The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

Chalmers, John; Korner, Paul I.; White, Saxon William

doi:10.1113/jphysiol.1966.sp007942

Cited by 30 publications

(46 citation statements)

References 39 publications

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“…Importantly, the metabolic cost of sodium reabsorption, as assessed by the quotient of sodium reabsorption and V O 2 , was not altered even during severe hypoxemia, reflecting the dependence of the bulk of renal sodium transport on aerobic metabolism (11,18). The fall in glomerular filtration rate during severe hypoxemia in the renal preparation is likely because of the associated fall in arterial pressure, which in turn can be explained by the local effect of hypoxia to induce vasodilation, particularly in skeletal muscle (4). The absence of a depressor response to ventilation with 11% oxygen in the hindlimb preparation presumably reflects the fact that these animals became less hypoxemic than the animals in which the kidney was studied.…”

Section: Discussionmentioning

confidence: 98%

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Evans

Goddard

Eppel

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Evans RG, Goddard D, Eppel GA, O'Connor PM. Factors that render the kidney susceptible to tissue hypoxia in hypoxemia. Am J Physiol Regul Integr Comp Physiol 300: R931-R940, 2011. First published January 19, 2011 doi:10.1152/ajpregu.00552.2010To better understand what makes the kidney susceptible to tissue hypoxia, we compared, in the rabbit kidney and hindlimb, the ability of feedback mechanisms governing oxygen consumption (V O2) and oxygen delivery (DO 2 ) to attenuate tissue hypoxia during hypoxemia. In the kidney (cortex and medulla) and hindlimb (biceps femoris muscle), we determined responses of whole organ blood flow and V O2, and local perfusion and tissue PO2, to reductions in DO2 mediated by graded systemic hypoxemia. Progressive hypoxemia reduced tissue PO2 similarly in the renal cortex, renal medulla, and biceps femoris. Falls in tissue PO2 could be detected when arterial oxygen content was reduced by as little as 4 -8%. V O2 remained stable during progressive hypoxemia, only tending to fall once arterial oxygen content was reduced by 55% for the kidney or 42% for the hindlimb. Even then, the fall in renal V O2 could be accounted for by reduced oxygen demand for sodium transport rather than limited oxygen availability. Hindlimb blood flow and local biceps femoris perfusion increased progressively during graded hypoxia. In contrast, neither total renal blood flow nor cortical or medullary perfusion was altered by hypoxemia. Our data suggest that the absence in the kidney of hyperemic responses to hypoxia, and the insensitivity of renal V O2 to limited oxygen availability, contribute to kidney hypoxia during hypoxemia. The susceptibility of the kidney to tissue hypoxia, even in relatively mild hypoxemia, may have important implications for the progression of kidney disease, particularly in patients at high altitude or with chronic obstructive pulmonary disease. hyperemia; hypoxia; ischemia; kidney circulation; oxygen tension; skeletal muscle ONE OF THE GREAT PARADOXES of physiology is the susceptibility of the kidney to tissue hypoxia. The kidneys are among the most highly perfused organs in the body, receiving approximately one-quarter of the cardiac output at rest yet comprise Ͻ1% of total body weight (14). Thus renal oxygen delivery (DO 2 ) greatly exceeds oxygen consumption (V O 2 ). Yet the kidney is extremely susceptible to hypoxic damage, which in turn appears to be a crucial event in the pathogenesis of chronic kidney disease (8,19,32,35) and acute kidney injury (7, 20, 24) of diverse etiology. Therefore, it is imperative that we improve our understanding of the structural and functional characteristics of the kidney that make it susceptible to development of hypoxia.Most organs respond to a reduction in oxygenation by increasing local blood flow and so DO 2 (14). The increased DO 2 then acts to increase tissue oxygenation and so attenuate development of hypoxia and tissue injury. In this regard, the control of blood flow to the kidney is unique in that it appears to be dominated by the func...

