Effect of sex steroid hormones on brain edema, intracranial pressure, and neurologic outcomes after traumatic brain injury

2010 ◽  
Vol 88 (4) ◽  
pp. 414-421 ◽  
Author(s):  
Nader Shahrokhi ◽  
Mohammad Khaksari ◽  
Zahra Soltani ◽  
Mehdi Mahmoodi ◽  
Nouzar Nakhaee

Recent studies have reported that estrogen and progesterone have a neuroprotective effect after traumatic brain injury (TBI); however, the mechanism(s) for this effect have not yet been elucidated. The aim of the present study was to investigate the role of sex steroid hormones on changes in brain edema, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) after TBI in ovariectomized (OVX) rats. In this study, 50 female rats were divided into 5 groups: control (intact), sham, and 3 TBI groups consisting of vehicle, estrogen (1 mg/kg), and progesterone (8 mg/kg). TBI was induced by the Marmarou method, and the hormones were injected i.p. 30 min after TBI. ICP was measured in the spinal cord, and CPP was calculated by subtracting the mean arterial pressure (MAP) from ICP. The results revealed that brain water content after TBI was lower (p < 0.001) in the estrogen and progesterone groups than in the vehicle group. After trauma, ICP was significantly higher in TBI rats (p < 0.001). The ICP in the estrogen and progesterone groups decreased at 4 and 24 h after TBI compared with vehicle (p < 0.001 and p < 0.05, respectively). The CPP in the estrogen and progesterone groups increased after 24 h compared with vehicle (p < 0.001). Also after TBI, the neurological score (veterinary coma scale) was significantly higher than vehicle at 1 h (p < 0.01) and 24 h (p < 0.001) in the group treated with estrogen. In conclusion, pharmacological doses of estrogen and progesterone improved ICP, CPP, and neurological scores after TBI in OVX rats, which implies that these hormones play a neuroprotective role in TBI.

2013 ◽  
Vol 30 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Ali Reza Sarkaki ◽  
Mohammad Khaksari Haddad ◽  
Zahra Soltani ◽  
Nader Shahrokhi ◽  
Mehdi Mahmoodi

2009 ◽  
Vol 21 (1) ◽  
pp. 192
Author(s):  
J.-H. Kim ◽  
K.-C. Choi ◽  
E.-B. Jeung

Calcium-related proteins include transient receptor potential vanilloid (TRPV) 5 and 6, plasma membrane calcium-ATPase 1b (PMCA1b), and calbindin-D9k and -D28k. The TRPV6 is a major calcium channel located in the apical and basolateral membranes of cell and distributed widely in many other organs, especially in the exocrine tissues such as intestine and uterus. TRPV6s are generally regulated by vitamin D, a dietary calcium ion and hormone. In particular, uterine TRPV6 appears to be affected by sex steroid hormones, which are altered according to estrous cycle and pregnancy. In order to discover the effect of sex steroid hormones on the regulation of TRPV6, we examined the expression of TRPV6 mRNA by using RT-PCR and real-time PCR, and protein expression of TRPV6 by immunohistochemistry (IHC) in the uterus, duodenum, and kidney. To evaluate the effect(s) of sex steroid hormones on its uterine, duodenal, and renal regulation, 17β-estradiol [E2; 40 μg kg–1 of body weight (bw)] and/or progesterone (P4; 4 mg kg–1 of bw) or vehicle (n = 6/each group) were subcutaneously injected into Sprague-Dawley immature female rats (14 days old, n = 24 in total) for 3 days. As a result, the treatments of immature rats with E2 or P4 increased TRPV6 mRNA for calcium function or regulation in the uterus of immature rats. To confirm the specificity of E2 or P4 through their receptors, we treated the immature rats (extra n = 24 in total) with an estrogen receptor-antagonist, ICI 182,780 (ICI; 30 μg kg–1 of bw), and/or progesterone receptor antagonist, RU 486 (10 mg kg–1 of bw), at 3 days prior to E2 or P4 injection. Consequently, an increase in TRPV6 mRNA was observed in the following 2 treatments; ICI plus E2/P4 and E2/P4 alone. In IHC, we further observed that the expression of duodenal TRPV6 was increased by E2 or P4 and E2 or P4 plus ICI, while no difference was observed in renal TRPV6 by the treatments of sex steroid hormones. In conclusion, these results indicate that the expressions of uterine and duodenal TRPV6 may be induced by E2 and P4, but its renal expression may not be controlled by these steroids.


