Muscle blood flow and functional capillary density evaluated by isotope clearance

1971 ◽  
Vol 322 (3) ◽  
pp. 197-216 ◽  
Author(s):  
R. E. Gosselin ◽  
L. F. Audino
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Capillary Density ◽  
Functional Capillary Density

scholarly journals Reduction of Functional Capillary Density in Human Brain after Stroke

1990 ◽  
Vol 10 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Albert Gjedde ◽  
Hiroto Kuwabara ◽  
Antoine M. Hakim
Keyword(s):  
Blood Flow ◽  
Brain Tissue ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Functional Density ◽  
Hemodynamic Variables ◽  
Cortical Gray Matter ◽  
Cerebral Ischemic ◽  
Reduced Density

The blood flow of brain tissue often returns to normal after an ischemic episode. As “luxury” rather than “reactive” reperfusion, this hyperemia is associated with low metabolism. It is not known to what extent the high blood flow accompanies a high, normal, or low density of capillaries. The resolution of this question may indicate whether the functional capillary density is variable and, if so, whether it is coupled to blood flow or metabolism. To answer these questions, we defined functional capillaries as capillaries that transport glucose. We then calculated the density of functional capillaries ( Dcap) and the mean time of transit of blood through the capillaries ( tcap) from hemodynamic variables obtained in vivo by positron tomography of five patients afflicted by cerebral ischemic stroke. Each patient was studied twice, within 36 h of the insult and 1 week later. We identified nominally “ischemic” regions in the first study as cortical gray matter regions, contiguous with the ischemic focus, in which the magnitude of blood flow did not exceed 20 ml 100 g−1 min−1. In these regions, values of metabolism and functional capillary density were proportionately low compared with normal values obtained in the contralateral hemisphere. The studies revealed a reduction of the functional density of exchange vessels in postischemic brain tissue as soon as 36 h after the insult. In “ischemic” regions, within 36 h of the insult, the net extraction of oxygen was inversely related to the capillary transit time and appeared to be limited mainly by the low functional density of the capillaries. Contrary to expectations, the reduced density persisted, even when more than adequate perfusion of the tissue returned. For these reasons, we concluded that changes of the capillary density were associated with changes of the metabolism of the tissue rather than with blood flow.

Oxidative capacity, blood flow, and capillarity of skeletal muscles

1980 ◽  
Vol 49 (4) ◽  
pp. 627-633 ◽  
Author(s):  
L. C. Maxwell ◽  
T. P. White ◽  
J. A. Faulkner
Keyword(s):  
Blood Flow ◽  
Skeletal Muscles ◽  
Muscle Blood Flow ◽  
Muscle Fibers ◽  
Capillary Density ◽  
Oxidative Capacity ◽  
Histochemical Demonstration ◽  
Capillary Endothelium ◽  
Fiber Types ◽  
Fiber Area

Our purpose was to test the hypothesis that the capillarity of mammalian skeletal muscles is correlated with the oxidate capacity of muscle fibers, or with the capacity for maximum blood flow. Capillarity of skeletal muscles from several species was determined using histochemical demonstration of phosphatase activity of capillary endothelium. Serial sections were incubated for succinate dehydrogenase activity as an indicator of muscle fiber oxidative capacity, and for myofibrillar ATPase activity. three types of muscle fibers were identified. Fiber area was determined by planimetry of projected cross sections. Succinate oxidase activity of whole homogenates was determined by differential respirometry. Muscle blood flow was determined experimentally or data were obtained from the literature. No consistent relation was observed for the different fiber types in the number of adjacent capillaries. Capillary density was negatively correlated with mean fiber area. Among adult animals of several species, skeletal muscles representing a 17-fold range of oxidative capacity demonstrated no relation between capillarity and oxidative capacity or muscle blood flow at maximum oxygen uptake. We find no support for relations between oxidative capacity of muscle blood flow and the capillarity of whole muscle or individual fibers and reject the hypothesis.

scholarly journals Effects of Cilnidipine on Muscle Fiber Composition, Capillary Density and Muscle Blood Flow in Fructose-Fed Rats.

2001 ◽  
Vol 24 (5) ◽  
pp. 565-572 ◽  
Author(s):  
Mikio TAKADA ◽  
Nobuyuki URA ◽  
Katsuhiro HIGASHIURA ◽  
Hideyuki MURAKAMI ◽  
Nobuhiko TOGASHI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Fiber ◽  
Muscle Blood Flow ◽  
Capillary Density ◽  
Fiber Composition

Vasomotion in critically perfused muscle protects adjacent tissues from capillary perfusion failure

2000 ◽  
Vol 279 (2) ◽  
pp. H550-H558 ◽  
Author(s):  
M. Rücker ◽  
O. Strobel ◽  
B. Vollmar ◽  
F. Roesken ◽  
M. D. Menger
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Capillary Flow ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Sprague Dawley ◽  
Capillary Perfusion ◽  
Peripheral Tissues ◽  
Flow Motion ◽  
Stepwise Reduction

We analyzed the incidence and interaction of arteriolar vasomotion and capillary flow motion during critical perfusion conditions in neighboring peripheral tissues using intravital fluorescence microscopy. The gracilis and semitendinosus muscles and adjacent periosteum, subcutis, and skin of the left hindlimb of Sprague-Dawley rats were isolated at the femoral vessels. Critical perfusion conditions, achieved by stepwise reduction of femoral artery blood flow, induced capillary flow motion in muscle, but not in the periosteum, subcutis, and skin. Strikingly, blood flow within individual capillaries was decreased ( P < 0.05) in muscle but was not affected in the periosteum, subcutis, and skin. However, despite the flow motion-induced reduction of muscle capillary blood flow during the critical perfusion conditions, functional capillary density remained preserved in all tissues analyzed, including the skeletal muscle. Abrogation of vasomotion in the muscle arterioles by the calcium channel blocker felodipine resulted in a redistribution of blood flow within individual capillaries from cutaneous, subcutaneous, and periosteal tissues toward skeletal muscle. As a consequence, shutdown of perfusion of individual capillaries was observed that resulted in a significant reduction ( P < 0.05) of capillary density not only in the neighboring tissues but also in the muscle itself. We conclude that during critical perfusion conditions, vasomotion and flow motion in skeletal muscle preserve nutritive perfusion (functional capillary density) not only in the muscle itself but also in the neighboring tissues, which are not capable of developing this protective regulatory mechanism by themselves.

