Heineman F W, Kupriyanov V V, Marshall R, Fralix T A, Balaban R S
Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Am J Physiol. 1992 Jan;262(1 Pt 2):H255-67. doi: 10.1152/ajpheart.1992.262.1.H255.
Myocardial O2 consumption (MVO2) was stimulated up to two-fold by either increasing afterload or beta-receptor stimulation in working normothermic isolated rabbit hearts while noninvasively monitoring the O2 delivery or phosphate compounds (total n = 48). Intracellular O2 delivery was estimated with the use of myocardial optical absorbance changes centered at 603.5 and 582 nm that correlate with cytochrome aa3 redox and myoglobin oxygenation states. Phosphate-containing metabolites (ATP, phosphocreatine, free ADP) were assessed using 31P nuclear magnetic resonance spectroscopy. Measurements were made both with intact autoregulation and after maximal vasodilation by 1 microM nitroprusside (NP). When afterload was used to increase MVO2, absorbance decreased at 603.5 nm and increased at 582 nm, consistent with a 10-15% increase in myocardial oxygenation, without an associated change in cardiac phosphate compounds. NP caused a further increase in myocardial oxygenation and venous PO2 consistent with an increase in the O2 supply-to-demand ratio. Increases in MVO2 due to beta-stimulation alone were not associated with changes in 603.5-nm absorbance or phosphate compounds, but in combination with NP were accompanied by increased oxygenation, venous PO2, and cardiac phosphocreatine. KCl arrest caused maximal increases in oxygenation and phosphocreatine. These findings suggest that neither cytochrome aa3 nor myoglobin in the isolated working rabbit heart is fully oxidized or oxygenated, respectively. Furthermore, the oxygenation state of the tissue varied both with afterload-induced changes in cardiac work and with changes in O2 supply/demand.
在正常体温下工作的离体兔心脏中，通过增加后负荷或β受体刺激，心肌耗氧量（MVO2）可被刺激增加至两倍，同时无创监测氧输送或含磷化合物（共48例）。利用以603.5和582nm为中心的心肌光吸收变化来估计细胞内氧输送，这些变化与细胞色素aa3氧化还原状态和肌红蛋白氧合状态相关。使用31P核磁共振波谱评估含磷代谢物（ATP、磷酸肌酸、游离ADP）。在完整的自动调节状态下以及在1μM硝普钠（NP）最大程度血管舒张后进行测量。当使用后负荷增加MVO2时，603.5nm处的吸光度降低，582nm处的吸光度增加，这与心肌氧合增加10 - 15%一致，而心脏含磷化合物没有相关变化。NP导致心肌氧合和静脉血氧分压进一步增加，这与氧供需比增加一致。仅由β刺激引起的MVO2增加与603.5nm吸光度或含磷化合物的变化无关，但与NP联合使用时，伴随着氧合增加、静脉血氧分压增加以及心脏磷酸肌酸增加。氯化钾停搏导致氧合和磷酸肌酸最大程度增加。这些发现表明，在离体工作的兔心脏中，细胞色素aa3和肌红蛋白分别没有完全被氧化或氧合。此外，组织的氧合状态随后负荷引起的心脏工作变化以及氧供需变化而变化。
