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K Tyml

Publications and source records attributed to K Tyml.

At least 37 records · Page 2Linked to original sources
PubMed1995

Microvascular response to ischemia, and endothelial ultrastructure, in disused skeletal muscle.

It has previously been demonstrated that muscle atrophy associated with aging and disuse is accompanied by changes in microvascular function including absolute loss of capillaries, increased mean red blood cell velocity (VRBC), and absence of reactive hyperemia. The purpose of the present study was to determine whether disuse could account for these changes. The right extensor digitorum longus muscle in male Fisher 344 rats was subjected to 15 days of disuse through the neural application of tetrodotoxin (TTX). Microvascular function, as assessed using intravital microscopy, was compared for muscles from control (n = 8) and TTX-treated (n = 5) animals. The TTX-induced disuse was associated with a 40.5% decrease in muscle weight, a 51.6% decrease in fiber cross-sectional area, a 62% decrease in mitochondrial volume density, and increased capillary damage (TTX, 11% control, 1.1%). Although capillary density in the disused muscle increased (by 139%), when corrected for muscle atrophy, the absolute number of capillaries was maintained. With TTX disuse, VRBC heterogeneity was not different from that in the control rats while the mean velocity increased 3.18x. TTX disuse did not alter the pattern of reactive hyperemia following 30 min of complete ischemia. These results suggest that short-term TTX-induced atrophy affects both microvascular structure and resting state blood flow in rat skeletal muscle, but it does not affect the vascular responsiveness following a metabolic challenge.

Animals↗
PubMed1995

Heterogeneity of red blood cell velocity in skeletal muscle decreases with increased flow.

OBJECTIVE: Effective material exchange between blood and tissue depends on the heterogeneity of microvascular flow. The objective was to address inconsistencies between intravital studies regarding this dependency. We tested the hypothesis that heterogeneity of red blood cell velocity (VRBC) in capillary beds varies with the strength of metabolic stimulus and with capillary bed geometry. METHODS: We used videomicroscopy to measure VRBC in a bed of 10-24 capillaries at the surface of extensor digitorum longus (EDL) muscle in anesthetized rats. The coefficient of variation (CV = standard deviation/mean; an index of spatial heterogeneity) was computed in the same bed before and after (i) 1, 2, 4, or 8 Hz supramaximal muscle contraction or (ii) adenosine superfusion (10(-7)-10(-3) M). Beds with or without arteriolar-venular capillary shunts were used. RESULTS: Although control VRBC differed between beds (shunt: 232 microns/s; no shunt: 130 microns/s), the percentage increases in postcontraction VRBC did not (range: 111-326%). In both beds, control CV varied greatly (overall range: 28-117%) and 2-8 Hz muscle contractions reduced CV significantly by 25%. Similar results were obtained for adenosine. In confirmatory experiments using the rat cremaster muscle, contractions (4 Hz) and adenosine (10(-4) M) also reduced CV. Based on all data, CV = 63-0.022 VRBC (r = 0.82, P < 0.001). CONCLUSIONS: The heterogeneity of VRBC decreased with metabolic stress, regardless of capillary bed geometry. We propose that both the large variability in control CV and the relatively shallow dependence of CV on velocity could be responsible for the present inconsistencies between intravital studies.

Analysis of Variance↗
PubMed1994

Evaluation of pulsatile and nonpulsatile flow in capillaries of goat skeletal muscle using intravital microscopy.

