Premium
Vasodilatation, oxygen delivery and oxygen consumption in rat hindlimb during systemic hypoxia: roles of nitric oxide
Author(s) -
Edmunds N. J.,
Marshall Janice M.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0251g.x
Subject(s) - hypoxia (environmental) , hindlimb , nitric oxide , sodium nitroprusside , endocrinology , vasodilation , medicine , nitric oxide synthase , vasoconstriction , chemistry , oxygen , anesthesia , biology , organic chemistry
1 We have investigated the relationship between O 2 delivery ( D O2 ) and O 2 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 O 2 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 μg 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 O 2 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 O 2 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.