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Review Article
Neurosurgery
The role of catecholamines in aneurysmal subarachnoid hemorrhage: a narrative review
Samantha Nalliah, Tariq Janjua, Luis Rafael Moscote-Salazar, Md Yunus, Amit Agrawal
Acute Crit Care. 2025;40(4):513-520.   Published online November 24, 2025
DOI: https://doi.org/10.4266/acc.001525
  • 6,989 View
  • 652 Download
  • 3 Web of Science
  • 3 Crossref
AbstractAbstract PDF
The marked release of catecholamines during subarachnoid hemorrhage is an important aspect of the pathobiology following aneurysmal rupture. This narrative review aims to identify how catecholamines influence aneurysmal subarachnoid hemorrhage (aSAH) outcomes. aSAH is a critical neurological condition characterized by hemorrhage into the subarachnoid space, leading to severe neurological deficits and mortality. Catecholamines, including epinephrine, norepinephrine, and dopamine, are the body's stress responses, which can lead to secondary injuries following aSAH. This review was conducted through a targeted literature search of relevant studies examining the relationship between aSAH, catecholamines, and clinical outcomes. Searches were performed in PubMed, Scopus, The Cochrane Library, Medline (Ovid), Embase (Ovid), and CINAHL, including publications up to July 2024. Search terms combined keywords and subject headings related to “subarachnoid hemorrhage” or “aSAH,” “catecholamines,” “epinephrine,” “norepinephrine,” “dopamine,” and outcome-related terms such as “prognosis,” “mortality,” and “neurological outcome.” Articles were selected based on relevance, and key findings were synthesized descriptively to provide a comprehensive overview of current knowledge in this area. Elevated levels of catecholamines are observed following aSAH and are associated with increased sympathetic nervous system activity. This catecholamine surge contributes to pathological processes, including vasospasm, blood-brain barrier disruption, cerebral edema, and neuronal damage. The review highlights the implications of catecholamine levels; where higher concentrations correlate with poorer outcomes and higher mortality rates. Understanding the mechanisms responsible for secondary injury due to catecholamines surge following aSAH shall facilitate the development of therapeutic approaches to prevent secondary brain injury and improve outcomes.

Citations

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  • Associations Between Serum Liver Enzymes and the Rupture Status of Intracranial Aneurysms
    Huan Luo, Lu Yu, Jiayuan Zhang, Qishan Chen, Tian Xu, Chao Yu
    Journal of Endovascular Therapy.2026;[Epub]     CrossRef
  • Glymphatic-meningeal lymphatic dysfunction drives remote organ injury after aneurysmal subarachnoid hemorrhage: a unified neuroimmune framework and time-stratified therapeutic roadmap
    Ying Dai, Jinshan Tie, Dan Zhu, Zhengchao Lv, Wei Wan, Haolun Chen, Wei Li, Chen Yu
    Reviews in the Neurosciences.2026;[Epub]     CrossRef
  • Glucose/Potassium Ratio, a Novel Biomarker for the Prognosis of Patients with Subarachnoid Hemorrhage: A Review
    Luis E. Fernández-Garza, Valeria A. Fernández-Garza, Daniela Mares-Custodio, Victor Gutiérrez-Ruano, Alexandro Navarrete-Rodríguez, Juan J. Arias-Alzate
    Journal of Vascular Diseases.2025; 4(4): 48.     CrossRef
Original Articles
Effects of Blood-Brain Barrier Disruption on Cerebral Oxygen Balance
Doo Ik Lee, Young Kyu Choi, Dong Ok Kim, Keon Sik Kim, Ok Young Shin, Moo Il Kwon
Korean J Crit Care Med. 1999;14(2):126-130.
  • 2,586 View
  • 9 Download
AbstractAbstract PDF
BACKGOUND: Disruption of the blood-brain barrier (BBB) can alter the internal milieu and may increase the release of excitatory amino acid neurotransmitters or catecholamines, which may affect metabolic rate or coupling. This study was performed to evaluate whether disruption of BBB by unilateral intracarotid injection of hyperosmolar mannitol would alter oxygen supply/consumption balance in the ipsilateral cortex.
METHODS
Rats were anesthetized with 1.4% isoflurane using mechanical ventilation via tracheostomy. 25% mannitol was administered at a rate of 0.25 mlxkg-1s-1 for 30 s through unilateral internal carotid artery. The BBB transfer coefficient (Ki) of 14C-alpha-aminoisobutyric acid was measured in one group (N=7) after administering mannitol. Regional cerebral blood flow (rCBF), regional arterial and venous O2 saturation and O2 consumption were measured in another group using a 14C-iodoantipyrine and microspectrophotometry (N=7).
RESULTS
Vital signs were similar before and after administering mannitol. Ki was significantly higher in the ipsilateral cortex (IC) than in the contralateral cortex (CC), (22.3+/-8.4 vs 4.4+/-1.1 microliterxg-1min-1). rCBF was similar between IC (105+/-21 mlxg-1min-1) and the CC (93+/-20). Venous O2 saturation was lower in the IC (43+/-7%) than in the CC (55+/-4). O2 consumption was higher in the IC (9.6+/-3.0 mlx100 g-1min-1) than in the CC (6.7+/-1.5).
CONCLUSIONS
Our data suggested that increasing permeability of the BBB increased cerebral O2 consumption and deteriorated cerebral oxygen balance.
The Effect of Cervical Sympathetic Nerve Block on Blood-brain Barrier Disruption with Mannitol Infusion in Rats
Bong Ki Moon, Soo Han Yoon, Young Joo Lee, Chul Ryung Hur, Chang Ho Kim, Sung Jung Lee, Young Seok Lee
Korean J Crit Care Med. 1997;12(1):69-74.
  • 2,491 View
  • 20 Download
AbstractAbstract PDF
BACKGOUND: The barrier can be altered by a number of insults to the brain (e.g., hypertension, freezing, trauma, drug). But the effect of the blood brain barrier distruction immediately after the neural change is unknown. In the present study, we focused on the BBBD after cervical sympathetic chain block.
METHODS
13 male Sprague-Dawley rats were divided into 2 groups. Group 1 (N=7) was blocked with 0.5% bupivacaine on the right cervical sympathetic chain and group 2 (N=6) was blocked with 0.5% bupivacaine on the bilateral cervical sympathetic chain. All rats received 37degrees C, 25% mannitol (1.75 g/kg) via right carotid artery and then, the effect of cervical sympathetic chain block on blood-brain barrier disruption of four cerebral compartment using 99mTc-human serum albumin and Evans blue was evaluated.
RESULTS
Both groups showed blood-brain barrier disruption and there was no significant difference between group 1 and group 2 in the anterior and posterior hemisphere of the right side brain. But group 2 showed significant blood-brain barrier disruption than group 1 in anterior and posterior hemisphere of the left brain (p<0.01).
CONCLUSIONS
This results suggest that cervical sympathetic chain block can increase the degree of mannitol-induced blood-brain barrier disruption via neural arch or blood flow change.

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