It is commonly believed that pulsatile flow generated by the pumping action of the heart is dampened out by the time it reaches the microcirculation. In clinical practice, most of the cardiopulmonary bypass pumps and ventricular assist devices are nonpulsatile. To test the hypothesis that pulsatile flow generated by the heart does exist at the microvascular level, intravital microscopy of a large animal model (goat) was developed to visualize and to videorecord the surface microcirculation of the flexor carpi ulnaris muscle from the right forelimb. Density of perfused capillaries and red blood cell velocity in capillaries were measured in five goats during pulsatile perfusion provided by the heart and during a subsequent 3-hr period of nonpulsatile perfusion provided by a centrifugal ventricular assist device (Centrimed, Sarns 3M) that bypassed the heart. Throughout the experiment, the heart rate, innominate artery mean blood pressure, and flow remained unchanged. During the pulsatile regimen, velocities showed regular fluctuations that coincided with the period of the cardiac cycle (range of periods: 0.5-0.8 sec). The peak velocity amplitudes (range: 0.25-0.55 mm/sec) correlated directly with the amplitude of the pulse pressure. During the nonpulsatile regimen, no such correlations were seen. During pulsatile flow and during the 3-hr nonpulsatile period, capillary density remained stable at 24 capillaries/mm of test line but there were significant increases in red cell velocity, from 0.8 to 1.2 mm/sec (P < 0.05), and in coefficient of variation of velocity (used as an index of flow heterogeneity), from 19 to 34% (P < 0.05). We conclude that (1) pulsatility exists in the capillary bed and that it directly correlates with the pumping action of the heart and (2) nonpulsatile flow produced by the ventricular assist device does not cause an acute deterioration in microvascular perfusion. We interpret the increase in heterogeneity of flow as an early sign of microvascular dysfunction. Prolonged use of the nonpulsatile device may, therefore, lead to deterioration in perfusion that could compromize the function of the organ.

Animals↗
PubMed1994

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

We hypothesized that normotensive sepsis affects the ability of the microcirculation to appropriately regulate microregional red blood cell (RBC) flux. An extensor digitorum longus muscle preparation for intravital study was used to compare the distribution of RBC flux and the functional hyperemic response in SHAM rats and rats made septic by cecal ligation and perforation (CLP). Using intravital microscopy, we found that sepsis was associated with a 36% reduction in perfused capillary density (from 35.3 +/- 1.5 to 22.5 +/- 1.0 capillaries/mm of test line) and a 265% increase in stopped-flow capillaries (from 0.9 +/- 0.2 to 3.3 +/- 0.4 capillaries/mm); the spatial distribution of perfused capillaries was also 72% more heterogeneous. Mean intercapillary distance (ICD) increased 30% (from 25.7 +/- 0.8 to 33.5 +/- 1.6 microns), and the proportion of capillary pairs with intercapillary distances > 33.8 microns (the 75th percentile of ICDSHAM) was greater with sepsis. Mean capillary RBC velocity increased 17% in CLP rats (391 vs 333 microns/s). Laser Doppler flowmetry was used to assess the functional hyperemic response of the extensor digitorum longus muscle before and after a period of maximal twitch contraction designed to increase oxygen demand. RBC flux was 36% lower in the CLP rats at rest. After contraction, RBC flux increased in both SHAM and CLP rats; however, the relative increase was less in the CLP group. We concluded that sepsis affects the ability of the skeletal muscle microcirculation to appropriately distribute RBC flux and to respond to increases in oxygen need.

Animals↗
PubMed1993

Evidence for sensing and integration of biological signals by the capillary network.

The aim of this study was to explore the phenomenon first described by Dietrich (Microvasc. Res. 38: 125-135, 1989) in which a local application of norepinephrine (NE) on a capillary can temporarily reduce flow via constriction of the feeding arteriole. Our objectives were to show that this phenomenon of remote response is not limited to vasoconstriction, can be elicited by materials other than NE, shows stimulus-strength dependency, and can be integrated within the capillary network. We used an intravital micropharmacological approach to iontophoretically apply (in mM concentrations in the pipette) NE, acetylcholine (ACh), 5'-N-ethylcarboxamidoadenosine (NECA, adenosine analogue), K+, and H+ on capillaries of the frog sartorius muscle in situ. Responses were measured in terms of changes in velocity of red blood cells (VRBC) in capillaries or in terms of changes in arteriolar diameter. ACh (3 mM) caused significant increases in diameter (from 34 to 37 microns) and in VRBC (from 250 to 340 microns/s, i.e., 36%). NE (3 mM) reduced VRBC by 16%. The magnitude of ACh and NE velocity responses increased with increasing pipette concentration and with increasing iontophoretic current. The ACh response was blocked by a local pretreatment with atropine. NECA, K+, and H+ caused 20-40% increases in VRBC. Dual application of NE on two capillaries fed by the same arteriole resulted in a greater VRBC reduction than for single NE application. Dual application of NE and ACh significantly attenuated the ACh response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Ischemia-reperfusion induced microvascular dysfunction in skeletal muscle: application of intravital video microscopy.

