Oxygen transport during anemic hypoxia in pigs: effects of digoxin on metabolism.
Oxygen transport during anemic hypoxia in pigs: effects of digoxin on metabolism.
复制标题
猪贫血缺氧期间的氧气输送：地高辛对代谢的影响。
DOI：
10.1152/ajpheart.1992.263.1.h208
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Lister,G
中科院分区：
文献类型：
--
作者：
Saltiel,A;Sanfilippo,DJ;Hendler,R;Lister,G
我们测试了地高辛是否可以通过改善外周O2分布或降低O2需求来限制重度贫血期间的组织缺氧。在8头对照猪和8头地高辛给药猪中，红细胞压积（Hct）从27-28%降低至17-18、11-12和7- 8%。在每个Hct下测定全身和后肢血流量、O2转运、O2提取和O2消耗以及血清儿茶酚胺（肾上腺素和去甲肾上腺素）。动脉和股静脉乳酸和氧赤字，以反映组织缺氧。与预期一样，地高辛组的心输出量显著增加（P <0.05），但后肢血流量无差异。此外，两组的全身和后肢O2提取量相同，O2转运水平相似，表明地高辛未改变局部循环中O2流量与代谢的关系。随着全身O2消耗量的下降，对照组比地高辛组积累更多（P <0.05）O2缺乏和动脉乳酸。此外，对照组（y = 1.11 + 0.06x）中乳酸盐相对于O2不足线性增加的斜率比地高辛组（y = 1.36 + 0.02x）陡得多，表明对于相当的O2不足，组织缺氧程度存在差异。这可能归因于儿茶酚胺反应的显著差异：Hct为7-8%时，对照组中肾上腺素较高，Hct为11-12和7- 8%时，去甲肾上腺素较高。地高辛可能抑制了儿茶酚胺的释放或减少了贫血时对儿茶酚胺分泌的刺激。我们推测，地高辛显着改善外周O2的供应和需求之间的平衡，在贫血抑制儿茶酚胺产热，从而降低O2的需求。这可能解释了糖苷类药物在心室功能正常的高输出量心力衰竭中的有益作用。
We tested whether digoxin would limit tissue hypoxia during severe anemia by improving peripheral O2 distribution or decreasing O2 demands. Hematocrit (Hct) was reduced in eight control and eight digoxin-treated pigs from 27-28% to 17-18, 11-12, and 7-8%. Whole body and hindlimb blood flow, O2 transport, O2 extraction, and O2 consumption and serum catecholamines (epinephrine and norepinephrine) were determined at each Hct. Arterial and femoral venous lactate and O2 deficit were obtained to reflect tissue hypoxia. Cardiac output was significantly greater (P less than 0.05) with digoxin, as expected, but there were no differences in hindlimb blood flow. Also, whole body and hindlimb O2 extractions were equal in both groups for similar levels of O2 transport, suggesting that digoxin did not alter the relationship of O2 flow to metabolism in regional circulations. As whole body O2 consumption fell, controls accumulated more (P less than 0.05) O2 deficit and arterial lactate than the digoxin group. Furthermore, the slope demonstrating the linear increase of lactate with respect to O2 deficit was much steeper in controls (y = 1.11 + 0.06x) than in digoxin (y = 1.36 + 0.02x), suggesting that there were differences in the degree of tissue hypoxia for comparable O2 deficit. This may be attributed to the marked differences in catecholamine response: epinephrine was higher in controls at Hct of 7-8% and norepinephrine was higher at Hcts of 11-12 and 7-8%. Digoxin may have inhibited the release of catecholamine or reduced the stimulus for catecholamine secretion during anemia. We speculate that digoxin markedly improved the balance between peripheral O2 supply and demand during anemia by inhibiting catecholamine thermogenesis, thereby decreasing O2 demands. This may explain some of the salutary effects of glycosides in high-output cardiac failure with normal ventricular function.