Methylprednisolone exacerbates acute critical illness-related corticosteroid insufficiency associated with traumatic brain injury in rats

2011 ◽  
Vol 1382 ◽  
pp. 298-307 ◽  
Author(s):  
Xin Chen ◽  
Bin Zhang ◽  
Yan Chai ◽  
Bo Dong ◽  
Ping Lei ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness ◽  
Corticosteroid Insufficiency

scholarly journals Corticosteroid receptor rebalancing alleviates critical illness-related corticosteroid insufficiency after traumatic brain injury by promoting paraventricular nuclear cell survival via Akt/CREB/BDNF signaling

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Bin Zhang ◽  
Miao Bai ◽  
Xiaojian Xu ◽  
Mengshi Yang ◽  
Fei Niu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness ◽  
Low Dose ◽  
Cell Loss ◽  
High Dose ◽  
Protective Effects ◽  
Signaling Mechanism ◽  
High Dose Methylprednisolone ◽  
Corticosteroid Insufficiency

Abstract Background We previously found that high-dose methylprednisolone increased the incidence of critical illness-related corticosteroid insufficiency (CIRCI) and mortality in rats with traumatic brain injury (TBI), whereas low-dose hydrocortisone but not methylprednisolone exerted protective effects. However, the receptor-mediated mechanism remains unclear. This study investigated the receptor-mediated mechanism of the opposite effects of different glucocorticoids on the survival of paraventricular nucleus (PVN) cells and the incidence of CIRCI after TBI. Methods Based on controlled cortical impact (CCI) and treatments, male SD rats (n = 300) were randomly divided into the sham, CCI, CCI + GCs (methylprednisolone 1 or 30 mg/kg/day; corticosterone 1 mg/kg/day), CCI + methylprednisolone+RU486 (RU486 50 mg/kg/day), and CCI + corticosterone+spironolactone (spironolactone 50 mg/kg/day) groups. Blood samples were collected 7 days before and after CCI. Brain tissues were collected on postinjury day 7 and processed for histology and western blot analysis. Results We examined the incidence of CIRCI, mortality, apoptosis in the PVN, the receptor-mediated mechanism, and downstream signaling pathways on postinjury day 7. We found that methylprednisolone and corticosterone exerted opposite effects on the survival of PVN cells and the incidence of CIRCI by activating different receptors. High-dose methylprednisolone increased the nuclear glucocorticoid receptor (GR) level and subsequently increased cell loss in the PVN and the incidence of CIRCI. In contrast, low-dose corticosterone but not methylprednisolone played a protective role by upregulating mineralocorticoid receptor (MR) activation. The possible downstream receptor signaling mechanism involved the differential effects of GR and MR on the activity of the Akt/CREB/BDNF pathway. Conclusion The excessive activation of GR by high-dose methylprednisolone exacerbated apoptosis in the PVN and increased CIRCI. In contrast, refilling of MR by corticosterone protects PVN neurons and reduces the incidence of CIRCI by promoting GR/MR rebalancing after TBI.

CORTICOSTEROID INSUFFICIENCY AFTER TRAUMATIC BRAIN INJURY.

2004 ◽  
Vol 52 ◽  
pp. S383
Author(s):  
P. Cohan ◽  
B. Armin ◽  
P. D. Christenson ◽  
D. McArthur ◽  
N. Mirza ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Corticosteroid Insufficiency

35 CORTICOSTEROID INSUFFICIENCY AFTER TRAUMATIC BRAIN INJURY.

2004 ◽  
Vol 52 (Suppl 2) ◽  
pp. S383.1-S383
Author(s):  
P. Cohan ◽  
B. Armin ◽  
P. D. Christenson ◽  
D. McArthur ◽  
N. Mirza ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Corticosteroid Insufficiency

Free and total catecholamines in critical illness

1988 ◽  
Vol 254 (3) ◽  
pp. E287-E291 ◽  
Author(s):  
P. D. Woolf ◽  
R. W. Hamill ◽  
L. A. Lee ◽  
J. V. McDonald
Keyword(s):  
Intensive Care Unit ◽  
Traumatic Brain Injury ◽  
Intensive Care ◽  
Brain Injury ◽  
Critical Illness ◽  
Glasgow Coma Score ◽  
Neurological Dysfunction ◽  
Surgical Patients ◽  
Range Of Values ◽  
Catecholamine Concentration

The magnitude of circulating free and total (free plus conjugated) catecholamine responses to a strong and sustained stimulus was investigated in four groups of patients: traumatic brain injury (n = 24), vascular brain injury (n = 10), polysystem trauma (n = 7) and medical/surgical patients in an intensive care unit (n = 29). Despite significant three- to sevenfold elevations in both free and total norepinephrine (NE) and epinephrine (E), the ratio of free to total NE and E remained constant over a very broad range of values. The proportion of free E was twice normal (30.1-33.5 vs. 16.2%) in all but patients with polytrauma, whereas the percentage of free NE was unchanged in all patients (43.0%). All dopamine (DA) parameters remained generally normal. In the patients with traumatic or vascular brain injury, significant inverse correlations were present between the degree of neurological dysfunction, as indicated by the concomitant Glasgow coma score, and free NE, E, and DA and total NE and DA levels. Thus, during conditions of intense and prolonged catecholamine release, the proportion of free catecholamine remains constant and the total as well as free catecholamine concentration is proportional to the Glasgow coma score.

1514: ROLE OF DELIRIUM AND CRITICAL ILLNESS IN MORTALITY AFTER TRAUMATIC BRAIN INJURY: A SIX-YEAR COHORT

2016 ◽  
Vol 44 (12) ◽  
pp. 454-454
Author(s):  
Laura Wilson ◽  
Jennifer Thompson ◽  
Madeline Morrell ◽  
Rameela Chandrasekhar ◽  
Joanna Stollings ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness

scholarly journals Autophagy is increased in mice after traumatic brain injury and is detectable in human brain after trauma and critical illness

Autophagy ◽  
2008 ◽  
Vol 4 (1) ◽  
pp. 88-90 ◽  
Author(s):  
Robert S.B. Clark ◽  
Hülya Bayir ◽  
Charleen T. Chu ◽  
Sean M. Alber ◽  
Patrick M. Kochanek ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness ◽  
Human Brain
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