Harding D P, Poole-Wilson P A
Cardiovasc Res. 1980 Aug;14(8):435-45. doi: 10.1093/cvr/14.8.435.
Calcium influx and efflux were measured during hypoxia and on reoxygenation in the isolated arterially perfused septum of the rabbit heart. The uptake of 47Ca2+ was continuously followed with a NaI crystal and counter. The extracellular space (ECS) was measured in a similar manner with 51Cr-EDTA. Calcium efflux was recorded by collection of effluent drops after labelling with 45Ca2+. Hypoxia caused a rapid decline of developed tension followed by a rise in resting tension. The ECS increased initially but decreased as resting tension rose. 51Cr-EDTA did not have free access to the intracellular fluid. Calcium efflux did not change and calcium influx was either unchanged or reduced. On reoxygenation calcium influx increased immediately but efflux was unaltered and 51Cr-EDTA did not enter the cell. The effects of hypoxia were altered by manipulation of temperature and substrate. The recovery of mechanical function was related to the size of the calcium influx on reoxygenation. The experiments show that a rise of resting tension during hypoxia can occur in the absence of a net gain of calcium, calcium accumulation is closely associated with the extent of tissue damage, and that calcium influx on reoxygenation is probably due to a specific abnormality and not gross disruption of the cell membrane.
在兔心脏离体动脉灌注间隔中,于缺氧期间及复氧时测量钙的流入和流出。用碘化钠晶体和计数器持续跟踪47Ca2+的摄取。用51Cr - 乙二胺四乙酸以类似方式测量细胞外间隙(ECS)。在用45Ca2+标记后,通过收集流出液滴记录钙流出。缺氧导致收缩张力迅速下降,随后静息张力升高。ECS最初增加,但随着静息张力升高而降低。51Cr - 乙二胺四乙酸无法自由进入细胞内液。钙流出未改变,钙流入要么未改变要么减少。复氧时钙流入立即增加,但流出未改变,且51Cr - 乙二胺四乙酸未进入细胞。缺氧的影响因温度和底物的改变而改变。机械功能的恢复与复氧时钙流入的大小有关。实验表明,缺氧期间静息张力升高可在无钙净增加的情况下发生,钙积累与组织损伤程度密切相关,且复氧时钙流入可能是由于特定异常而非细胞膜的严重破坏。