Nutrition and the regulation of higher animals in hypoxia

Hyoixia(10.5或7.6%)delayed gastric emptying and suppressed gastric acid secretion inconscious rats. In addition, although the concentration of plasma gastrin，gastric acid secretion, increased under hypoxic conditions，the oral administration of HCL abolished the hyposha -stimulated gastrin release，indicating that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrinrelease through positive feedback regulation.The 10.5% oi D22 D2 hyposia -suppressed gastric acidsecretion was restored to nearly the level in normoxia by the adrenal medullectomy. WithD22 hypoxia, the operation also caused an increase in the level of gastric acid output，虽然the extent was lower than that with 10.5% oi D22 D2hypoxia. Similar results were obtainedwhen reserpine, which causes an adrenaergic discharge, was administered. Furthermorean α2-adrenoceptor blocking agent, yohimbine，almost completely removed the inhibitory effectMore f10.5% and 7.6% oi D22 D2hypoxia on gastric and secretion. Epinephrine release isstimulated by 10.5% D22 hypoxiaand not only epinephrine but also norepinephrine releases are enhanced by D22 D2hypoxia. Itsuggested that the hyposia -stimulated adrenergic response acts on the α2-adrenoceptor on thevagus cholinergic endings in the gastric wall，and the deareased acetylcholine release thereby inhibits gastric acid secretion.Epo functionedas a competence factor for RBECs and maximally stimulated DNA synthesis of RBECs at theconcentration of 1u /ml （the serum concentrations of Epo in most animals are in the range 10 - 30）mU/ml under normal physiological conditions and increase more than 100-fold in hypoxemia resulting来自anemia and hypoxic exposure). Furthermore, both RBECs and MBECs expressed two form epor mNRA，the authentic form （aEpo-R）和the intron 5-inserted form (15epo - r). RBECs had a single class oflow affinity (860 pM) binding site for Epo. These results suggest that rat and murine 15epo - rsmodulate the functions of Epo by the binding of Epo with the authentic receptor as amembran -bound form and a soluble form, respectively，Epo acts on endothelial cells as a competent factor when excess Epo is induced byhyposia . hypoxia (2) stimulated the expression of GAPDH mRNA in all cell typed testedMBEC4, Hep G2 CHO cells，Ba/F3 cells and rat sooth muscle cells). Some transition metals (coy D12+ die D1, Ni D12+ die D1，Zn D12+ D12+ D12+ D1 and DFX also upregulated the transcription of GAPDH gene in MBEC4，suggesting that GAPDH is regulated through a mechanism其中heme protein participates. iNOS也可以induced in hypoxia， then cGMP was extremelyformed,suggesting that cGMP acts as a intracellular information transmitter.Vitamin B - D212 - D2 is known asa developmental factor of blood cell. We have studied how the vitamin B - 212 - D2 affects on thedevelopment of blood cell in hypoxia. Less

Hyoixia (10.5 or 7.6%OィイD22ィエD2) delayed gastric emptying and suppressed gastric acid secretion in conscious rats. In addition, although the concentration of plasma gastrin, the principal stimulant of gastric acid secretion, increased under hypoxic conditions, the oral administration of HCL abolished the hypoxia-stimulated gastrin release, indicating that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrin release through positive feedback regulation.The 10.5%OィイD22ィエD2 hypoxia-suppressed gastric acid secretion was restored to nearly the level in normoxia by the adrenal medullectomy. With 7.6%OィイD22ィエD2hypoxia, the operation also caused an increase in the level of gastric acid output, although the extent was lower than that with 10.5%OィイD22ィエD2hypoxia. Similar results were obtained when reserpine, which causes an adrenaergic discharge, was administered. Furthermore, an α2-adrenoceptor blocking agent, yohimbine, almost completely removed the inhibitory effect o … More f 10.5% and 7.6% OィイD22ィエD2hypoxia on gastric and secretion. Epinephrine release is stimulated by 10.5%OィイD22ィエD2hypoxia, and not only epinephrine but also norepinephrine releases are enhanced by 7.6%OィイD22ィエD2hypoxia. It is suggested that the hypoxia-stimulated adrenergic response acts on the α2-adrenoceptor on the vagus cholinergic endings in the gastric wall, and that the deareased acetylcholine release thereby inhibits gastric acid secretion.Epo functioned as a competence factor for RBECs and maximally stimulated DNA synthesis of RBECs at the concentration of 1 U/ml (the serum concentrations of Epo in most animals are in the range 10 - 30 mU/ml under normal physiological conditions and increase more than 100-fold in hypoxemia resulting from anemia and hypoxic exposure). Furthermore, both RBECs and MBECs expressed two form Epo-R mNRA, the authentic form (aEpo-R) and the intron 5-inserted form (15 Epo-R). RBECs had a single class of low affinity (860 pM) binding site for Epo. These results suggest that rat and murine 15Epo-Rs modulate the functions of Epo by competing the binding of Epo with the authentic receptor as a membrane-bound form and a soluble form, respectively, and that Epo acts on endothelial cells as a competent factor when excess Epo is induced by hypoxia.Hypoxia (2%OィイD22ィエD2) stimulated the expression of GAPDH mRNA in all cell typed tested (MBEC4, Hep G2 CHO cells, Ba/F3 cells and rat sooth muscle cells). Some transition metals (CoィイD12+ィエD1, NiィイD12+ィエD1, ZnィイD12+ィエD1 and MnィイD12+ィエD1) and DFX also upregulated the transcription of GAPDH gene in MBEC4, suggesting that GAPDH is regulated through a mechanism, in which heme protein participates. iNOS was also induced in hypoxia and then cGMP was extremely formed, suggesting that cGMP acts as a intracellular information transmitter.Vitamin BィイD212ィエD2 is known as a developmental factor of blood cell. We have studied how the vitamin BィイD212ィエD2 affects on the development of blood cell in hypoxia. Less