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Ring segments of dog thoracic ducts precontracted with a high concentration of norepinephrine (NE) relaxed in a concentration-dependent manner in response to acetylcholine (ACh) or sodium nitroprusside (SNP). Pretreatment with atropine inhibited the ACh-induced relaxation in a competitive manner. The Schild plot showed a slope of 1.1 +/- 0.2 and a pA2 value of 10.4 +/- 0.4 (n = 6 ring segments). Removal of endothelium caused a complete inhibition of the ACh-induced relaxations in precontracted dog thoracic ducts. ACh, which failed to relax precontraction of the ring segment when mounted separately, induced relaxation in the same preparation when it was mounted as a "sandwich" with the longitudinal strip. The ACh-induced relaxations in the lymphatic preparations with endothelium were suppressed or abolished by pretreatment with oxyhemoglobin (10(-6) and 10(-5) M), methylene blue (10(-6) and 10(-5) M), and NG-monomethyl-L-arginine (3 x 10(-5) M), but the relaxations were unaffected by aspirin (10(-5) M). Pretreatment with methylene blue (10(-5) M) also caused a significant reduction of the SNP-induced relaxations in the precontracted thoracic ducts. It may be concluded that ACh-induced relaxation in dog thoracic ducts precontracted with NE is mediated by high-affinity muscarinic receptors in the lymphatic endothelial cells. Also, stimulation of the endothelial muscarinic receptors liberates a transferable endothelium-derived relaxing factor, which results in the relaxation of the lymphatic smooth muscles via the accumulation of cellular guanosine 3',5'-cyclic monophosphate.

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A low molecular weight, heat-resistant hepatotrophic factor in an extract from the bovine intestinal mucosa was purified and identified as ethanolamine by structural analyses. The mode of action of ethanolamine in vitro and in vivo coincided with that of the crude extract of the tissue, indicating that ethanolamine is the active component. Ethanolamine synergistically elevated the stimulation of DNA synthesis in hepatocytes in primary culture when added together with a growth factor, such as epidermal growth factor, with the ED 50 being 20 M, although it showed little stimulatory effect by itself. Contrary to these in vitro results, the intraperitoneal administration of ethanolamine hydrochloride (24 mg of ethanolamine per kg of body weight) enhanced hepatocyte proliferation in regenerating rat livers after two-thirds hepatectomy without the administration of any growth factors. In the regenerating liver, hepatocyte proliferation may be initiated by an endogenous growth factor, but the supply of ethanolamine in circulation may not be sufficient for optimal hepatocyte proliferation; thus, the exogenous administration of ethanolamine may further enhance hepatocyte proliferation. Ethanolamine in circulation may be a humoral hepatotrophic factor.Previously we reported that the proliferation of hepatocytes in primary culture was synergistically stimulated by a low molecular weight (LMW, Ͻ1,000) and a high molecular weight (HMW, Ͼ10,000) factor that were derived from the bovine small intestine mucosa, separated by their solubility in methanol (1). The LMW factor synergistically enhanced the basal level of stimulation by the HMW factor, while it had little effect when added alone. Since the LMW factor could enhance the level of DNA synthesis in hepatocytes that were stimulated by epidermal growth factor (EGF) or hepatocyte growth factor (HGF), it acts by amplifying the effects of a growth factor. Contrary to the in vitro result, the LMW factor could stimulate hepatocyte proliferation in regenerating livers even when added alone. We speculate that an endogenous growth factor(s) is probably produced in the animals with the regenerating liver, but the supply of the LMW factor is below the optimal level, thus the exogenous supply of the LMW factor can further stimulate hepatocyte proliferation. The LMW factor may function as a humoral hepatotrophic factor for liver regeneration.We purified the LMW factor from the bovine small intestinal mucosa, and we identified it as ethanolamine (Etn). The commercially available Etn had effects identical to those of the LMW factor before purification; i.e., Etn synergistically stimulated the proliferation of hepatocytes in primary culture when added with the HMW factor, and it stimulated hepatocyte proliferation in the regenerating liver when administered alone. Etn can synergistically enhance DNA synthesis in hepatocytes when added with EGF, suggesting that it enhances the actions of hepatotrophic growth factors. Etn in circulation may function as a humoral hepatotrophic factor ...

We have investigated whether acidity can be used to control the physicochemical properties of chitin nanofibers (ChNFs). In this study, we define acidity as the molar ratio of dissociated protons from the acid to the amino groups in the raw chitin powder. The effect of acidity on the physicochemical properties of and -ChNFs was compared. The transmittance and viscosity of the -ChNFs drastically and continuously increased with increasing acidity, while those of the -ChNFs were not affected by acidity. These differences are because of the higher ability for cationization based on the more flexible crystal structure of -chitin than -chitin. In addition, the effect of the acid species on the transmittance of -ChNFs was investigated. The transmittance of -ChNFs can be expressed by the acidity regardless of the acid species, such as hydrochloric acid, phosphoric acid, and acetic acid. These results indicate that the acidity defined in this work is an effective parameter to define and control the physicochemical properties of ChNFs.