Video microscopy of red cell flow in capillaries at the surface of skeletal muscle provided the opportunity to quantitate ischemia-reperfusion (I-R) induced microcirculatory changes, in vivo. Extensor Digitorum Longus (EDL) muscles of 22 male Wistar rats (300-400 g), anesthetized with sodium pentobarbital (Somnotol, 65 mg kg,-1 IP), were used to measure the number of perfused capillaries (CDper: mm-1) crossing lines drawn perpendicular to the muscle axis, and red blood cell velocity (VRBC: mm/s) within individual capillaries from controls (n = 6), and after 2 hr (n = 4), 3 hr (n = 4), and 4 hr (n = 5) of no-flow ischemia with the muscle temperature maintained at its normal value of 32 degrees C. Ischemia was induced by tightening a tourniquet placed around the limb above the EDL muscle. Measurements were made after 30, 60, and 90 min of reperfusion. To test the usefulness of this skeletal muscle model for evaluating proposed interventions in I-R, the effect of hypothermia (24 degrees C) on the microcirculation following 4 hr ischemia (n = 3) was measured. Edema formation was estimated from the wet/dry weight ratio of the ischemic and contralateral control EDL muscles. Capillary perfusion at the surface of the control muscles was remarkably stable over the 5 hr period studied, while significant changes occurred following the ischemic periods. Significantly lower CDper was measured 30 min following all periods of normothermic ischemia. However, unlike the 2 and 4 hr ischemic periods 3 hr normothermic ischemia resulted in a progressive decline in CDper throughout the reperfusion period. VRBC showed evidence of a hyperemic response following 2 hr normothermic ischemia (control: 0.12 mm/s +/- 0.19 compared to 0.26 mm/s +/- 0.03 following 90 min reperfusion; mean +/- sem). However, no such hyperemia was measured following either 3 or 4 hr normothermic ischemia (i.e., 3 hr control: 0.24 mm/s +/- 0.01 compared to 0.07 mm s +/- 0.003 following 90 min reperfusion). In fact, VRBC was essentially zero 90 min following 4 hr normothermic ischemia (0.01 mm/s +/- 0.01). However, when the muscle was allowed to cool to 24 degrees C during 4 hr ischemia no significant change in either VRBC or CDper was measured compared to pre-ischemic controls. Evidence of edema was found after 3 and 4 hr normothermic ischemia. This study establishes a skeletal muscle model of I-R, which may be useful in testing hypotheses regarding mechanisms of I-R injury, and effectiveness of proposed treatments of I-R.

Animals↗
PubMed1992

Microvascular flow response to localized application of norepinephrine on capillaries in rat and frog skeletal muscle.

Recently, Dietrich (1989, Microvasc. Res. 38, 125-135) demonstrated that a local application of a minute amount of norepinephrine (NE, 5.5 mM, 0.01-88 pmole) on a capillary in rat mesentery can elicit constriction of the feeding arteriole 0.5-1.0 mm away. This constriction can reduce or even stop blood flow in capillaries supplied by the arteriole. The main objective here was to show that the phenomenon of reduced flow occurs not only in the rat mesentery but also in other tissues and species. We chose to study the rat tibialis anterior and frog sartorius muscles. Using the same intravital video-microscopic approach as in the mesentery, strong NE stimuli (3 mM) were applied iontophoretically 48 times to 19 capillaries in 10 rats anesthetized with pentobarbital. They resulted in significant reductions (average: 80%) of the red blood cell velocity (VRBC) in capillaries. The onset of these reductions (i.e., 10% decrease from control) occurred within 3-52 sec (average: 20.9 sec) from the time of NE application. Reductions lasted 6.0 min. The same stimuli were applied 42 times to 15 capillaries in 6 frogs anesthetized with urethane. The average VRBC reduction was 86%. The onset occurred within 30.6 sec while the reduction lasted 6.6 min. Under the same conditions, arteriolar diameters in the sartorius muscle decreased significantly from 28.5 to 22.5 microns (n = 8). We also used local microinjection of small droplets of NE (30 mM) to 13 capillaries in 7 frogs. This resulted in a significant VRBC reduction of 64% with an onset time of 44.2 sec and a reduction duration of 17.2 min. Weak NE stimuli (3 microM) applied iontophoretically to 10 capillaries in 5 frogs resulted in marginal, but significant, VRBC reductions (9%). The present study demonstrates that the phenomenon of reduced flow after local application of NE may be a general phenomenon as it occurs also in skeletal muscle in both rat and frog. Our accompanying paper addresses the hypothesis that the phenomenon reflects communication of a NE-induced signal along the capillary.

