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
Citations to this article as recorded by
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
Background Dopamine is an inotropic agent that is often selected for continuous infusion. For hemodynamic stability, the rate of infusion is controlled in the range of 5-15 μg/kg/min. This study aimed to compare the time intervals from the administration of dopamine to the onset of its hemodynamic effects when dopamine was administered through three different peripheral veins (the cephalic vein [CV], the great saphenous vein [GSV], and the external jugular vein [EJV]).
Methods Patients in group 1, group 2, and group 3 received dopamine infusions in the CV, GSV, and EJV, respectively. A noninvasive continuous cardiac output monitor (NICCOMO™, Medis, Ilmenau, Germany) was used to assess cardiac output (CO) and systemic vascular resistance (SVR). Six minutes after intubation, baseline heart rate (HR), systolic blood pressure (BP), diastolic BP, mean arterial pressure (MAP), CO, and SVR values were recorded and dopamine infusion was initiated at a dose of 10 μg/kg/min. Hemodynamic changes at 0, 4, 8, 12, and 15 minutes postinfusion were recorded.
Results No statistically significant differences were observed among the three groups with respect to the rate of hemodynamic change. In all groups, systolic BP, diastolic BP, MAP, and SVR tended to increase after decreasing for the first 4 minutes; in contrast, HR and CO decreased until 8 minutes, after which they tended to reach a plateau.
Conclusions For patients under general anesthesia receiving dopamine at 10 μg/kg/min, there were no clinical differences in the effect of dopamine administered through three different peripheral veins.
Citations
Citations to this article as recorded by
Impact of dopamine on baroreflex-mediated sympathetic arterial pressure regulation in rats: an open-loop analysis Nana Hiraki, Toru Kawada, Masafumi Fukumitsu, Takuya Nishikawa, Hiroki Matsushita, Yuki Yoshida, Kei Sato, Hidetaka Morita, Masahiro Otake, Kenta Ohba, Kazunori Uemura, Joe Alexander, Keita Saku American Journal of Physiology-Regulatory, Integrative and Comparative Physiology.2025; 329(2): R329. CrossRef
BACKGROUND Incorrect infusion of dopamine can be potentially life threatening. If the actual volume of a 100 ml intravenous bag or bottle used to mix dopamine solutions is greater than the labeled volume, overdilution of dopamine can occur, resulting in ineffective hemodynamic response. To determine the significance of dopamine overdilution induced by the excessive volume, dopamine concentration and hemodynamic effect were compared in the manually mixed dopamine and the manufactured premixed dopamine. METHODS: For 5% dextrose water (D5W) 100 ml intravenous bottle mixed with 160 mg (4 ml) of dopamine (group 1), D5W 96 ml mixed with 160 mg of dopamine (group 2), premixed dopamine with 1.6 mg/ml of concentration manufactured 2 months ago (group 3), premixed dopamine with 1.6 mg/ml of concentration manufactured 6 months ago (group 4), and D5W 100 ml intravenous bottle mixed with 160 mg (4 ml) of dopamine after removal of 4 ml dextrose water (group 5), dopamine concentration was measured by High performance liquid chromatography (HPLC). Hemodynamic data was obtained from 10 mongrel dogs for each group at baseline (T1), 15 minutes after dopamine infusion at a rate of 3 microgram/kg/min (T2), 8 microgram/kg/min (T3), and 15 microgram/kg/min (T4). RESULTS Dopamine concentrations of group 1, 2, 3, 4, and 5 were 1.51+/- 0.09, 1.60 +/- 0.10, 1.63 +/- 0.06, 1.57+/- 0.08 and 1.57+/- 0.07 mg/ml, respectively. Group 1 showed a significantly low concentration (p< 0.05). There was no significant differences in all hemodynamic data between group 1, 2, 3, and 4. In group 1, however, there was no significant increase in both mean blood pressure at T4 and mixed venous oxygen saturation at T3 compared with T1. CONCLUSIONS The actual volume of D5W in 100 ml intravenous bottle is greater than the labeled, and therefore can cause significant overdilution of dopamine. Premixed dopamine, however, has the same concentration and hemodynamic effects as the dopamine mixed manually but precisely.
BACKGROUND Norepinephrine, which is frequently administered as a vasopressor to the patients with septic shock, can decrease splanchnic and renal blood flows and aggravate splanchnic and renal ischemia. The low-dose dopamine (LDD) has been frequently combined with norepinephrine to ameliorate renal and splanchnic hypoperfusion in patients with septic shock. However, the effect of the LDD on the splanchnic and renal blood flow has not been fully elucidated. This investigation was carried out to determine the effect of the LDD on the splanchnic and renal blood flow in the patients with septic shock under the treatment of norepinephrine. METHODS Eleven patients with septic shock were included in this study. All of them were under the norepinephrine treatment as the mean arterial pressure (MAP) was less than 70 mm Hg in spite of the adequate fluid resuscitation. With stabilization of MAP, the LDD (2 g/kg/min) was administered for two hours in each patients. Hemodynamics, gastric intramucosal pH (pHi), gastric regional PCO2 (rPCO2), rPCO2 - PaCO2, urine volume, urine sodium excretion and creatinine clearance were compared between with and without the LDD infusion. Diuretics was not used during the study period. RESULTS Age of patients (n=11) was 64 12 and the APACHE III score was 84 17. The mortality rate of the subjects was 64%.
Dosage of norepinephrine was 0.55 0.63 g/kg/min during the study period. There were no significant differences in hemodynamics (central venous pressure, cardiac output, pulmonary artery occlusion pressure, mixed venous gas), pHi, rPCO2, rPCO2 - PaCO2 depending on the concomitant infusion of the LDD. The volume of urine tended to increase (P=0.074) after concomitant LDD, but the changes in urine sodium excretion and creatinine clearance were not significantly different. CONCLUSIONS The combined infusion of the LDD with norepinephrine did not improve splanchnic and renal blood flow in the patients with septic shock.