testosterone/hemorrhage

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Attenuation of vascular endothelial dysfunction by testosterone receptor blockade after trauma and hemorrhagic shock.

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OBJECTIVE The salutary effects of the testosterone receptor antagonist flutamide on the depressed immune and cardiovascular functions after hemorrhage and resuscitation are related to improved endothelial cell function, which can subsequently lead to an increase in organ blood flow, oxygen delivery,

Attenuation of cerebral vasospasm and secondary injury by testosterone following experimental subarachnoid hemorrhage in rabbit.

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BACKGROUND The vasodilatator effects of testosterone have been widely studied and demonstrated. Based on previous studies of these vasodilatatory activities, we hypothesized that testosterone might have potential effects on subarachnoid hemorrhage-induced cerebral vasospasm. METHODS Thirty-two adult

Testosterone: the crucial hormone responsible for depressing myocardial function in males after trauma-hemorrhage.

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OBJECTIVE To determine whether testosterone depletion in males before trauma-hemorrhage has any salutary effects on cardiac performance after hemorrhage and resuscitation. BACKGROUND Studies indicate that castration of male mice before trauma-hemorrhage prevents the immunodepression seen after

Testosterone receptor blockade after trauma-hemorrhage improves cardiac and hepatic functions in males.

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Although studies have shown that testosterone receptor blockade with flutamide after hemorrhage restores the depressed immune function, it remains unknown whether administration of flutamide following trauma and hemorrhage and resuscitation has any salutary effects on the depressed cardiovascular

Sex-specific p38 MAP kinase activation following trauma-hemorrhage: involvement of testosterone and estradiol.

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Although immune functions are markedly depressed in males and not in proestrous females following trauma-hemorrhage (T-H), the mechanisms responsible for the divergent responses remain unknown. Because sex steroids modulate the activation of p38, our aim was to determine whether differences in the

Hereditary hemorrhagic telangiectasia, liver disease and elevated serum testosterone (Osler-Weber-Rendu syndrome): a case report.

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BACKGROUND A Sri Lankan girl with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) is described. METHODS She presented with recurrent spontaneous epistaxis, pulmonary arterio venous malformation and oral telangiectasia. A diagnosis of Hereditary hemorrhagic telangiectasia

Testosterone: the culprit for producing splenocyte immune depression after trauma hemorrhage.

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Studies indicate that, whereas immune functions in males are depressed, they are enhanced in females after trauma hemorrhage. Moreover, castration of male mice (i.e., androgen depletion) before trauma hemorrhage prevented the depression of cell-mediated immunity. Nonetheless, it remains unknown

Testosterone receptor blockade after trauma and hemorrhage attenuates depressed adrenal function.

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Although the testosterone receptor antagonist flutamide restores the depressed immune function in males after trauma and hemorrhage, it remains unknown whether this agent has any salutary effects on adrenal function. To study this, male rats underwent laparotomy and were bled to and maintained at a

Testosterone depletion or blockade in male rats protects against trauma hemorrhagic shock-induced distant organ injury by limiting gut injury and subsequent production of biologically active mesenteric lymph.

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BACKGROUND We tested the hypothesis that testosterone depletion or blockade in male rats protects against trauma hemorrhagic shock-induced distant organ injury by limiting gut injury and subsequent production of biologically active mesenteric lymph. METHODS Male, castrated male, or flutamide-treated

Testosterone receptor blockade after hemorrhage in males. Restoration of the depressed immune functions and improved survival following subsequent sepsis.

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BACKGROUND Recent studies suggest that androgen depletion by castration before hemorrhage has protective effects on cell-mediated immunity in male mice after soft tissue trauma and hemorrhagic shock. OBJECTIVE To determine whether treatment with an androgen receptor blocker (eg, flutamide) after

Testosterone and/or low estradiol: normally required but harmful immunologically for males after trauma-hemorrhage.

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BACKGROUND Previous studies indicate that after severe hemorrhage, immune functions are markedly depressed in males, whereas females do not show any depression. Although androgen depletion by castration of mice before soft-tissue trauma and hemorrhagic shock prevents the depression of cell-mediated

Vaginal bleeding and spotting in transgender men after initiation of testosterone therapy: A prospective cohort study (ENIGI)

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Background: Previous studies have cross-sectionally described amenorrhea in cohorts of transgender men on intramuscular or subcutaneous testosterone injections. It remains uncertain which testosterone preparations most effectively

Early post-haemorrhagic stroke testosterone and oestradiol levels and long-term risk of death.

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The influence of oestrogen and testosterone replacement on stroke risk has been examined, as well as mechanisms by which oestrogen may protect from post-stroke damage. However, whether testosterone levels in the early time period after haemorrhagic stroke influence long-term mortality has not

Mechanism of immunosuppression in males following trauma-hemorrhage. Critical role of testosterone.

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OBJECTIVE To determine whether male sex steroids contribute to the depression in cell-mediated immunity following trauma-hemorrhage and resuscitation. METHODS Two weeks before the induction of soft-tissue trauma (2.5-cm midline laparotomy) and hemorrhagic shock (mean [+/-SEM] blood pressure, 35 +/-

Testosterone and estrogen differently effect Th1 and Th2 cytokine release following trauma-haemorrhage.

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The object of the study was to determine whether male and female sex steroids produce divergent effects on Th1 and Th2 cytokine release following trauma-haemorrhage. Recent studies indicate that androgens are responsible for the depressed splenocyte Th1 cytokine release in males following

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