【摘要】 新西兰兔33只,分成4组:对照组、去甲基肾上腺素(NE)组、美托洛尔(MP)组和酚妥拉明(R)组。NE组静滴NE 1mg/kg,MP和R组则在静滴NE前10分钟分别静注β受体阻滞剂MP或α受体阻滞剂R。测定21种代谢产物。结果发现,在NE组中磷酸二羟丙酮和丙酮酸明显增加,提示三磷酸甘油醛脱氨酶和丙酮酸脱氨酶活性显著降低,同时伴乳酸浓度增高(P<0.01),ATP和磷酸肌酸降低(P<0.05),能荷值降低(P<0.05)。MP组呈现与NE组相似的改变,而R组与NE组相比代谢紊乱呈明显逆转。因NE已知为α受体和β受体两者的兴奋剂,而在未研究中α受体阻滞剂R,而不是β受体阻滞剂MP,可显著减轻代谢紊乱,故NE心肌病的代谢紊乱系由α受体兴奋所致。更多还原

【Abstract】 33 New Zealand rabbits were divided into the following 4 groups: control group, nor.epinephrine (E) group, metoprolol (MP) group and regitine (R) group. To norepinephrine (NE)group, 1 mg NE/kg body weight was given intravenously. To the MP group and the R group, β-blocker MP or α-blocker R was given 10 minutes prior to the NE infusion respectively.Intermediate metabolites and related enzymes of the glycolysis and tricarboxylic acid cycle weremeasured. In NE group, activities of both 3-phosphoglyceraldehyde dehydrogenase and pyruvatedehyrdogenase were decreased significantly with concomitant increase in the concentration oflactate (P<0.01), a reduction in ATP and creatine phosphate (P<0.05), and energy charge (P<0.05). Rabits of the MP group showed similar changes. Whereas in rabbits of the R group,metabolic disturbances were just the reverse. Hence, the authors are of the opinion thatmetabolic disturbances occurring in NE caused cardiomyopathy are due to the stimulation of theα-adrenereceptor.更多还原