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Influence of Experimental Edema on Metabolically Determined Blood Flow

To evaluate the effects of edema and elevated tissue pressure on metabolically determined blood flow, forelimb vascular resistance was determined by two techniques. Peak reactive hyperemic blood flow after release of a 5-minute arterial occlusion was bilaterally measured in the brachial arteries of...

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Published in:Circulation research 1974-04, Vol.34 (4), p.482-490
Main Authors: ZELIS, ROBERT, LEE, GARRETT, MASON, DEAN T
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MASON, DEAN T
description To evaluate the effects of edema and elevated tissue pressure on metabolically determined blood flow, forelimb vascular resistance was determined by two techniques. Peak reactive hyperemic blood flow after release of a 5-minute arterial occlusion was bilaterally measured in the brachial arteries of 11 dogs before and after venous congestion of one limb for 4 hours at 70 mm Hg and after infusion of 1,000 ml of 6% Dextran 70. Before determining peak reactive hyperemic blood flow, congestion was released; venous pressure was then similar in both limbs. Congestion reduced peak reactive hyperemic blood flow from 23.9 ± 5.7 (SE) to 16.0 ± 3.6 ml/min 100 g (P < 0.05). Peak reactive hyperemic blood flow was unchanged in the uncongested control limb (21.2 ± 5.2 to 20.4 ± 4.5 ml/min 100 g, P > 0.5) at the time when it was reduced in the congested limb. Total tissue pressure measured with a needle was greater in the congested limb (9.1 ± 1.7 mm Hg) than it was in the uncongested limb (2.5 ± 1.5 mm Hg, P < 0.01). Likewise, pressure in a chronically implanted perforated capsule was −2.1 ± 2.0 mm Hg in the control limb but was +7.2 ± 1.5 mm Hg (P < 0.01) in the contralateral limb following congestion. Dextran 70 was infused after venous congestion; this procedure produced peak reactive hyperemic blood flows and tissue pressures which were similar in both limbs. Similarly, minimum vascular resistance following an ischemic stimulus in an isolated, denervated constant-perfused forelimb was increased from 17.7 ± 2.2 to 23.9 ± 1.8 mm Hg/ml min 100 g (P < 0.01) following congestion in five dogs. Brachial arterial sodium content was unchanged in four dogs following 4 hours of congestion. These data suggest that, in the presence of edema, metabolic arteriolar dilation may be impaired.
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Peak reactive hyperemic blood flow after release of a 5-minute arterial occlusion was bilaterally measured in the brachial arteries of 11 dogs before and after venous congestion of one limb for 4 hours at 70 mm Hg and after infusion of 1,000 ml of 6% Dextran 70. Before determining peak reactive hyperemic blood flow, congestion was released; venous pressure was then similar in both limbs. Congestion reduced peak reactive hyperemic blood flow from 23.9 ± 5.7 (SE) to 16.0 ± 3.6 ml/min 100 g (P &lt; 0.05). Peak reactive hyperemic blood flow was unchanged in the uncongested control limb (21.2 ± 5.2 to 20.4 ± 4.5 ml/min 100 g, P &gt; 0.5) at the time when it was reduced in the congested limb. Total tissue pressure measured with a needle was greater in the congested limb (9.1 ± 1.7 mm Hg) than it was in the uncongested limb (2.5 ± 1.5 mm Hg, P &lt; 0.01). Likewise, pressure in a chronically implanted perforated capsule was −2.1 ± 2.0 mm Hg in the control limb but was +7.2 ± 1.5 mm Hg (P &lt; 0.01) in the contralateral limb following congestion. Dextran 70 was infused after venous congestion; this procedure produced peak reactive hyperemic blood flows and tissue pressures which were similar in both limbs. Similarly, minimum vascular resistance following an ischemic stimulus in an isolated, denervated constant-perfused forelimb was increased from 17.7 ± 2.2 to 23.9 ± 1.8 mm Hg/ml min 100 g (P &lt; 0.01) following congestion in five dogs. Brachial arterial sodium content was unchanged in four dogs following 4 hours of congestion. 