Effects of emphysema on diaphragm microvascular oxygen pressure

Pulmonary emphysema impairs lung and respiratory muscle function leading to restricted physical capacity and accelerated morbidity and mortality conse quent to respiratory muscle failure. In the absence of direct evidence, an O-2 supply-demand imbalance within the diaphragm and other respiratory musc les in emphysema has been considered the most likely explanation for this f ailure. To test this hypothesis, we utilized phosphorescence quenching tech niques to measure mean microvascular PO2 (Po(2)m) within the medial costal diaphragm of control (C, n = 10) and emphysematous (E, elastase instilled, n = 7) hamsters. Po(2)m and mean arterial pressure (MAP) were measured in t he spontaneously breathing anesthetized hamster at inspired O-2 percentages of 10, 21, and 100, and across a range of mean MAPs from 40 to 115 mm Hg. At each inspired O-2, diaphragm Po(2)m was significantly (p < 0.05) lower i n E animals (10%: C, 19 +/- 3; E, 9 +/- 2; 21%: C, 32 +/- 2; E, 21 +/-: 2; 100%: C, 60 +/- 8; E, 36 +/- 9 mm Hg). At 21% inspired O-2, the Po,m decrea se was correlated with reduced MAP in both C (r = 0.968) and E (r = 0.976) animals. We conclude that diaphragmatic Po,m (and therefore microvascular O -2 content) is decreased in emphysematous hamsters reflecting a greater dia phragmatic O-2 utilization at rest and a lower O-2 extraction reserve. Acco rding to Fick's law, this lower Po(2)m will mandate an exaggerated fall in intramyocyte Po(2)m, which is expected to accelerate muscle glycogen deplet ion and consequently fatigue. This provides empirical evidence in support o f one possible mechanism for respiratory muscle failure in emphysema.