Hemodynamics and O2 uptake during maximal knee extensor exercise in untrained and trained human quadriceps muscle: effects of hyperoxia

2004 ◽  
Vol 97 (5) ◽  
pp. 1796-1802 ◽  
Author(s):  
M. Mourtzakis ◽  
J. González-Alonso ◽  
T. E. Graham ◽  
B. Saltin
Keyword(s):  
Blood Flow ◽  
Peak Power ◽  
Fiber Type ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Capillary Density ◽  
Quadriceps Muscle ◽  
Peak Power Output ◽  
Vascular Conductance ◽  
Type Composition

To elucidate the potential limitations on maximal human quadriceps O2 capacity, six subjects trained (T) one quadriceps on the single-legged knee extensor ergometer (1 h/day at 70% maximum workload for 5 days/wk), while their contralateral quadriceps remained untrained (UT). Following 5 wk of training, subjects underwent incremental knee extensor tests under normoxic (inspired O2 fraction = 21%) and hyperoxic (inspired O2 fraction = 60%) conditions with the T and UT quadriceps. Training increased quadriceps muscle mass (2.9 ± 0.2 to 3.1 ± 0.2 kg), but did not change fiber-type composition or capillary density. The T quadriceps performed at a greater peak power output than UT, under both normoxia (101 ± 10 vs. 80 ± 7 W; P < 0.05) and hyperoxia (97 ± 11 vs. 81 ± 7 W; P < 0.05) without further increases with hyperoxia. Similarly, thigh peak O2 consumption, blood flow, vascular conductance, and O2 delivery were greater in the T vs. the UT thigh (1.4 ± 0.2 vs. 1.1 ± 0.1 l/min, 8.4 ± 0.8 vs. 7.2 ± 0.8 l/min, 42 ± 6 vs. 35 ± 4 ml·min−1·mmHg−1, 1.71 ± 0.18 vs. 1.51 ± 0.15 l/min, respectively) but were not enhanced with hyperoxia. Oxygen extraction was elevated in the T vs. the UT thigh, whereas arteriovenous O2 difference tended to be higher (78 ± 2 vs. 72 ± 4%, P < 0.05; 160 ± 8 vs. 154 ± 11 ml/l, respectively; P = 0.098) but again were unaltered with hyperoxia. In conclusion, the present results demonstrate that the increase in quadriceps muscle O2 uptake with training is largely associated with increases in blood flow and O2 delivery, with smaller contribution from increases in O2 extraction. Furthermore, the elevation in peak muscle blood flow and vascular conductance with endurance training seems to be related to an enhanced vasodilatory capacity of the vasculature perfusing the quadriceps muscle that is unaltered by moderate hyperoxia.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

scholarly journals Endothelial deletion of PKCδ prevents VEGF inhibition and restores blood flow reperfusion in diabetic ischemic limb

2021 ◽  
Vol 18 (2) ◽  
pp. 147916412199903
Author(s):  
Laura Croteau ◽  
Clément Mercier ◽  
Étienne Fafard-Couture ◽  
Alexandre Nadeau ◽  
Stéphanie Robillard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Phosphatase Activity ◽  
Capillary Density ◽  
Artery Ligation ◽  
Vegf Signaling ◽  
Post Surgery ◽  
Src Homology ◽  
Artery Disease ◽  
Ischemic Muscle

Aims: Peripheral artery disease is a complication of diabetes leading to critical hindlimb ischemia. Diabetes-induced inhibition of VEGF actions is associated with the activation of protein kinase Cδ (PKCδ). We aim to specifically investigate the role of PKCδ in endothelial cell (EC) function and VEGF signaling. Methods: Nondiabetic and diabetic mice, with ( ec-Prkcd−/−) or without ( ec-Prkcdf/f) endothelial deletion of PKCδ, underwent femoral artery ligation. Blood flow reperfusion was assessed up to 4 weeks post-surgery. Capillary density, EC apoptosis and VEGF signaling were evaluated in the ischemic muscle. Src homology region 2 domain-containing phosphatase-1 (SHP-1) phosphatase activity was assessed in vitro using primary ECs. Results: Ischemic muscle of diabetic ec-Prkcdf/f mice exhibited reduced blood flow reperfusion and capillary density while apoptosis increased as compared to nondiabetic ec-Prkcdf/f mice. In contrast, blood flow reperfusion and capillary density were significantly improved in diabetic ec-Prkcd−/− mice. VEGF signaling pathway was restored in diabetic ec-Prkcd−/− mice. The deletion of PKCδ in ECs prevented diabetes-induced VEGF unresponsiveness through a reduction of SHP-1 phosphatase activity. Conclusions: Our data provide new highlights in mechanisms by which PKCδ activation in EC contributed to poor collateral vessel formation, thus, offering novel therapeutic targets to improve angiogenesis in the diabetic limb.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document