The purpose of this study was to determine whether there are local regions in resting skeletal muscle in which the oxygen delivery is insufficient to support oxidative metabolism. This hypothesis was tested by stopping the blood supply to the exteriorized cat sartorius muscle for 5 min while monitoring NADH fluorescence in localized tissue areas 15-25 microns in diameter. A rise in fluorescence was taken to indicate a shift to anaerobic metabolism. Tissue sites in the arteriolar and venular regions of the capillary network were selected for study. After flow stoppage, fluorescence did not change for an average of 48 +/- 22 (SD) s and then rose over a period of 61 +/- 27 s to an average value 55 +/- 19% above control for arteriolar and venular sites combined. Fluorescence began to rise within 5 s of flow stasis in only 1 of 61 sites and within 10 s in 2 sites. There was no difference in the time course or magnitude of fluorescence changes at arteriolar and venular sites. The data indicate that in resting skeletal muscle, oxygen supply appears sufficient to support oxidative metabolism in over 95% of the tissue.
The objective of the present work was a theoretical evaluation of pial arterial pressures in normotensive rats and spontaneously hypertensive rats based on the geometry and topography of the pial arterial system as well as on various topological models of the vascular trees. Pial branches of the middle cerebral artery in the diameter range of 30-320 microns were selectively visualized by corrosion compound, and the diameter and length of vascular segments were measured. The vessels were classified into branching orders by the methods of Horsfield and Strahler. The steady-state pressure distribution in the pial arterial system was calculated assuming that the flow at the bifurcations was partitioned in proportion to a given power of the diameters of the daughter branches (diameter exponent). The maximum number of vascular segments along the longest branch varied between 16 and 33. The mean branching ratio was 4.14 +/- 0.23 (SD). The mean diameter of vessels classified into Strahler orders 1-5 were: 50 +/- 12, 71 +/- 19, 106 +/- 22, 168 +/- 22, and 191 +/- 7 microns, respectively. The calculated pressure drop in the pial trees of normotensive rats was approximately twice as large in proximal orders 3 and 4 than in distal orders 1 and 2. The mean pressure in arteries of order 1 ranged from 54.4 to 58.4 mm Hg in the normotensive rat (input pressure: 83 mm Hg), and from 77.2 to 89.0 mm Hg in the spontaneously hypertensive rat (input pressure: 110 mm Hg). The coefficient of variation of terminal pressures in vessels of order 1 increased linearly with the mean pressure drop in the system. The coefficient of variation in terminal pressure had a minimum as a function of the diameter exponent in case of each pial tree. At its minimum, it was higher in all spontaneously hypertensive rats (10.1-22.9%) than in any normotensive rats (6.0-8.5%). The corresponding diameter exponents were in most cases lower in the spontaneously hypertensive rat (1.3-2.5) than in the normotensive rat (2.5-3.0). Topologically consistent models of the pial arterial network predicted significantly less variation in intravascular pressures than was obtained by direct calculations. More idealized models suggested the dependence of coefficient of variation in terminal pressure on the total number of vascular segments contained by the tree. All models predicted the existence of the minimum of coefficient of variation in terminal pressure in function of the diameter exponent.(ABSTRACT TRUNCATED AT 400 WORDS)
An in vivo microscope system has been developed that can measure fluorescence emission and/or light absorption at up to five wavelengths in a tissue area of 18-30 microns diam while imaging adjacent microcirculatory vessels with a video system. The system also incorporates a computer-controlled stage and data acquisition system for rapid and repeated measurements from a number of tissue sites. The tissue area monitored for fluorescence or absorption can be defined further by a confocal arrangement of the microscope optics. Tests of the system for NADH fluorescence measurements show good agreement between the fluorescence at 450 nm and NADH concentration in vitro and in skeletal muscle. The instrument can also be used simultaneously for spectrophotometric determination of O2 saturation and hematocrit in microcirculatory vessels. In vitro tests indicate suitable accuracy for such measurements. The open architecture and modular arrangement of the instrument facilitates its use for a variety of simultaneous measurements of parenchymal cell and microcirculatory function.
Tó th A, Pal M, Intaglietta M, Johnson PC. Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle. Am J Physiol Heart Circ Physiol 292: H2643-H2653, 2007. First published February 16, 2007 doi:10.1152/ajpheart.00207.2006.-Elevated blood flow (reactive hyperemia) is seen in many organs after a period of blood flow stoppage. This hyperemia is often considered to be due in part to a shift to anaerobic metabolism during tissue hypoxia. The aim of our study was to test this hypothesis in skeletal muscle. For this purpose we measured NADH fluorescence at localized tissue areas in cat sartorius muscle during and after arterial occlusions of 5-300 s. In parallel studies, red blood cell (RBC) velocity was measured in venules. Tissue NADH fluorescence rose significantly with occlusions of 45 s or greater, reaching a maximum of 44% above control at 180 s. Peak RBC velocity rose to four times control as occlusion duration was increased from 5 to 45 s, but hyperemia duration was stable at ϳ70 s. With occlusions of 45-240 s, hyperemia duration increased progressively to 210 s while peak flow was unchanged. However, after 300-s occlusions, peak flow rose to six times above control and hyperemia duration fell to 140 s. With occlusions of 45-300 s the time integral both of increased NADH fluorescence and of reduced fluorescence following occlusion release showed a high degree of correlation with the additional hyperemia. We conclude that in this muscle anaerobic vasodilator metabolites are responsible for the increase in reactive hyperemia with arterial occlusions longer than 45 s. Since the durations of reactive hyperemia and reduced fluorescence are substantially different, vasodilator metabolite removal may be due to washout by the bloodstream rather than metabolic uptake. anoxia; vasodilator metabolites; metabolic feedback; NADH fluorescence; red blood cell velocity; microcirculation; blood flow regulation REACTIVE HYPEREMIA is the increase in blood flow above resting levels that occurs after a period of blood flow stoppage, usually induced by arterial occlusion. This phenomenon has been demonstrated in a wide variety of vascular beds including skeletal muscle (4), myocardium (9), liver (14), kidney (16), intestine (36), and skin (27). The hyperemia is often attributed to accumulation of vasodilator metabolites produced by anaerobic metabolism during tissue hypoxia (1,13,28,47). However, occlusions of a few seconds' duration also elicit a hyperemic response, although this is too brief to deplete oxygen stores as noted initially by Bayliss in 1902 (3). This finding suggests that other mechanisms such as the myogenic response may contribute, since a fall in intravascular pressure during arterial occlusion would lead to arteriolar relaxation and a subsequent hyperemia when the pressure is restored. Studies on skeletal muscle (21, 25) supported the suggestion that the response following short-term (5-30 s) occlusions in resting skeletal muscle is primarily myogenic. However, with reports of additional flo...
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