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Peak reactive hyperemic blood flow after release of a 5-minute arterial occlusion was bilaterally measured in the brachial arteries of 11 dogs before and after venous congestion of one limb for 4 hours at 70 mm Hg and after infusion of 1,000 ml of 6% Dextran 70. Before determining peak reactive hyperemic blood flow, congestion was released; venous pressure was then similar in both limbs. Congestion reduced peak reactive hyperemic blood flow from 23.9 ± 5.7 (SE) to 16.0 ± 3.6 ml/min 100 g (P &lt; 0.05). Peak reactive hyperemic blood flow was unchanged in the uncongested control limb (21.2 ± 5.2 to 20.4 ± 4.5 ml/min 100 g, P &gt; 0.5) at the time when it was reduced in the congested limb. Total tissue pressure measured with a needle was greater in the congested limb (9.1 ± 1.7 mm Hg) than it was in the uncongested limb (2.5 ± 1.5 mm Hg, P &lt; 0.01). Likewise, pressure in a chronically implanted perforated capsule was −2.1 ± 2.0 mm Hg in the control limb but was +7.2 ± 1.5 mm Hg (P &lt; 0.01) in the contralateral limb following congestion. Dextran 70 was infused after venous congestion; this procedure produced peak reactive hyperemic blood flows and tissue pressures which were similar in both limbs. Similarly, minimum vascular resistance following an ischemic stimulus in an isolated, denervated constant-perfused forelimb was increased from 17.7 ± 2.2 to 23.9 ± 1.8 mm Hg/ml min 100 g (P &lt; 0.01) following congestion in five dogs. Brachial arterial sodium content was unchanged in four dogs following 4 hours of congestion. 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Peak reactive hyperemic blood flow after release of a 5-minute arterial occlusion was bilaterally measured in the brachial arteries of 11 dogs before and after venous congestion of one limb for 4 hours at 70 mm Hg and after infusion of 1,000 ml of 6% Dextran 70. Before determining peak reactive hyperemic blood flow, congestion was released; venous pressure was then similar in both limbs. Congestion reduced peak reactive hyperemic blood flow from 23.9 ± 5.7 (SE) to 16.0 ± 3.6 ml/min 100 g (P &lt; 0.05). Peak reactive hyperemic blood flow was unchanged in the uncongested control limb (21.2 ± 5.2 to 20.4 ± 4.5 ml/min 100 g, P &gt; 0.5) at the time when it was reduced in the congested limb. Total tissue pressure measured with a needle was greater in the congested limb (9.1 ± 1.7 mm Hg) than it was in the uncongested limb (2.5 ± 1.5 mm Hg, P &lt; 0.01). Likewise, pressure in a chronically implanted perforated capsule was −2.1 ± 2.0 mm Hg in the control limb but was +7.2 ± 1.5 mm Hg (P &lt; 0.01) in the contralateral limb following congestion. Dextran 70 was infused after venous congestion; this procedure produced peak reactive hyperemic blood flows and tissue pressures which were similar in both limbs. Similarly, minimum vascular resistance following an ischemic stimulus in an isolated, denervated constant-perfused forelimb was increased from 17.7 ± 2.2 to 23.9 ± 1.8 mm Hg/ml min 100 g (P &lt; 0.01) following congestion in five dogs. Brachial arterial sodium content was unchanged in four dogs following 4 hours of congestion. These data suggest that, in the presence of edema, metabolic arteriolar dilation may be impaired.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>4826925</pmid><doi>10.1161/01.RES.34.4.482</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Blood Flow Velocity
Brachial Artery - metabolism
Denervation
Dextrans - pharmacology
Dilatation
Dogs
Edema - physiopathology
Forelimb - blood supply
Forelimb - innervation
Heart Failure - physiopathology
Hyperemia
Regional Blood Flow
Sodium - metabolism
Vascular Resistance - drug effects
Venous Pressure
title Influence of Experimental Edema on Metabolically Determined Blood Flow
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