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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。
33 New Zealand white rabbits were divided into 4 groups: control group, NE group, metoprolol (MP) group and Phentolamine (R) group. In NE group, 1 mg / kg NE was intravenously administered, while in MP and R groups, β-blockers MP or α-blockers R were administered intravenously 10 minutes before NE bolus. Twenty-one metabolites were determined. The results showed that dihydroxyacetone phosphate and pyruvate increased significantly in NE group, suggesting that glyceraldehyde deaminase triphosphate and pyruvate deaminase activities were significantly decreased, accompanied by increased lactate concentration (P <0.01), ATP and phospho-muscle Acid decreased (P <0.05), the charge value decreased (P <0.05). The MP group showed similar changes as the NE group, but the metabolic disorder was significantly reversed in the R group compared with the NE group. Because NE is known as both an alpha receptor and a beta receptor agonist, and in the absence of alpha-blockers R, but not beta-blockers MP, can significantly reduce metabolic disorders, so NE myocardium Diseased metabolic disorders are caused by alpha receptor agonism.