Gerdin B, McCann E, Lundberg C, Arfors K E
Int J Tissue React. 1985;7(5):373-80.
Manganese chloride (MnCl2), with or without the addition of trace amounts of 54Mn2+, was administered as a 7-min i.v. infusion in rats. Tissue accumulation of 54Mn2+ was determined 0-15 min after the infusion, and cardiac output, regional blood flows and vascular resistances were measured 5 and 60 min after the infusion by the microsphere technique. The plasma half-life of 54Mn2+ was found to be 4.7 min. Mn2+ accumulated in several organs, the highest relative concentrations being seen in the liver, duodenum, jejunum, kidney and heart, and intermediate concentrations in the ileum, colon, stomach and spleen. There was no uptake in the lung, skeletal muscle or brain. During the infusion of 180 mumol/kg b.w. of Mn2+, the arterial blood pressure fell from a mean of 123 +/- 5 mm Hg to a minimum of 85 +/- 7 mm Hg, and thereafter returned to normal. Five minutes after termination of the infusion, there was a decrease in cardiac output and minute work but not in total peripheral resistance, a finding interpreted as a negative inotropic effect of Mn2+. At this time blood flow was decreased in the stomach, ileum, colon, spleen and skin, and increased in duodenum, jejunum and liver. The blood flows were normalized 60 min after termination of the infusion in all organs except the liver and heart. The effects are probably due to the calcium-antagonistic properties of Mn2+ and the tissue accumulation is most probably a result of intracellular accumulation through calcium channels. The relation between tissue accumulation and tissue selectivity of blood-flow alterations is unexplained.
给大鼠静脉输注7分钟氯化锰(MnCl₂),添加或不添加微量⁵⁴Mn²⁺。输注后0 - 15分钟测定⁵⁴Mn²⁺的组织蓄积情况,输注后5分钟和60分钟采用微球技术测量心输出量、局部血流量和血管阻力。发现⁵⁴Mn²⁺的血浆半衰期为4.7分钟。Mn²⁺在多个器官中蓄积,在肝脏、十二指肠、空肠、肾脏和心脏中相对浓度最高,在回肠、结肠、胃和脾脏中浓度中等。肺、骨骼肌或脑无摄取。在输注180 μmol/kg体重的Mn²⁺期间,动脉血压从平均123±5 mmHg降至最低85±7 mmHg,随后恢复正常。输注终止5分钟后,心输出量和每分功降低,但总外周阻力未降低,这一发现被解释为Mn²⁺的负性肌力作用。此时,胃、回肠、结肠、脾脏和皮肤的血流量减少,十二指肠、空肠和肝脏的血流量增加。输注终止60分钟后,除肝脏和心脏外,所有器官的血流量均恢复正常。这些作用可能归因于Mn²⁺的钙拮抗特性,组织蓄积很可能是通过钙通道细胞内蓄积的结果。组织蓄积与血流改变的组织选择性之间的关系尚无法解释。