Animals↗
PubMed1992

Capillary as a communicating medium in the microvasculature.

The preceding study (Dietrich and Tyml, 1992. Microvasc. Res. 43) demonstrated that a local application of norepinephrine (NE) on a capillary in a skeletal muscle produces a temporary reduction in blood flow within this capillary. The reduction is mediated via constriction of the supplying arteriole. The objective of the present study was to address the mechanism by which the local NE stimulus is propagated from the capillary to the arteriole. Using intravital video microscopy we measured red blood cell velocity in capillaries, and diameter of supplying arterioles, in the sartorius muscle in anesthetized frogs. Velocity responses were measured following iontophoretic application of NE (3 mM in the pipette) on the capillary, with or without pretreatment with 0.9 mM tetrodotoxin (nerve-specific sodium channel blocker), 30 mM lidocaine (nonspecific sodium channel blocker), and 30 mM yohimbine (alpha 2-receptor blocker). Diameter responses were measured before and after capillary damage introduced by microcautery. Tetrodotoxin did not block the NE-induced velocity reduction (i.e., from 0.2 to 0.07 mm/sec), while lidocaine attenuated it. Yohimbine blocked it only when applied on the same site as NE. Capillary damage abolished the NE-induced arteriolar constriction (i.e., from 27.8 to 21.5 microns). We conclude that the observed responses were not due to (1) direct diffusion of NE from the capillary to the arteriole, (2) conduction along adrenergic nerves, or (3) venous-arteriolar diffusional cross-talk. We interpret our data to indicate that the capillary itself could function as a communicating medium.

Animals↗
PubMed1992

Distribution of red blood cell velocity in capillary network, and endothelial ultrastructure, in aged rat skeletal muscle.

Although age-related structural and functional changes in skeletal muscle have been described extensively, little is known about the accompanying hemodynamic and structural changes in the microvasculature. The objective of this study was to use the extensor digitorum longus muscle in mid-aged (12 months) and old (28 months) Fisher 344 male rats to evaluate (1) the distribution of microvascular flow in the resting state, (2) the distribution response to a complete 30-min tourniquet ischemia, and (3) the extent of damage of capillary endothelium. Using intravital video microscopy, the mean resting velocity of red cells in capillaries was found to be 3x larger in old rats while the distribution of velocity within the microvascular bed was as heterogeneous as that in mid-aged rats. The postischemic response was characterized by the same mean peak velocity, but a slower return to velocity to the preischemic level. Within the microvascular bed, there was a less uniform postischemic response among capillaries. No long-term effect of ischemia was seen as velocity was already stable at the preischemic level 20 min after the tourniquet release. There were no differences in the pre- and postischemic densities of perfused capillaries, wet/dry weight ratios, or the occurrence of damaged capillaries. Thus, in this muscle model, aging was associated with an increased resting flow but a remarkably unaffected long-term flow response to a vasodilatory stimulus and endothelial ultrastructure.

Aging↗
PubMed1992

Effect of isovolemic hemodilution on microvascular perfusion in rat skeletal muscle during a low flow state.

