Epinephrine is an enhancer of rat intestinal absorption.

Some physiological substances, including acetylcholine and nitric oxide, are useful candidates for stimulation of intestinal absorption of drugs. In the present study, we elucidated the ability of epinephrine (Epi) to stimulate the intestinal absorption of drugs. We evaluated the ability of Epi to enhance absorption of macromolecules using dextran (Mw 4000 Da), which is poorly absorbed from the intestine, as a model compound in situ in a closed loop of the rat jejunum. Treatment of the jejunum with Epi resulted in significant increase in absorption of dextran in a dose-dependent fashion. The area under the curve (AUC) from 0 to 4 h in the Epi-treated jejunum was 13-fold higher than that in the vehicle-treated jejunum. The absorption-enhancing activity of Epi was 40-fold higher than that of caprate, a clinically used absorption-enhancer of drugs. In the experimental conditions used in this study, histological injury of the mucosa and perturbation of the mucosal membrane were not observed in the Epi-treated jejunum. Treatment with an antagonist of alpha-adrenergic receptors attenuated the stimulation of intestinal absorption by Epi, and treatment with an agonist of alpha-adrenergic receptors resulted in enhancement of intestinal absorption. While an antagonist of beta-adrenergic receptors enhanced the absorption-enhancing effect of Epi, an agonist of beta-adrenergic receptors stimulated intestinal absorption. These results indicate that stimulation of adrenergic receptors may be a novel strategy for intestinal absorption of drugs.     

Biological significance of enhanced mitochondrial ketogenesis during the early stages after 70% hepatectomy in rats

Ketogenic capacity of mitochondria from the remnant liver of 70% hepatectomized rats was studied in relation to mitochondrial phosphorylative activity. Ketogenic capacity increased to a maximum of 6.04 +/- 0.39 from 3.84 +/- 0.13 of control, with an enhancement of mitochondrial phosphorylative activity 6 hr after hepatectomy, and then decreased to normal levels within 24 hr. Adenylate energy charge, (ATP + 1/2ADP)/(ATP + ADP + AMP), of the remnant liver decreased to 0.825 +/- 0.006 as compared to 0.849 +/- 0.002 of control 6 hr after operation. At 12 hr, total ketone body concentrations of the arterial blood increased concomitant with a fall in ketone body ratio (acetoacetate/3-hydroxybutyrate) which reflects the decreased liver mitochondrial redox (NAD+/NADH) state. These findings suggest that an enhancement of mitochondrial fatty acid oxidation and ketogenesis occurs concomitant with an enhancement of mitochondrial phosphorylative activity in the remnant liver in response to a decreased energy charge after 70% hepatectomy.     

Availability of 4'galactosyllactose (O-beta-D-galactopyranosyl-(1----4)-O-beta-D-galactopyranosyl-(1----4)- D-glucopyranose) in rat

O-beta-D-Galactopyranosyl-(1----4)-O-beta-D-galactopyranosyl-(1----4)-D- glucopyranose (designated as 4'GL) is produced from lactose by Cryptococcus laurentii. The influence of chronic ingestion of 4'GL on body weight gain, organ weight, serum lipids, and liver lipids was investigated in rats. The body weight gains of the 5% and 10% 4'GL-diet groups were higher than that of the control group. Food intake and fecal dry weight were significantly increased (p less than 0.05) by 4'GL feeding. The 4'GL diet produced a significant increase (p less than 0.01) in the wet weight and contents of both the cecum and the colon. However, no significant increase was observed in the weight of the stomach, small intestine, liver, or other organs. The effects of 4'GL on serum and liver lipid levels were not observed in this experiment. The digestion of 4'GL was measured in vitro using the artificial gastric juice, alpha-amylase of human saliva, alpha-amylase of hog pancreas, and mucosa of rat intestine. 4'GL was not hydrolyzed by these enzymes. Long-term ingestion of 4'GL did not cause any induction of 4'GL hydrolyzing enzyme activity in the rat small intestine.     

Q-Switched Alexandrite Laser Therapy for Pigmentation of the Lips Owing to Laugier-Hunziker Syndrome

BACKGROUND: Laugier-Hunziker (LH) syndrome is a rare benign condition in which hyperpigmentation of the lips and buccal mucosa occurs with no systemic associations. OBJECTIVE: We report the response to treatment with the Q-switched alexandrite laser (QSAL) because there are few reports on therapy for LH syndrome. METHODS: The QSAL was used for pigmentation of the lips in a 63-year-old woman with LH syndrome. Laser irradiation was done at 5.0 J/cm2 with a 3 mm spot size. RESULTS: There was 100% clearance of pigmentation of the lips with a single laser treatment, and recurrence was not observed after 6 months. CONCLUSION: The QSAL is very effective for pigmentation owing to LH syndrome.