include impairment of the first-line defense performed by specialized phagocytes against bacteria. The hypothesis that these changes enhance susceptibility to acquired infections is supported by our observation that on admission oxidative burst in monocytes was more impaired in patients with stroke with subsequent stroke-associated infections.

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Section: March 2014supporting

confidence: 93%

Section: In Vitro Effects Of Stress Hormones and Acetylcholine On Phamentioning

confidence: 99%

Stroke Alters Respiratory Burst in Neutrophils and Monocytes

Ruhnau

Schulze

Gaida

et al. 2014

Stroke

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“…Following stroke, there is an increase in inflammatory biomarkers in the bloodstream [2,3], but at the same time activation of the sympathetic nervous system mediates a systemic immunodepression that includes a defect in the T helper 1 response [4,5]. This sympathetically mediated immunodepression likely contributes to an increase in the risk of poststroke infection [6]. Poststroke infection, primarily pneumonia, is independently associated with increased morbidity and mortality [7,8].…”

mentioning

confidence: 99%

Stroke, Inflammation and the Immune Response: Dawn of a New Era

Becker

Buckwalter

2016

Neurotherapeutics

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“…BPV is under the influence of numerous extrinsic (administered and preexisting medication, arrhythmia requiring β-blocker, vegetative and emotional stressors, and positional [eg, lying versus upright] and continuous recording versus manual measurement) and intrinsic (arterial hypertension, fluid balance, stroke subtype, recanalization, and autonomic regulation or dysregulation) factors. 37,38 Even so, attempts to explain BPV in the multivariable analysis by all available patients baseline characteristics left 92% variance unexplained in our study.…”

Section: July 2017mentioning

confidence: 72%

Reciprocal Interaction of 24-Hour Blood Pressure Variability and Systolic Blood Pressure on Outcome in Stroke Thrombolysis

Kellert

Hametner

Ahmed

et al. 2017

Stroke

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Background and Purpose-Significance and management of blood pressure (BP) changes in acute stroke care are unclear.Here, we aimed to investigate the impact of 24-hour BP variability (BPV) on outcome in patients with acute ischemic stroke treated with intravenous thrombolysis. . Analyzing successive variation for analysis of BPV as a function of pre-treatment, systolic BP significantly improved the prediction of functional outcome (mRS score of 0-1, mRS score of 0-2, neurological improvement, mRS-shift: all P interaction <0.01). Excluding patients with atrial fibrillation in a sensitivity analysis gave consistent results overall. Conclusions-This study suggests the need for a more individual BP management accounting for pre-treatment BP and the acute BP course (ie, BPV) to achieve best possible outcome for the patient. Methods-From

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Catecholamines, infection, and death in acute ischemic stroke

Cited by 173 publications

References 47 publications

Stroke Alters Respiratory Burst in Neutrophils and Monocytes

Stroke Alters Respiratory Burst in Neutrophils and Monocytes

Stroke, Inflammation and the Immune Response: Dawn of a New Era

Reciprocal Interaction of 24-Hour Blood Pressure Variability and Systolic Blood Pressure on Outcome in Stroke Thrombolysis

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