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Standard clinical practice recommends minimal doses of vasoactive drugs during weaning of patients from mechanical ventilation. However there are currently no clinical data to inform clinicians about whether the use of noradrenaline during weaning predisposes to weaning failure. The objective of this study was to evaluate whether the necessity of the vasopressor noradrenaline in mechanically ventilated patients recovering from septic shock changed the extubation outcome. A total of 656 patients recovering from septic shock on mechanical ventilation were selected from intensive care units in two university hospitals. Patients receiving noradrenaline at the time of weaning and case-controls not taking noradrenaline were matched for age, gender, haemodynamic and ventilatory parameters, aetiology of respiratory failure and APACHE II score. One hundred and forty-five patients who successfully tolerated a spontaneous breathing trial were extubated while on noradrenaline therapy and the reintubation rate was measured. In the noradrenaline group, the mean dose of noradrenaline during initial shock treatment was 0.52+/-0.29 microg/kg/min and 0.12+/-0.10 microg/kg/min during weaning. The reintubation rate was 12/63 (19%) in the noradrenaline group and 15/82 (18.3%) in the control group (P=1.00). Intensive care unit mortality was also similar in both groups (10/63, 15.9%) for noradrenaline patients and (11/82, 13.4%) for control patients (P=0.81). Arterial blood gases and ventilatory and haemodynamic parameters were similar in all patients regardless of weaning success. We did not find that the use of noradrenaline at the time of weaning was associated with extubation failure. Low doses of noradrenaline may not preclude weaning from mechanical ventilation.

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BACKGROUND: Long-term administration of carbon tetrachloride is an accepted experimental model to produce hepatic fibrosis. Oxidative stress has been postulated as a major molecular mechanism involved in carbon tetrachloride hepatotoxicity, where the reactive oxygen species play an important role in the pathogenesis of liver fibrosis. AIMS: This study was conducted to evaluate the effectiveness of an experimental model of hepatic cirrhosis induced by carbon tetrachloride inhalation as well as the importance of lipid peroxidation and the characteristics of the ascitic fluid in this model. METHODS: At first the hepatic histologic findings were assessed using the hematoxilineosin technique in different moments of carbon tetrachloride inhalation (5th, 7th, 9th, 12th weeks). Later, at the end of 15 weeks of the study the rats were divided in three groups (control; control + phenobarbital; and carbon tetrachloride + phenobarbital) for lipid peroxidation, ascitic fluid and histologic characteristics evaluation. For the lipid peroxidation analysis, thiobarbituric acid and QL techniques were used. Cytologic and bacteriologic parameters were analysed in the ascitic fluid. RESULTS: Cirrhosis was established in 100% of carbon tetrachloride rats between the 12th and 15th weeks with an elevation in the lipid peroxidation carbon tetrachloride rats' livers. Ascitic fluid infection was observed in one of seven rats who has developed ascites. CONCLUSIONS: The carbon tetrachloride inhalation method developed in this study is effective in cirrhosis induction and ascites formation, and the carbon tetrachloride cirrhosis physiopathogenesis is probably related to the oxidative stress installation.

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Secretion of the alpha-subunit of pituitary glycoprotein hormones usually follows the secretion of intact gonadotropins and is increased in gonadal failure and decreased in isolated gonadotropin deficiency. The aim of the present study was to determine the levels of the alpha-subunit in the serum of patients with cirrhosis of the liver and to compare the results obtained for eugonadal cirrhotic patients with those obtained for cirrhotic patients with hypogonadotropic hypogonadism. Forty-seven of 63 patients with cirrhosis (74.6%) presented hypogonadism (which was central in 45 cases and primary in 2), 7 were eugonadal, and 9 women were in normal menopause. The serum alpha-subunit was measured by the fluorimetric method using monoclonal antibodies. Cross-reactivity with LH, TSH, FSH and hCG was 6.5, 1.2, 4.3 and 1.1%, respectively, with an intra-assay coefficient of variation (CV) of less than 5% and an interassay CV of 5%, and sensitivity limit of 4 ng/l. The serum alpha-subunit concentration ranged from 36 to 6253 ng/l, with a median of 273 ng/l. The median was 251 ng/l for patients with central hypogonadism and 198 ng/l for eugonadal patients. The correlation between the alpha-subunit and basal LH levels was significant both in the total sample (r = 0.48, P < 0.01) and in the cirrhotic patients with central hypogonadism (r = 0.33, P = 0.02). Among men with central hypogonadism there was a negative correlation between alpha-subunit levels and total testosterone levels (r = -0.54, P < 0.01) as well as free testosterone levels (r = -0.53, P < 0.01). In conclusion, although the alpha-subunit levels are correlated with LH levels, at present they cannot be used as markers for hypogonadism in patients with cirrhosis of the liver.

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Secretion of the alpha-subunit of pituitary glycoprotein hormones usually follows the secretion of intact gonadotropins and is increased in gonadal failure and decreased in isolated gonadotropin deficiency. The aim of the present study was to determine the levels of the alpha-subunit in the serum of patients with cirrhosis of the liver and to compare the results obtained for eugonadal cirrhotic patients with those obtained for cirrhotic patients with hypogonadotropic hypogonadism. Forty-seven of 63 patients with cirrhosis (74.6 percent) presented hypogonadism (which was central in 45 cases and primary in 2), 7 were eugonadal, and 9 women were in normal menopause. The serum alpha-subunit was measured by the fluorimetric method using monoclonal antibodies. Cross-reactivity with LH, TSH, FSH and hCG was 6.5, 1.2, 4.3 and 1.1 percent, respectively, with an intra-assay coefficient of variation (CV) of less than 5 percent and an interassay CV of 5 percent, and sensitivity limit of 4 ng/l. The serum alpha-subunit concentration ranged from 36 to 6253 ng/l, with a median of 273 ng/l. The median was 251 ng/l for patients with central hypogonadism and 198 ng/l for eugonadal patients. The correlation between the alpha-subunit and basal LH levels was significant both in the total sample (r = 0.48, P<0.01) and in the cirrhotic patients with central hypogonadism (r = 0.33, P = 0.02). Among men with central hypogonadism there was a negative correlation between alpha-subunit levels and total testosterone levels (r = 0.54, P<0.01) as well as free testosterone levels (r = -0.53, P<0.01). In conclusion, although the alpha-subunit levels are correlated with LH levels, at present they cannot be used as markers for hypogonadism in patients with cirrhosis of the liver

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In this work, the authors report the case of a female patient with 24 years of age with hyperprolactinemia, who presented a pituitary stalk calcification as seen by CT scan. Once other possible etiologies were excluded, we concluded that the calcification was probably related to hyperprolactinemia caused by interruption of the input of dopamine to the pituitary gland.

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