The objective was to evaluate the hemodynamic effect of hemodilution during a state of experimentally reduced microvascular flow. We measured red blood cell velocity (VRBC) and density of capillaries with moving and stationary red cells (CDPER, CDSTAT) at the surface of extensor digitorum longus muscle in 26 rats anesthetized with pentobarbital. The low flow state was achieved by reducing the femoral blood pressure to 30 mmHg via a partial occlusion of the abdominal aorta. Hemodilution with a 6% PVP-40 (polyvinylpyrrolidone) solution (average hematocrit reduction from 47 to 22%) was introduced either 90 minutes before or 30 minutes after the onset of low flow state. When compared with the control state, this state was associated with significantly reduced VRBC (from 0.14 to 0.016 mm/s) and CDPER (from 32.5 to 18.7 cap/mm of test line), and significantly increased CDSTAT (from 4.5 to 13.8 cap/mm), percentage of capillaries with low VRBC, 0-0.05 mm/s, (from 35 to 94%) and VRBC heterogeneity (coefficient of variation increased from 91 to 152%). Pre-hemodilution improved microvascular perfusion dramatically during the low flow state. VRBC and CDPER increased significantly by 387 and 51%, while CDSTAT, percentage of low VRBC capillaries, and heterogeneity decreased significantly by 52, 51 and 32%. Post-hemodilution, on the other hand, showed no improvement as none of these parameters changed significantly from the low flow state. We conclude that, based on this rat model, hemodilution is more suitable as a preventive measure, rather than as a treatment, of microcirculatory disorders associated with compromised flow.

Animals↗
PubMed1991

A new preparation of rat extensor digitorum longus muscle for intravital investigation of the microcirculation.

The extensor digitorum longus (EDL) muscle is a fast contracting muscle with 60% of Type IIB fibres at the surface. We developed a surgical procedure for exposing this surface from which the microcirculation can be visualized via intravital microscopy. From video recorded microscopic images we determined that microvascular perfusion at the surface is fairly stable for at least 5 hours. Among 7 anaesthetized rats (male Wistar), the density of perfused capillaries decreased at a rate of 4% per hr. The average velocity of red cells in perfused capillaries remained constant at 0.14 mm/s. In order to demonstrate the usefulness of the preparation we report 2 sample experiments involving muscle contraction and aging. The major advantages of EDL preparation are (1) absence of mechanical manipulation of the muscle during exposure, (2) no requirement for surface superfusion following exposure, and (3) independence of the visibility of the microcirculation from rat size and age.

Animals↗
PubMed1991

Heterogeneity of microvascular flow in rat skeletal muscle is reduced by contraction and by hemodilution.

The objective was to test the hypothesis that heterogeneity of microvascular perfusion in a mammalian muscle will decrease with increased flow. We used the extensor digitorum longus muscle in rats to quantify, via intravital video microscopy, (1) the spatial distribution of red cell velocity, VRBC, and (2) density of capillaries with moving and stationary red cells (CDPER, CDSTAT) within a large capillary bed (1.05 x 0.78 mm) at the muscle surface. From the VRBC distribution, the coefficient of variation (CV = SD/mean) was used as an index of VRBC heterogeneity. The flow was increased by two procedures: (1) 1 min supramaximal muscle contraction, and (2) hematocrit reduction from 49 to 21% by isovolemic hemodilution with a 6% PVP-40 (polyvinylpyrrolidone) solution. Among 5 rats studied, the post-contraction and post-hemodilution mean VRBC's were significantly larger than the resting VRBC (1.08 and 0.17 vs. 0.11 mm/s). The corresponding CV's were significantly lower (33 and 49 vs. 60%). The percentages of capillaries with low velocity (0-0.1 mm/s) were also significantly lower (0 and 27 vs. 52%). CDPER values did not differ from the resting level (30.8 cap/mm of test line) but CDSTAT was significantly smaller after contraction (0.8 vs. 4.9 cap/mm). The present data demonstrate that heterogeneity of VRBC in rat skeletal muscle decreases after contraction and after hemodilution. The study shows that hemodilution has a major effect on improving flow in a population of poorly perfused capillaries. Since heterogeneity also decreased after contraction in an amphibian muscle (Tyml, Microvasc. Res. 32: 84-98, 1986), the study supports the view that heterogeneity, in general, is a microcirculatory parameter that reflects the vascular network response to a given tissue stimulus.

