AJP - Heart and Circulatory Physiology, Vol 272, Issue 6 2757-H2764, Copyright © 1997 by American Physiological Society

ARTICLES

Capillary red blood cell flow and activation of white blood cells in chronic muscle ischemia in the rat

S. I. Anderson, O. Hudlicka and M. D. Brown
Department of Physiology, University of Birmingham, United Kingdom.

Increased activity of ischemic skeletal muscles in which functional hyperemia is impaired has been linked with capillary endothelial swelling postcapillary white blood cell (WBC) adherence. The perfusion pattern of capillaries under these conditions and time course of WBC activation is not known. Capillary microcirculation was studied by videomicroscopy at rest and after muscle contractions (1 Hz, 10 min) in extensor digi-torum longus muscles of pentobarbital sodium-anesthetized rat during the early stages of chronic ischemia (unilateral ligation of the common iliac artery for 3 days) and in ischemic muscles subjected to increased activity (7 days of ischemia or 3 days of ischemia plus indirect electrical stimulation via planted electrodes, 10 Hz, 7 x 10 min on-90 min off/day) to investigate how perfusion was affected. All ischemic muscles had more intermittently flowing capillaries than did unoperated control) muscles. Temporal heterogeneity of perfusion at rest, assessed by velocity, time spent stationary, and stop/start frequency of red blood cells, was similar to control values in ischemic muscles but greater in ischemic muscles subjected to additional activity. Hyperemic responses to contractions were severely blunted in all ischemic groups. The portion of morphologically nonspherical WBCs, taken to indicate activation, was 24 +/- 3% in venous blood after 3 days of ischemia vs. 14 +/- 1% in control muscles and increased further by 7 days (42 +/- 2%) when activated cells were also found in arterial blood. Thus increased muscular activity may exacerbate the adverse effects of ischemia on capillary perfusion, and WBC activation, evident before endothelial swelling is apparent, provides the potential as a circulating signal for capillary swelling in the ischemic and other muscles.

This article has been cited by other articles:

				O. Hudlicka, A. Garnham, R. Shiner, and S. Egginton Attenuation of changes in capillary fine structure and leukocyte adhesion improves muscle performance following chronic ischaemia in rats J. Physiol., October 15, 2008; 586(20): 4961 - 4975. [Abstract] [Full Text] [PDF]

				D. C. Poole, M. D. Brown, and O. Hudlicka Counterpoint: There is not capillary recruitment in active skeletal muscle during exercise J Appl Physiol, March 1, 2008; 104(3): 891 - 893. [Full Text] [PDF]

				T. Loizidis, A. Sioga, L. Economou, A. Frosinis, A. Kyparos, A. Zotou, and M. Albani The role of ascorbic acid and exercise in chronic ischemia of skeletal muscle in rats J Appl Physiol, January 1, 2007; 102(1): 321 - 330. [Abstract] [Full Text] [PDF]

				M. Milkiewicz, O. Hudlicka, M. D. Brown, and H. Silgram Nitric oxide, VEGF, and VEGFR-2: interactions in activity-induced angiogenesis in rat skeletal muscle Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H336 - H343. [Abstract] [Full Text] [PDF]