Intracarotid histamine administration results in dose-dependent vasogenic brain oedema formation in new-born pigs

1997 ◽  
Vol 46 (13) ◽  
pp. 45-46 ◽  
Author(s):  
L. Németh ◽  
C. A. Szabó ◽  
M. A. Deli ◽  
J. Kovács ◽  
I. A. Krizbai ◽  
...  
Keyword(s):  
Brain Oedema ◽  
Oedema Formation ◽  
New Born ◽  
Dose Dependent ◽  
Vasogenic Brain Oedema

scholarly journals Endothelial Acid Phosphatase May Participate in the Histamine-Induced Vasogenic Brain Oedema Formation in Newborn Pigs 137

1996 ◽  
Vol 40 (3) ◽  
pp. 538-538
Author(s):  
J Kovács ◽  
L Németh ◽  
C A Szabó ◽  
M A Deli ◽  
I Krizbai ◽  
...  
Keyword(s):  
Acid Phosphatase ◽  
Brain Oedema ◽  
Oedema Formation ◽  
Newborn Pigs ◽  
Vasogenic Brain Oedema

scholarly journals Glucocorticoid In Cytotoxicity Followed by Delayed Edema

2020 ◽  
Vol 10 (1) ◽  
pp. 45-51
Author(s):  
Md Amir Ali ◽  
Aminul Islam ◽  
RU Chowdhury ◽  
Al Amin Salek ◽  
Sudipta Kumer Mukherjee ◽  
...  
Keyword(s):  
Brain Oedema ◽  
Corticosteroid Treatment ◽  
Military Hospital ◽  
Pathological State ◽  
Oedema Formation ◽  
Vasogenic Oedema ◽  
First Time ◽  
Cytotoxic Brain Oedema ◽  
Cytotoxic Oedema ◽  
Vasogenic Brain Oedema

Background: Cytotoxicity is the toxicity to cell. Any type of brain oedema producing raised intracranial pressure (ICP) which may be a fatal pathological state. Corticosteroid is contraindicated in cytotoxic brain oedema but in vasogenic oedema, it is beneficial. Cytotoxic oedema in its consequences induces vasogenic oedema where the corticosteroid may helpful. Objectives: To determine the effects of corticosteroid on tertiary vasogenic brain oedema from cytotoxic edema. Methods: Total of 328 patients was diagnosed as brain oedema and they had been first time reported & all were admitted in Combined Military Hospital (CMH) Dhaka, between Jan 2017 to Jun 2019. Out of 328 patients, brain oedema due to spontaneous ICHs was 219 (66.77%) and traumatic ICHs were 109(33.33%). Diagnosis was based upon history, clinical examination and non-contrast Computed Tomography (CT) scan of brain. Results: Total 328 admitted patients in CMH Dhaka from Jan 2017-Jun 2019 were included in our study who full-fill the criteria. Males were 231 (70.43%); females were 97(29.57%) and were aged between 1 to 95 year. Intracranial haemorrhage rate among age group less than 55 years old being 76 (34.70%) and 55 years or above 143 (65.30%) of total 219 patients. Traumatic ICHs were 109 and 1 to 44 years age is most vulnerable, 69(63.30%) and 45 years and above 40 (36.70%) patients. Corticosteroid was used after vasogenic brain oedema formation following cytotoxic oedema which was diagnosed mainly radiologically. Cytotoxic oedema induced by 24 hours and vasogenic oedema in two to four days of brain insult. Vasogenic oedema developed in 24 -48 hours, 65 (19.82%) patients and 117 (35.67 %) by 48-72 hours and above 72 hours rest 146 (44.51%) patients after brain insult. After vasogenic oedema formation, out of 164 patients that is 50% patients were treated with corticosteroid and GOS was assessed- GOS 4,5 -103(62.80%), GOS 3-34 (20.73%), GOS 2- 23(14.02%) and GOS 1-4(2.44%) whereas without corticosteroid treatment of rest vasogenic oedema 164 (50%) , GOS was- GOS 4,5 -85(51.83%), GOS 3-43 (26.22%), GOS 2- 27(16.46%) and GOS 1-9(5.49%) at 30 days of incidence. There is more than two times mortality without corticosteroid therapy than with steroid therapy. Conclusion: Cytotoxic brain oedema is contraindicated for steroid but we observed that corticosteroid gives better GOS in vasogenic oedema which develops after cytotoxic brain oedema. Outcome in cytotoxic oedema followed by vasogenic oedema is beneficial for corticosteroid. Bang. J Neurosurgery 2020; 10(1): 45-51