Animals↗
PubMed1990

Microvascular response to ischemia, and tissue structure, in normal and atrophied skeletal muscle.

The objective of this study was to explain why the normally observed reactive hyperemia in frog sartorius muscle following ischemia is absent when this muscle atrophies. Two possibilities were addressed: (1) absence is due to lowered O2 consumption, making the muscle more tolerant to ischemia, and (2) absence is linked to impaired vascular function in atrophy. We used 10 frogs after 2-3 months and 8 frogs after 7-14 months of laboratory captivity. Animals in the latter group had a significantly lower sartorius muscle weight, i.e., 85 +/- 33 vs 24 +/- 11 SD mg. Using intravital video microscopy, we measured red cell velocity in capillaries at the muscle surface, and densities of capillaries with moving (NCPER) and stationary red cells (NCSTAT) before and after 30 min ischemia. Ischemia induced a significant temporary increase in overall velocity (from 0.10 to 0.27 mm/sec) in normal muscles, but no increase in atrophied muscles. It resulted in no difference in NCPER between the two groups (preischemic levels in both groups: 15.0 cap/mm of test line), but in a significant difference in NCSTAT (3.8 vs 11.5 cap/mm in atrophy). Using light and electron microscopy, we also measured structural and ultrastructural parameters in both groups. In atrophied muscles the mean fiber cross-sectional area was lower (568 vs 1935 microns 2) and anatomical capillary density higher (892 vs 282 cap/mm2) than in normal muscles. Mitochondrial volume density was not statistically different from the 1.5% level in the normal muscle, while the lipid droplet volume density was larger (2.33 vs 0.58%). The percentage of capillaries with damaged endothelium was larger (33.5 vs 12.6%). Using histology, the white cell volume density per capillary volume was also found to be larger in atrophy (1.96 vs 0.83%). From the discrepancy between the lack of intergroup difference in preischemic NCPER and the 3.2-fold difference in anatomical capillary density we estimate that about 60% of capillaries were perfused with red cells in atrophied muscles. Although the preischemic rate of perfusion in these capillaries was comparable between the two groups, the postischemic response was not: reactive hyperemia was absent in atrophy. Our mitochondrial and lipid volume density data do not support the possibility that this absence was due to lowered O2 consumption, as these densities did not decrease with atrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Variation in axial velocity profile of red cells passing through a single capillary.

We have used an analysis of the velocity of individual red cells as the cells pass through a capillary in order to estimate the variability in cross-sectional area of the capillary lumen available for flow along the length of the vessel. The purpose of the study was to determine if there were irregularities of sufficient magnitude and frequency to support Secomb's hypothesis that local constrictions in the capillary lumen could hinder blood flow at low driving pressure, due to the energy required to deform red cells as they pass through the constriction. All capillary segments analyzed to date, in both rat and frog, have shown regions where the velocity of individual cells is consistently faster or slower than that of the mean velocity of all other cells in the same segment. There are approximately two constrictions per 100 microns in the rat and one per 100 microns in the frog. On average these constrictions appear to reduce the cross-sectional area by 30% in the rat and 16% in the frog. These results provide evidence in support of Secomb's hypothesis. In addition, our results from one bifurcation indicate that the capillary lumen increases in cross-sectional area as one moves from the parent vessel to the region of the bifurcation. Downstream of the bifurcation the lumen rapidly decreases in area by 45 to 54%. Thus a red cell must undergo even greater deformation as it passes through a capillary bifurcation than it will in most other sections of the capillary network.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Localized heterogeneity of red cell velocity in skeletal muscle at rest and after contraction.

Using intravital video microscopy, the present study focussed on a detailed analysis of Vrbc heterogeneity in a 2.4 x 1.8 x 0.15 surface volume of a frog sartorius muscle, before and after supramaximal contraction. Heterogeneity of Vrbc was evaluated (1) for an entire population of capillaries seen in this volume, (2) for a series of optical cross-sections, (3) along a series of longitudinal muscle strips, and (4) in terms of an asymmetry ratio for pairs of concurrent capillaries surrounding a muscle fibre. All four types of analysis showed an increased Vrbc homogeneity after contraction. Velocities became more homogeneous along rather than across muscle fibres. The mean asymmetry ratio became significantly larger during post-contraction hyperemia suggesting that each fibre receives a more uniform blood supply that will contribute to an improved exchange of materials across the capillary wall. The analysis of localized Vrbc heterogeneity provides new means of pinpointing the sources of perfusion heterogeneity. It enables, therefore, a specific experimental intervention that is aimed at an improved perfusion under both normal and abnormal conditions.

