Heller L J, Mohrman D E
Department of Physiology, University of Minnesota, Duluth 55812.
J Mol Cell Cardiol. 1988 Jun;20(6):509-23. doi: 10.1016/s0022-2828(88)80078-6.
The adenosine concentration of exudate formed on the surface of isolated perfused rat hearts has been used to obtain estimates of interstitial values. At a constant perfusion of approximately 15 ml/min/g, exudate was collected from below ring seals that either fitted snugly (compressing seals) or that acted as wicks (wicking seals) to deflect venous effluent away from the apical surface. Steady state exudates flows obtained below each of these seals were 0.96 +/- 0.05 ml/min and 0.18 +/- 0.02 ml/min, respectively. Adenosine concentration of surface exudate and venous effluent from hearts with the compressing seal were 130 +/- 8 nM and 23 +/- 3 nM, respectively, and from those with the wicking seal were 770 +/- 93 nM and 36 +/- 9 nM, respectively. Interstitial adenosine concentration in a situation with no net filtration may be slightly higher than that achieved in the exudate from preparations with the wicking seal. Addition of exogenous adenosine to the perfusate (1.0 microM) decreased vascular resistance and automaticity of all preparations, increased the venous effluent adenosine concentration to 236 +/- 18 nM and 251 +/- 30 nM with the compressing and wicking seals, respectively, but did not significantly alter the exudate adenosine concentration with either of the seals. This finding suggests that increases in vascular adenosine may influence functional characteristics without altering interstitial levels. Perfusion with 10 microM adenosine increased adenosine concentration in both effluent and exudate in all preparations but the gradient was reversed so that effluent levels were significantly higher than exudate levels. We conclude that venous adenosine determinations significantly underestimate the interstitial adenosine concentration associated with endogenous adenosine production and significantly overestimate the interstitial levels achieved by infusion of exogenous adenosine.
已利用在离体灌注大鼠心脏表面形成的渗出液中的腺苷浓度来估算组织间隙值。在以约15 ml/min/g的恒定灌注速率下，从紧密贴合（压缩密封）或用作灯芯（灯芯密封）以将静脉流出液从心尖表面引开的环形密封下方收集渗出液。在这些密封中的每一个下方获得的稳态渗出液流速分别为0.96±0.05 ml/min和0.18±0.02 ml/min。带有压缩密封的心脏表面渗出液和静脉流出液中的腺苷浓度分别为130±8 nM和23±3 nM，带有灯芯密封的心脏表面渗出液和静脉流出液中的腺苷浓度分别为770±93 nM和36±9 nM。在无净滤过的情况下，组织间隙腺苷浓度可能略高于灯芯密封制剂渗出液中的浓度。向灌注液中添加外源性腺苷（1.0 μM）可降低所有制剂的血管阻力和自律性，使用压缩密封和灯芯密封时，静脉流出液中的腺苷浓度分别增加至236±18 nM和251±30 nM，但两种密封方式下均未显著改变渗出液中的腺苷浓度。这一发现表明，血管内腺苷的增加可能影响功能特性而不改变组织间隙水平。用10 μM腺苷灌注可使所有制剂的流出液和渗出液中的腺苷浓度均升高，但梯度反转，使得流出液水平显著高于渗出液水平。我们得出结论，静脉腺苷测定显著低估了与内源性腺苷产生相关的组织间隙腺苷浓度，并且显著高估了通过输注外源性腺苷所达到的组织间隙水平。
