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Vasodilatation, oxygen delivery and oxygen consumption in rat hindlimb during systemic hypoxia: roles of nitric oxide

N. J. Edmunds and Janice M. Marshall

1. We have investigated the relationship between O₂ delivery (D_O2) and O₂ consumption (V_O2) in hindlimb muscle of anaesthetised rats during progressive systemic hypoxia. Since muscle vasodilatation that occurs during hypoxia is nitric oxide (NO) dependent, we examined the effects of the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME).

2. In control rats (n = 8), femoral vascular conductance (FVC) increased at each level of hypoxia. Hindlimb D_O2 decreased with the severity of hypoxia, but muscle V_O2 was maintained until the critical D_O2 value (D_O2,crit) was reached at 0.64 ± 0.06 ml O₂ min^-1 kg^-1; below this V_O2 declined linearly with D_O2. This is a novel finding for the rat but is comparable to the biphasic relationship seen in the dog.

3. In another group of rats (n = 6), L-NAME caused hindlimb vasoconstriction and attenuated the hypoxia-evoked increases in FVC D_O2 was so low after L-NAME administration that V_O2 was dependent on D_O2 at all levels of hypoxia.

4. In a further group (n = 8), femoral blood flow and D_O2 were restored after L-NAME by infusion of the NO donor sodium nitroprusside (20 g kg^-1 min^-1. Thereafter, hypoxia-evoked increases in FVC were fully restored. Nevertheless, D_O2,crit was increased relative to control (0.96 ± 0.07 ml O₂ min^-1 kg^-1, P < 0.01).

5. As NOS inhibition limited the ability of muscle to maintain V_O2 during hypoxia, we propose that hypoxia-induced dilatation of terminal arterioles, which improves tissue O₂ distribution, is mediated by NO. However, since the hypoxia-evoked increase in FVC was blocked by L-NAME but restored by the NO donor, we propose that the dilatation of proximal arterioles is dependent on tonic levels of NO, rather than mediated by NO.

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