turpentine/hypoxia

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Normal response to erythropoietin or hypoxia in rats made anemic with turpentine abscess.

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21-aminosteroids prevent the down-regulation of hepatic cytochrome P450 induced by hypoxia and inflammation in conscious rabbits.

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1 This study was conducted to assess whether a 21-aminosteroid, U74389G, could prevent the down-regulation of hepatic cytochrome P450 (P450) induced by acute moderate hypoxia or an inflammatory reaction. 2 The rabbits of two groups (n = 6 per group) were subjected to acute moderate hypoxia (PaO2

Effect of hypoxia alone or combined with inflammation and 3-methylcholanthrene on hepatic cytochrome P450 in conscious rabbits.

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1 To investigate the effect of moderate hypoxia alone or combined with an inflammatory reaction or after 3-methylcholanthrene (3MC) pre-treatment on cytochrome P450 (P450), conscious rabbits were exposed for 24 h to a fractional concentration of inspired O2 of 10% (mean PaO2 of 34 mmHg). Hypoxia

Effects of turpentine-induced inflammation on the hypoxic stimulation of intestinal Fe3+ absorption in mice.

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Chronic subcutaneous turpentine administration (weekly for 6 weeks) induced a mild normocytic anaemia in mice. In-vitro and in-vivo intestinal Fe3+ absorption parameters were, however, not significantly altered from values in saline-treated or untreated mice. Normal mice, when exposed to 3 days

In vivo and in vitro effect of cimetidine, inflammation, and hypoxia on propofol kinetics.

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Propofol is rapidly cleared from the body by biotransformation; however, the repercussions of changes in cytochrome P-450 activity on propofol rate of elimination are unknown. To assess how changes in cytochrome P-450 activity affect propofol kinetics, one group of rabbits (N = 6) was pretreated

The iron regulatory peptide hepcidin is expressed in the heart and regulated by hypoxia and inflammation.

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The peptide hormone hepcidin plays a central role in iron homeostasis. It is predominantly expressed in the liver and regulated by iron, hypoxia, and inflammation. Although it has been shown that iron plays a key pathophysiological role in cardiac diseases, including iron-overload cardiomyopathy,

The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation.

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The present study was aimed at determining whether hepcidin, a recently identified peptide involved in iron metabolism, plays a role in conditions associated with both iron overload and iron deficiency. Hepcidin mRNA levels were assessed in two models of anemia, acute hemolysis provoked by

Effect of nifedipine on the elimination of theophylline in the rabbit subjected to hypoxia or to an inflammatory reaction.

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This study was performed to assess whether nifedipine could prevent the decrease in hepatic cytochrome P450 induced by acute moderate hypoxia or an inflammatory reaction. Rabbits were subjected to acute moderate hypoxia (PaO2 > 37 mmHg), with or without pretreatment with nifedipine (0.5 mg kg-1

[Characteristics of the morphology of metaphase chromosomes in white rat hematopoietic cells].

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Comparative study of morphological structure of chromosomes in different hematogenous cells of experimental white rats was carried out on the 5th day after ablation of spleen, on the 6th day after intermittent action of hypoxia in an altitude chamber and on the 6th day in case of aseptic

Hepatic changes of erythropoietin gene expression in a rat model of acute-phase response.

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An acute-phase response is the systemic reaction of an organism to insult (e.g. infection, trauma and burning). It represents the 'first line' of defence of the body to tissue-damaging attacks. In the present work, we used a rat model of an intra-muscular turpentine oil (TO) injection to analyse

Cellular and molecular mechanisms regulating the hepatic erythropoietin expression during acute-phase response: a role for IL-6.

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The source of circulating erythropoietin (EPO), the mediators and the mechanisms involved in the upregulation of EPO gene expression during acute-phase reaction are still poorly understood. Acute-phase reaction was induced by either intramuscular turpentine oil (TO) or intraperitoneal

Intravenous hydrocarbon abuse.

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The case of a man who injected turpentine intravenously in an attempt to kill himself is reported. The patient developed immediate pulmonary edema and hypoxia, followed later by cellulitis at the site of injection. Although only one death to date has been attributed to this form of chemical abuse,

Induction of type 3 deiodinase activity in inflammatory cells of mice with chronic local inflammation.

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During illness, changes in thyroid hormone metabolism occur, so-called nonthyroidal illness (NTI). NTI has been characterized by a fall of serum T(3) due to decreased extrathyroidal conversion of T(4) into T(3) by liver type 1 deiodinase (D1), without an increase in serum TSH. Type 3 deiodinase (D3)

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