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Objectives To investigate the effects ofβ2-adrenergic antagonist on cytosolic Ca2 + ([Ca2+]i) in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending coronary artery of rat hearts. Rats in the control group were sham-operated. Cardiomyocytes were dissociated at two, four, eight weeks after myocardial infarction (MI) and [Ca2+]i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol in presence or absence of betal-adrenergic antagonist atenolol, beta2-adrenergic antagonist ICI118, 551 or non-selectiveβ1, 2- adrenergic antagonists propranolol was examined. Results The followings were found that ICI118, 551 had no significant effects on the rise of [Ca2+]i induced by isoproterenol in normal ventricular myocytes (P > 0.05 ), ICI118, 551 only significantly attenuated the rise of [Ca2+]i induced by isoproterenol at four weeks and eight weeks after MI (24.5%±5.7% vs 57.8%±13.2%, P<0.01; 12.2%±7.9% vs 44.6%±11.3%, P< 0.01). Atenolol had suppressive effects only in the control group and the post-Mi group of two weeks (P< 0.05 ) , and propranolol had suppressive effects in the control and all the three post-Mi groups (P < 0.01). Conclusions Beta2-adrenergic antagonist ICI118, 551 may exert negative effects on Ca2+ overload initiated by sympathetic stimulation after MI.
Objectives To investigate the effects of β2-adrenergic antagonist on cytosolic Ca2 + ([Ca2 +] i) in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending coronary artery of rat hearts. Rats in the control group were sham- operated. Cardiomyocytes were dissociated at two, four, eight weeks after myocardial infarction (MI) and [Ca2 +] i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol in presence or absence of betal- adrenergic antagonist atenolol, beta2- Results The following articles were found that ICI118, 551 had no significant effects on the rise of [Ca2 +] i induced by isoproterenol in normal ventricular myocytes (P> 0.05 ), ICI118, 551 only significantly attenuated the rise of [Ca2 +] i induced by isoproterenol at four weeks and eight weeks after MI (24.5% ± 5.7% vs 57.8% ± 13.2%, P <0.01; 12.2% ± 7.9% vs 4 4.6% ± 11.3%, P <0.01). Atenolol had suppressive effects only in the control group and the post-Mi group of two weeks (P <0.05), and propranolol had suppressive effects in the control and all the three post-Mi groups (P <0.01). Conclusions Beta2-adrenergic antagonist ICI118, 551 may exert negative effects on Ca2 + overload initiated by sympathetic stimulation after MI.