The American journal of physiology
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Hepatopulmonary syndrome (HPS) causes impaired oxygenation due to intrapulmonary vasodilatation in patients with cirrhosis. Chronic common bile duct ligation (CBDL) in the rat results in gas-exchange abnormalities similar to HPS, but intrapulmonary vasodilatation has not been evaluated. We assess intrapulmonary vasodilatation, measured in vivo, after CBDL. ⋯ No lung injury was observed. CBDL, but not PVL, causes progressive intrapulmonary vasodilatation, which accompanies worsening arterial gas exchange. These findings validate CBDL as a model to study HPS.
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Clinical Trial Controlled Clinical Trial
Melatonin and S-20098 increase REM sleep and wake-up propensity without modifying NREM sleep homeostasis.
The pineal hormone melatonin has been implicated in the circadian regulation of sleep. In a crossover design, we investigated the effect of acute administration of 5 mg melatonin and a melatonin agonist (S-20098, 5 and 100 mg) in healthy young men when given 5 h before bedtime on sleep structure and electroencephalogram (EEG) power density. Each trial comprised a baseline, a treatment, and a posttreatment sleep episode. ⋯ On the posttreatment night after melatonin and S-20098 administration, more wakefulness was present in the latter one-half of the sleep episode. EEG power density between 0.25 and 20 Hz during either non-REM (NREM) or REM sleep did not differ from placebo. Thus a single early evening dose of melatonin or the agonist S-20098 increases REM sleep propensity and advances sleep termination while, at the same time, the EEG in NREM sleep remains unaffected.
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The present studies investigated the significance of glucoprivic metabolic signals, particularly those of central origin, to the regulation of pituitary luteinizing hormone (LH). Groups of gonadectomized (GDX) adult male rats were treated with 2-deoxy-D-glucose (2-DG), an inhibitor of glycolysis, by either intravenous (50, 100, or 200 mg/kg) or intracerebroventricular (5, 20, or 100 microg/rat) administration. Systemic drug treatment caused a significant decrease in mean plasma LH levels compared with saline-treated controls. ⋯ In summary, treatment of GDX rats with the glucose antimetabolite, 2-DG, decreased plasma LH, suggesting that metabolic signaling of cellular glucose oxidation is of physiological importance to the regulation of pituitary hormone secretion. Findings that plasma LH was diminished in animals treated intracerebroventricularly with 2-DG implicate central glucoprivic receptors in neuroendocrine mechanisms governing the reproductive endocrine axis. Attenuation of 2-DG-induced decreases in circulating LH by opioid receptor antagonists suggests that these receptors, particularly the mu-subtype, mediate central effects of glucoprivation on circulating LH.