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[Effect of AMG-1 on free intrasynaptosome calcium level and on the isolated artery contraction induced by norepinephrine].

Li Wp, Feng Yp, Zhang Jt

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Abstract

Recently, the intracellular free calcium overload has been considered as an important factor in the development of ischemic brain damage. In this paper, the effect of AMG-1 on free calcium concentration ([Ca2+]i) in rat intrasynaptosome and on the isolated rat tail artery contraction induced by norepinephrine (NE) were studied by using Fura-2 fluorescence technique and contraction force measurement, respectively. The results show that: 1. AMG-1 10 mumol.L-1 and 100 mumol.L-1 reduced the KCl induced [Ca2+]i increase by 19 +/- 11% and 57 +/- 12%. 2. AMG-1 100 mumol.L-1 markedly decreased the NE-dependent intracellular calcium induced contraction force (43 +/- 11%). In our previous study, AMG-1 was shown to have improving effect on ischemic damage following middle cerebral artery occlusion in rats. On the basis of these results, we suggest that the mechanism of AMG-1 in improving cerebral ischemic damage may be due to the decrease of [Ca2+]i.

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What this paper is about

Recently, the intracellular free calcium overload has been considered as an important factor in the development of ischemic brain damage. In this paper, the effect of AMG-1 on free calcium concentration ([Ca2+]i) in rat intrasynaptosome and on the isolated rat tail artery contraction induced by norepinephrine (NE) were studied by using Fura-2 fluorescence technique and contraction force measurement, respectively. The results show that: 1. AMG-1 10 mumol.L-1 and 100 mumol.L-1 reduced the KCl induced [Ca2+]i increase by 19 +/- 11% and 57 +/- 12%. 2. AMG-1 100 mumol.L-1 markedly decreased the NE-dependent intracellular calcium induced contraction force (43 +/- 11%). In our previous study, AMG-1 was shown to have improving effect on ischemic damage following middle cerebral artery occlusion in rats. On the basis of these results, we suggest that the mechanism of AMG-1 in improving cerebral ischemic damage may be due to the decrease of [Ca2+]i.

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Available abstract

Recently, the intracellular free calcium overload has been considered as an important factor in the development of ischemic brain damage. In this paper, the effect of AMG-1 on free calcium concentration ([Ca2+]i) in rat intrasynaptosome and on the isolated rat tail artery contraction induced by norepinephrine (NE) were studied by using Fura-2 fluorescence technique and contraction force measurement, respectively. The results show that: 1. AMG-1 10 mumol.L-1 and 100 mumol.L-1 reduced the KCl induced [Ca2+]i increase by 19 +/- 11% and 57 +/- 12%. 2. AMG-1 100 mumol.L-1 markedly decreased the NE-dependent intracellular calcium induced contraction force (43 +/- 11%). In our previous study, AMG-1 was shown to have improving effect on ischemic damage following middle cerebral artery occlusion in rats. On the basis of these results, we suggest that the mechanism of AMG-1 in improving cerebral ischemic damage may be due to the decrease of [Ca2+]i.

Key concepts: Contraction (grammar), Calcium, Fura-2, Chemistry, Calcium in biology, Intracellular, Ischemia, Internal medicine

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[Effect of AMG-1 on free intrasynaptosome calcium level and on the isolated artery contraction induced by norepinephrine]. — Research Paper | ScholarLens