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家兔结扎前降枝24h后,心肌乳酸及K~+分别由正常摄取+17±1.0％及±2.1±0.08％转变为产生-196±60.2％及-83±8.2％。m-Nif 15,30,50μg·kg~(-1)使心肌乳酸产生及失K~+分别较结扎组减少69,76,88％及61,79,97％;Nif30μg·kg~(-1)减少76％及56％;普萘洛尔1mg·kg~(-1)使乳酸减少91％,心肌K~+反转为摄取+2±0.05％,结扎组与溶剂对照组的MIA％分别为18.7±3.3及19±4％,上述剂量的m-Nif分别为12.6±1.1,8.4±0.4和5.6±0.3％,Nif30μg·kg~(-1)9.2±0.9％,普萘洛尔3.2±0.5％,各给药组均减轻ST段上升。
After 24 hours, the lactic acid and K ~ + in myocardium changed from normal ± 17 ± 1.0% and ± 2.1 ± 0.08% to -196 ± 60.2% and -83 ± 8.2%, respectively. Compared with the ligation group, m-Nif 15, 30 and 50 μg · kg -1 decreased myocardial lactate production and loss of K ~ + by 69,76,88% and 61,79 and 97%, respectively; Nif30μg · kg -1 ) Were decreased by 76% and 56%, propranolol 1 mg · kg -1 decreased lactate by 91% and myocardial K + by + 2 ± 0.05% respectively. MIA% of ligation group and solvent control group were respectively Were 18.7 ± 3.3 and 19 ± 4% respectively. The above-mentioned doses of m-Nif were 12.6 ± 1.1, 8.4 ± 0.4 and 5.6 ± 0.3%, Nif 30 μg · kg -1 9.2 ± 0.9%, propranolol 3.2 ± 0.5%, all the treatment groups reduce the ST segment rise.