cain1981

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<p>Adv. Physiol. Sci. Vol. 25. Oxygen Transport to Tissue</p><p>A. G. B. Kovach, E. Dora, M. Kessler, I. A. Silver (eds)</p><p>Vasodilatation in the hindlimb that usually resulted from prolonged</p><p>and severe hypoxia was prevented in anesthetized dogs given the ^-blocker</p><p>propranolol (Cain and Chapler, 1979). In other dogs given the a-blocker</p><p>phenoxybenzamine, it appeared that reoxygenation shut off chemoreflex</p><p>stimulation of 3-vasodilators whose action had been unmasked by a-block</p><p>(Cain and Chapler, 1980). The results suggested that neural vasodilatation</p><p>was more evident than that arising from any local factors resulting from</p><p>hypoxia. To test this hypothesis, we denervated the hindlimb of anesthe-</p><p>tized dogs and made them hypoxic.</p><p>METHODS: In 10 anesthetized and paralyzed dogs ventilated by pump, the</p><p>venous outflow of the intact left hindlimb less the paw was isolated to the</p><p>femoral vein. Isolation was verified by quantitative collection of dye</p><p>injected into the artery. Limb blood flow and oxygen uptake (V02)> total</p><p>V02 and cardiac output were measured and reported per kg of either muscle</p><p>weight in the limb or body weight. Vascular resistances were expressed as</p><p>the quotient of mean arterial pressure and flow. The hindlimb was dener-</p><p>vated by cutting the sciatic and femoral nerves. After a 40-min control</p><p>period breathing air, the dogs were ventilated at the same rate for 20 min</p><p>using 9.1% oxygen and then for 40 min on air again. A second group of 10</p><p>was treated the same but the hindlimb was not denervated.</p><p>RESULTS: With the exception of a significantly greater V02 in the dener-</p><p>vated group ( D ) , the whole body measurements during the control period were</p><p>comparable. Limb blood flow, vascular resistance, and oxygen extraction</p><p>all differed significantly between the groups as a result of the denerva-</p><p>tion. Hypoxia lowered arterial P02 from 10.9 ± 1 . 1 kPa to 3.0 ± 0.2 kPa in</p><p>the innervated group (I) and from 11.0 ± 0.7 to 3.1 ± 0.3 kPa in the D</p><p>group. Femoral venous P02 during hypoxia was 1.8 ± 0.3 and 2.0 ± 0.-4 kPa</p><p>respectively in the I and D groups. Both total and limb V02 were signifi-</p><p>cantly decreased by hypoxia in both groups. Limb resistances of both groups</p><p>are shown in Fig. 1 for the last 5 min of normoxia during the control period,</p><p>the first and last 5 min of hypoxia, and the first 5 min of normoxic re-</p><p>covery. A prompt increase was seen in the I group with a slower and lesser</p><p>increase in the D group as the animals became hypoxic. During the inter-</p><p>vening 10 min of hypoxia, limb resistance in the D group continued to in-</p><p>crease but was always significantly lower than in the I group. When the</p><p>animals were returned to breathing room air, there was a marked transient</p><p>hyperemia and fall in limb resistance in the I group but there was no</p><p>233</p><p>RESISTANCE TO BLOOD FLOW IN</p><p>DENERVATED CANINE HIND LI MB</p><p>DURING HYPOXIA</p><p>S t e p h e n M . Ca in a n d C h r i s t o p h e r K. Chapter</p><p>Departments of Physiology, University of Alabama in Birmingham, Birmingham, Alabama 35294 USA</p><p>and</p><p>Queen's University, Kingston, Ontario K7L 3N6, Canada</p><p>significant change during the first minutes of recovery in the D group.</p><p>Fig. 1: Changes in limb vascular resistance with onset and relief of</p><p>hypoxia.</p><p>DISCUSSION: The significant difference in total V02 between the two groups</p><p>during the control period may have been attributable to the central stim-</p><p>ulation caused by denervating the limb. The increased flow, and decreased</p><p>02 extraction ratio and resistance in the limbs of the denervated group</p><p>reflected the loss of vasoconstrictor tone which is normally present. With</p><p>the onset of hypoxia, vasoconstrictor tone was increased in the limbs of</p><p>the I group by chemoreflex activity. In the D group, flow changed propor-</p><p>tionately to arterial pressure at first but the resistance began to* in-</p><p>crease significantly by the 4th and 5th minutes of hypoxia. This may have</p><p>been the autoregulatory response to the increased arterial pressure caused</p><p>by making the whole animal hypoxic. Of most interest was the absence of</p><p>any sharp fall in limb resistance in the D group upon return to room air.</p><p>Since they had been just as hypoxic for just as J o n g as the I group and</p><p>since both groups sustained a decrease in limb V02 during hypoxia, local</p><p>vasodilator factors should have been present in equal amounts in both</p><p>groups. The hyperemic response and fall in limb resistance in the I group</p><p>is usually explained as a washing out of local vasodilator substances as</p><p>the dominant vasoconstrictor tone was removed by increase in P02 at the</p><p>peripheral chemoreceptor. Either denervation somehow prevented the accumu-</p><p>lation of any local factors or posthypoxic hyperemia and dilatation were</p><p>more a central and chemoreflex phenomenon. Because the delayed increase</p><p>in limb resistance was similar in both groups and probably was due to a</p><p>washout of vasodilator substance, the latter reason appears more plausible.</p><p>REFERENCES:</p><p>Cain, S.M. and C.K. Chapler (1979) Oxygen extraction by canine hindlimb</p><p>during hypoxic hypoxia. J, Appl. Physiol. 46: 1023-1028.</p><p>Cain, S.M. and C.K. Chapler (1980) O2 extraction by canine hindlimb</p><p>during a-adrenergic blockade and hypoxic hypoxia. J. Appl. Physiol. 48:</p><p>(in press).</p><p>234</p>