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Section: Discussionmentioning

confidence: 98%

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Evans

Goddard

Eppel

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The renal and portal catheters were inserted by direct puncture of the vessel wall, and were fixed by means of the tissue adhesive methyl 2-cyanoacrylate or isobutyl acrylate (Ethicon Inc. Sommerville, N.J., U.S.A.). Details of the operative procedure have been described elsewhere (Chalmers et al 1966;White, Chalmers, Hilder & Korner, 1967). Experiments were carried out in normal animals 3-5 days after the preliminary operation when they had fully recovered.…”

Section: Methodsmentioning

confidence: 99%

“…Local thermodilution curves were recorded after rapid injection of room temperature injectate about 11-12 mm upstream from the thermistor using a mechanical injector. Flow in the various veins was calculated using the formulae and corrections described previously (Chalmers et al 1966;White et al 1967). Muscle blood flow was estimated as the difference between iliac vein flow (assumed to equal total hindlimb flow) and limb skin flow.…”

Section: Methodsmentioning

confidence: 99%

Local and reflex factors affecting the distribution of the peripheral blood flow during arterial hypoxia in the rabbit

Chalmers

Korner²,

White³

1967

The Journal of Physiology

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SUMMARY1. The effects of severe arterial hypoxia on the blood flow in the portal vein, and in kidney, muscle and skin beds have been determined in normal unanaesthetized rabbits, in animals without functioning autonomic effectors, and in rabbits with section of the carotid sinus and aortic nerves.2. The resting blood flows in the above regions were not significantly different in the three groups.3. The susceptibilities of the various beds to the local dilator effects of arterial hypoxia (assessed from the responses of animals without functioning autonomic effectors) were markedly different; vasodilatation was by far the greatest in the portal bed, followed in order by the renal, skin and muscle beds.4. Section of the carotid sinus and aortic nerves completely abolished reflex activity, and the pattern of peripheral blood flow changes was similar to that of animals without functioning autonomic effectors. The findings suggest that the arterial chemoreceptors are the primary afferent source of reflex control of the peripheral circulation in arterial hypoxia.5. In normal animals with intact reflexes there was sustained vasoconstriction throughout the treatment period in the portal and renal bed. The net vasomotor effects in muscle and limb skin were small owing to the operation of a number of factors, which opposed the effects of reflexly increased sympathetic nerve activity.

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“…6). It seems probable therefore that the increase in sympathetic vasoconstrictor activity to the ear during arterial hypoxia must normally be small and much less marked than to the hind-limb skin, or to muscle (Chalmers et al 1966).…”

Section: Introductionmentioning

confidence: 99%

“…The preliminary operations for the insertion of an aortic thermistor catheter, for transposition of the trachea, for bilateral adrenalectomy, for lumbar sympathectomy, and for section of the carotid sinus and aortic nerves were carried out as described elsewhere (Komer, 1965b;White, 1966;Komer &White, 1966;Chalmers, Komer & White, 1966). On the day of the experiment, catheterization of the central ear artery and insertion of a tracheotomy tube were carried out using local anaesthesia exactly as described previously (Korner, 1965b;Chalmers et al 1966). …”

Section: Introductionmentioning

confidence: 99%

Effects of arterial hypoxia on the cutaneous circulation of the rabbit

Chalmers

Korner²

1966

The Journal of Physiology

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SUMIARY1. Changes in blood flow of the skin of the rabbit's ear and hind limb have been studied during arterial hypoxia by a calibrated heat conductivity method, together with changes in arterial pressure and aortic blood temperature.2. There is little change in the blood flow of the hind-limb skin during the early phase of arterial hypoxia, reflecting a balance between the local dilator effects of hypoxia and the increased constrictor activity mediated through the sympathetic nerves as a result of arterial chemoreceptor excitation. During more prolonged arterial hypoxia there is a small gradual dilatation of the vessels of the hind-limb skin as a result of some diminution in the initial intensity of vasoconstrictor activity.3. There is much more extensive vasodilatation in the ear than in the hind-limb skin during arterial hypoxia. Vasoconstrictor activity is slight in this region. Comparison of the ear responses to arterial and to primary tissue hypoxia suggests that in the former type of hypoxia stimulation of the arterial chemoreceptors inhibits thermoregulatory vasoconstriction to the ear, whilst in the latter type of hypoxia baroreceptor reflexes maintain or intensify it.

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The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

Cited by 30 publications

References 39 publications

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Local and reflex factors affecting the distribution of the peripheral blood flow during arterial hypoxia in the rabbit

Effects of arterial hypoxia on the cutaneous circulation of the rabbit

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