https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38581 Wed 23 Feb 2022 15:53:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:665 Thu 25 Jul 2013 09:10:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12687 Sat 24 Mar 2018 08:16:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12662 35 mm Hg) in the rabbit, muscle blood flow did not change, although cardiac output increased. During moderate hypoxia (Po₂ 30 - 35 mm Hg) there was initial vasoconstriction in muscle, followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (Po₂ < 30 mm Hg) the initial vasoconstriction was less marked, and during the 'steady state' there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated. 3. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation. 4. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia. The peripheral dilator (β-)effects of adrenaline oppose the peripheral constrictor (α-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxia.]]> Sat 24 Mar 2018 08:15:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12658 Sat 24 Mar 2018 08:15:48 AEDT ]]>