2013 ◽  
Vol 33 (9) ◽  
pp. 1457-1464 ◽  
Author(s):  
Erik C Brockman ◽  
Hülya Bayir ◽  
Brian Blasiole ◽  
Steven L Shein ◽  
Ericka L Fink ◽  
...  

Polynitroxylated-pegylated hemoglobin (PNPH), a bovine hemoglobin decorated with nitroxide and polyethylene glycol moieties, showed neuroprotection vs. lactated Ringer’s (LR) in experimental traumatic brain injury plus hemorrhagic shock (TBI + HS). Hypothesis: Resuscitation with PNPH will reduce intracranial pressure (ICP) and brain edema and improve cerebral perfusion pressure (CPP) vs. LR in experimental TBI + HS. C57/BL6 mice ( n = 20) underwent controlled cortical impact followed by severe HS to mean arterial pressure (MAP) of 25 to 27 mm Hg for 35 minutes. Mice ( n = 10/group) were then resuscitated with a 20 mL/kg bolus of 4% PNPH or LR followed by 10 mL/kg boluses targeting MAP > 70 mm Hg for 90 minutes. Shed blood was then reinfused. Intracranial pressure was monitored. Mice were killed and %brain water (%BW) was measured (wet/dry weight). Mice resuscitated with PNPH vs. LR required less fluid (26.0 ± 0.0 vs. 167.0 ± 10.7 mL/kg, P < 0.001) and had a higher MAP (79.4 ± 0.40 vs. 59.7 ± 0.83 mm Hg, P < 0.001). The PNPH-treated mice required only 20 mL/kg while LR-resuscitated mice required multiple boluses. The PNPH-treated mice had a lower peak ICP (14.5 ± 0.97 vs. 19.7 ± 1.12 mm Hg, P = 0.002), higher CPP during resuscitation (69.2 ± 0.46 vs. 45.5 ± 0.68 mm Hg, P < 0.001), and lower %BW vs. LR (80.3 ± 0.12 vs. 80.9 ± 0.12%, P = 0.003). After TBI + HS, resuscitation with PNPH lowers fluid requirements, improves ICP and CPP, and reduces brain edema vs. LR, supporting its development.


1995 ◽  
Vol 268 (1) ◽  
pp. G171-G176 ◽  
Author(s):  
T. S. Chen ◽  
M. L. Doong ◽  
F. Y. Chang ◽  
S. D. Lee ◽  
P. S. Wang

In vitro studies have shown that estrogen and progesterone can affect the contractile response and myoelectric activity of the gastrointestinal smooth muscle. The present study was designed to investigate the effect of sex steroid hormones on gastric emptying and gastrointestinal transit were assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and 51Cr. Gastric emptying was determined by measuring the amount of labeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating both the geometric center of distribution of the radiolabeled marker and the charcoal transit in the intestine. The experimental animals included diestrus rats; ovariectomized rats treated with vehicle, estradiol, and/or progesterone; and normal male and orchiectomized rats treated with vehicle or testosterone. Female rats in diestrus had a slower gastric emptying and a lesser geometric center value than ovariectomized rats. Estradiol inhibited gastric emptying but did not affect gastrointestinal transit. Progesterone increased gastric emptying. Progesterone at lower dose (10 mg/kg) decreased the geometric center compared with higher doses (20 or 40 mg/kg) or vehicle controls. A mixture of estradiol (10 micrograms/kg) and progesterone (20 mg/kg) inhibited gastric emptying to a similar degree as estradiol (10 micrograms/kg) did. Testosterone had no influence on gastric emptying or gastrointestinal transit. These results suggest that estradiol and a mixture of estradiol and progesterone inhibit, whereas progesterone enhances, gastric emptying. Testosterone did not play a role in gastrointestinal motility.


2013 ◽  
Vol 44 (4) ◽  
pp. 251-258 ◽  
Author(s):  
Fatemeh Dehghan ◽  
Mohammad Khaksari Hadad ◽  
Gholamreza Asadikram ◽  
Hamid Najafipour ◽  
Nader Shahrokhi

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