Effect of alpha-adrenoreceptor stimulation on the diaphragmatic oxygen delivery-consumption relationship

In the vascularly isolated canine hemidiaphragm, we tested the hypothesis that alpha-adrenoreceptor stimulation may influence diaphragmatic function and O2 extraction during reductions in O2 delivery (QO2di).

The diaphragm was perfused using a constant flow pump with blood diverted from the left femoral artery. QO2di was reduced in a stepwise fashion by progressive reductions in pump flow. The tension generated by the contracting diaphragm (3 Hz), the critical O2 delivery (QO2di,c) below which O2 consumption (VO2di) becomes dependent on O2 supply and the oxygen extraction ratio at this critical point (ERc) were assessed in two groups of animals. Phenylephrine (10(-5) mol/L) was infused into the phrenic artery in one group and saline was infused in another group.

In the contracting diaphragm, VO2di was higher in the phenylephrine infused group than in the control group (5.2 +/- 0.5 vs 2.11 +/- 0.3 mL/min/100 g). QO2di,c and ERc were also higher in the phenylephrine group than in the control group (6.16 +/- 0.43 vs 3.1 +/- 0.5 mL/min/100 g and 0.87 +/- 0.035 vs 0.63 +/- 0.05, respectively). In the resting diaphragm, VO2di was not significantly different between the two groups and no critical oxygen delivery could be identified in either group.

These results indicate that alpha-adrenoreceptor activation may increase the tension generated by the diaphragm as well as its oxygen consumption and oxygen extraction. Although this may be beneficial during moderate reductions in oxygen delivery, in more severe shock states, activation of these receptors by endogenous or exogenously administered catecholamines may hasten the development of delivery limitation of VO2di and compromise the ability to sustain ventilation.