Histamine-Induced Vasogenic Brain Oedema Formation in Newborn Pigs

1997 ◽  
pp. 479-483
Author(s):  
Csilla Andrea Szabó ◽  
Maria Anna Deli ◽  
László Németh ◽  
István Krizbai ◽  
József Kovács ◽  
...  
Keyword(s):  
Brain Oedema ◽  
Oedema Formation ◽  
Newborn Pigs ◽  
Vasogenic Brain Oedema

Autacoids as Mediators of Vasogenic Brain Oedema

1995 ◽  
pp. 147-157 ◽  
Author(s):  
M. Wahl ◽  
L. Schilling ◽  
A. Unterberg ◽  
A. Baethmann
Keyword(s):  
Brain Oedema ◽  
Vasogenic Brain Oedema

scholarly journals Aquaporin-4 water channel expression in human vasogenic brain oedema

2002 ◽  
Vol 200 (5) ◽  
pp. 523-534 ◽  
Author(s):  
F. Geeson ◽  
S. Saadoun ◽  
M. C. Papadopoulos ◽  
B. A. Bell ◽  
D. C. Davies
Keyword(s):  
Brain Oedema ◽  
Water Channel ◽  
Aquaporin 4 ◽  
Channel Expression ◽  
Vasogenic Brain Oedema

Neutrophil extracellular traps mediate joint hyperalgesia induced by immune inflammation

Rheumatology ◽  
2020 ◽  
Author(s):  
Ayda Henriques Schneider ◽  
Caio Cavalcante Machado ◽  
Flávio Protásio Veras ◽  
Alexandre Gomes de Macedo Maganin ◽  
Flávio Falcão Lima de Souza ◽  
...  
Keyword(s):  
Clinical Investigation ◽  
Neutrophil Extracellular Traps ◽  
Arginine Deiminase ◽  
Human Neutrophils ◽  
Oedema Formation ◽  
Extracellular Traps ◽  
Mechanical Threshold ◽  
Articular Pain ◽  
Dose Dependent

Abstract Objective To evaluate the role of neutrophil extracellular traps (NETs) in the genesis of joint hyperalgesia using an experimental model of arthritis and transpose the findings to clinical investigation. Methods C57BL/6 mice were subjected to antigen-induced arthritis (AIA) and treated with Pulmozyme (PLZ) to degrade NETs or Cl-amidine to inhibit NET production. Oedema formation, the histopathological score and mechanical hyperalgesia were evaluated. NETs were injected intra-articularly in wild type (WT), Tlr4−/−, Tlr9−/−, Tnfr1−/− and Il1r−/− mice, and the levels of cytokines and Cox2 expression were quantified. NETs were also quantified from human neutrophils isolated from RA patients and individual controls. Results AIA mice had increased NET concentration in joints, accompanied by increased Padi4 gene expression in the joint cells. Treatment of AIA mice with a peptidyl arginine deiminase 4 inhibitor or with PLZ inhibited the joint hyperalgesia. Moreover, the injection of NETs into joints of naïve animals generated a dose-dependent reduction of mechanical threshold, an increase of articular oedema, inflammatory cytokine production and cyclooxygenase-2 expression. In mice deficient for Tnfr1, Il1r, Tlr4 and Tlr9, joint hyperalgesia induced by NETs was prevented. Last, we found that neutrophils from RA patients were more likely to release NETs, and the increase in synovial fluid NET concentration correlated with an increase in joint pain. Conclusion The findings indicate that NETs cause hyperalgesia possibly through Toll-like receptor (TLR)-4 and TLR-9. These data support the idea that NETs contribute to articular pain, and this pathway can be an alternative target for the treatment of pain in RA.

The Role of Histamine in Brain Oedema Formation

1994 ◽  
pp. 76-78
Author(s):  
Ferenc Joó ◽  
J. Kovács ◽  
P. Szerdahelyi ◽  
P. Temesvári ◽  
Á. Tósaki
Keyword(s):  
Brain Oedema ◽  
Oedema Formation
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