経壁刺激および化学刺激に対する摘出モルモット胆のうの収縮反応に及ぼす低温保存の影響

抄録

The present report describes the effects of cold storage (1_??_7 days) on the mechanical response of isolated guinea-pig gallbladder to transmural and chemical stimulation. Results obtained are as follows: in the cumulative dose-response analysis, the maximal contractile response to exogenous ACh was gradually reduced during the 1 to 7-day cold storage, however it was not abolished. The pD₂ and pA₂ (of atropine) values were not significantly different between on fresh and cold-stored preparations. The monophasic contraction induced by transmural stimulation was reduced more rapidly during the 1 to 4-day storage and abolished during the 4 to 7-day cold storage. Tetrodotoxin (TTX) or atropine prevented the contractile response to transmural stimulation. On the other hand, atropine, but not TTX, blocked the exogenous ACh-induced contraction. The maximal contractions induced by KCl and by BaCl₂ were gradually reduced during the 1 to 7-day cold storage, while pD₂ and pD₂' (of papaverine) values on cold-stored preparations were not remarkably different from those on fresh preparations. Cold storage reduced the maximal contractile response to phenylephrine, but did not affect the maximal relaxation induced by isoprenaline. The pD₂ and pA₂ (of antagonist) values were not, however, significantly different between fresh and cold-stored preparations. In the K⁺-free medium, ouabain (10^-5M), but not propranolol (3.5×10^-5M) abolished the biphasic response of cold-stored preparations induced by treatment with 5.4mM KCl or by replacement of normal Ringer's solution. These results suggest that the ACh release mechanism of postganglionic cholinergic fibers was blocked after a 4-day storage at 2°C and that the specific receptor level as well as the contractile actomyosin system were unaffected by cold storage up to 7 days. The maximal contractile response was, however, gradually reduced during a one-week period of cold storage. Thus, it appears that the cold storage procedure produces a partial depolarization of cell membrane.