Biomedical subjects
Publications and source records attributed to J H Bridge.
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Heart cells were loaded with sodium by treatment with toxic doses of acetyl strophanthidin. After this treatment, an increase in extracellular calcium resulted in a transient net outward sodium flux against its electrochemical gradient and in net cellular uptake of calcium. It is concluded that the free energy for the net outward sodium movement was derived from the increased calcium gradient and that these ion movements took place through the sodium-calcium exchange. While in the normal physiological state the sodium-calcium exchange produces calcium extrusion from the cell, these experiments demonstrate its reversibility.
A new gamma-labeled marker for extracellular space is the cobaltic form of 58Co-ethylenediaminetetraacetic acid (58Co-EDTA). The cobaltic ion has a much higher affinity for EDTA than the cobaltous ion; it is prepared as a potassium salt, K+(58Co3+-EDTA4-), and is apparently biologically inert. Testing by equilibration in intact rabbits and comparing the myocardial content with that of [14C]sucrose give values of the volume of distribution in the myocardium of 0.294 +/- 0.052 ml/g for 58Co-EDTA and 0.303 +/- 0.051 ml/g for [14C]sucrose (SD, n = 130, for two hearts), with the ratios of 58Co-EDTA/sucrose averaging 0.973 +/- 0.043 (n = 130). The average value of the extracellular fluid measured in isolated rabbit interventricular septum using Co-EDTA was 0.51 +/- 0.05 ml/g (SD, n = 16) and 0.46 +/- 0.04 ml/g using [14C]sucrose as an extracellular fluid space (ECF) marker. Flushing with a high concentration of nontracer Co-EDTA does not reveal any release from binding sites. The gamma-energy (811 KeV), long half-life (71.4 days), stability, and lack of binding to tissue components make 58Co-EDTA a useful marker for ECF.
1. The washout of (22)Na, (45)Ca and (58)CoEDTA(-) has been observed in arterially perfused rabbit interventricular septa both in the presence and absence of intoxicating doses of the aglycone, 3 acetylstrophanthidin (ACS).2. The washout of (22)Na from paced septa (21.0/min) was rapid with approximately 99% of the exchange occurring in 30 min.3. Septa labelled with (22)Na and washed out in the presence of 10(-5)m-ACS were quiescent, exhibited marked contracture and a slowed (22)Na exchange with 99% of the initial (22)Na leaving the tissue in approximately 200 min.4. Comparison of the washout of the extracellular marker (58)CoEDTA(-) from paced and intoxicated septa revealed no differences, suggesting that regions of the extracellular space had not become inexchangeable as a result of the contracture that these septa exhibited.5. Simultaneous measurements of the distribution of (22)Na and (58)CoEDTA(-) in the presence of 10(-5)m-ACS revealed an apparent cellular Na concentration of 54.8+/-10.4 (s.e.). This was considerably in excess of the maximum amount of Na contributing to the slowest component of Na efflux from intoxicated septa. Origins of this discrepancy are considered.6. The slowest component of (22)Na efflux from intoxicated septa could be markedly stimulated by increasing the external Ca concentration from a nominal 1.5 to 16 mm. The magnitude of stimulation was 44.3+/-7.8% (s.e.). Increases in the concentration of Mg from 1.0 to 16.0 mm were without effect on the (22)Na efflux.7. Application of 10(-5)m-ACS produced marked depolarization of the membrane to new stable levels that lay between -10 and -20 mV.8. Washout of ACS after several hours of intoxication resulted in a partial decline in contracture tension, an acceleration of Ca efflux, little change in (22)Na efflux and a repolarization of the cell membrane.9. Some of the Na and Ca movements reported in this paper have been interpreted by supposing that there is, in this preparation, a coupled exchange of three Na ions for a single Ca ion.