Animals↗
PubMed1988

Evidence for increased perfusion heterogeneity in skeletal muscle during reduced flow.

Recently, it has been demonstrated (D. Cousineau, C. P. Rose, D. Lamoureux, and C. A. Goresky, 1983, Cir. Res., 53, 719-730; K. Tyml, 1986, Microvasc. Res., 32, 84-98) that heterogeneity of microvascular flow depends on tissue metabolism. The objective of this study was to examine the possibility that, independent of metabolism, heterogeneity is also a function of flow. Using an intravital video-microscopic approach, we evaluated heterogeneity in the frog sartorius muscle at different flow rates while maintaining the muscle in the same exercised state. The flow was altered via partial aortal clamping. Exercised state was achieved by direct electrical stimulation. Heterogeneity of flow was evaluated in terms of the coefficient of variation (CV = SD/mean) computed from simultaneous measurements of red cell velocities in a capillary network. In addition to velocity analysis, the number of perfused capillaries crossing a 1-mm test line on the video monitor was counted. Among 10 networks from eight muscles, the overall preocclusion hyperemic velocity and CV were 0.42 +/- 0.15 SD mm/sec and 40 +/- 12%, respectively. The overall capillary count was 16.4 +/- 3.0 cap/mm. In all networks, increasing clamping reduced the mean hyperemic velocity and increased CV. For reductions to less than 50% of the preocclusion velocity, CV increased significantly (P less than 0.05), up to 88%. In 6 networks only, increasing clamping reduced capillary count, down to 10.2 cap/mm. This reduction was due to flow stoppages in capillaries situated randomly throughout the network. The data demonstrate for the first time that, for the same exercised state, heterogeneity of velocity depends on the mean velocity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Heterogeneity of microvascular response to ischemia in skeletal muscle.

The aim of this study was to use the video-microscopic approach to analyze simultaneously, at very low magnification, red cell velocity (VRBC) and density of perfused capillaries (CD) in an entire capillary network of a frog sartorius muscle before and after 3 s, 1 min and 30 min arterial occlusions. In 11 muscles studied, the 3 s occlusion caused a significant increase in the overall peak hyperemic VRBC and CD (from 0.14 +/- 0.08 to 0.28 +/- 0.16 S.D. mm/s, and from 104 +/- 41 to 126 +/- 42 S.D. cap/mm2). All muscles participated in this overall response. On average, 71% of capillaries per network showed hyperemia. The 1 min occlusion also caused significant increases in overall VRBC and CD (from 0.14 +/- 0.08 to 0.34 +/- 0.17 S.D. mm/s, and from 94 +/- 44 to 123 +/- 44 S.D. cal/mm2). In contrast to the 3 s response, only 9 out of 11 muscles participated in this response, with an average capillary participation of 80%. The 30 min occlusion caused a significant increase in overall VRBC (from 0.13 +/- 0.07 to 0.24 +/- 0.17 S.D. mm/s) but no change in CD. Only 6 out of 11 muscles participated in this response, with an average capillary participation of 56%. In terms of these microvascular data, the present study demonstrate for the first time ever (1) an appreciable spatial heterogeneity of responses within the capillary network in a single muscle following all three types of occlusions, and (2) a progressively larger muscle-to-muscle heterogeneity of responses with longer duration of occlusion. Since the spatial heterogeneity (i.e. increase, no change or even decrease in flow) was associated with groups of similarly behaving capillaries supplied by a common arteriole, the existence of a flow-suppressing arteriolar mechanism (in addition to metabolic and myogenic vasodilating mechanisms) is postulated to explain the dramatic heterogeneity of response to ischemia in this muscle.

Animals↗