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Cardiorespiratory and Vascular Dynamics Laboratory, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
Submitted 7 April 2003 ; accepted in final form 20 August 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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hyperemia; endothelium; shear stress; ischemic exercise; blood flow
Between-laboratory comparisons of the magnitude of FMD are often difficult because of different experimental protocols that might examine different physiological aspects of FMD. Even in healthy volunteers, the range of reported FMD can be from a few percent to 22% (1, 3, 7, 11, 16, 20, 27). The magnitude of FMD appears to be related to many factors, including the method of measurement (e.g., echo wall tracking versus echo Doppler imaging), artery studied (brachial versus radial), site of occlusion (either proximal or distal to the measurement site), duration of occlusion, and presence or absence of exercise. To date, there has not been a systematic examination of several of these factors for a common measurement site. In the present experiments, we observed FMD in the brachial artery during five different protocols designed to achieve different levels of reactive hyperemia. The magnitude and duration of reactive hyperemia were modified by occluding different volumes of tissue by upper arm, forearm, and wrist occlusion protocols and by including exercise during the forearm and wrist protocols. This allowed us to test the general hypothesis that the magnitude of FMD was proportional to the peak or total magnitude of reactive hyperemia. We further explored the specific hypothesis that the type of occlusion of the brachial artery (that is, proximal or distal to the site of measurement) would alter the magnitude of FMD even though the magnitude of reactive hyperemia was similar under both conditions.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Physiological measurements. Measurements were made in a quiet room of relatively constant temperature (22–24°C). Signals from an electrocardiograph (model VS4, Cambridge Instruments; Cambridge, UK), finger-cuff photoplethysmograph (Finapres 2300, Ohmeda), and pulsed Doppler ultrasound (model 500V, Multigon Industries) were recorded at 100 Hz on a computer to allow measurement of heart rate, mean arterial pressure, and mean blood velocity, respectively. Forearm blood flow was calculated beat by beat (25, 26) from the product of the mean blood velocity and the cross-sectional area of the brachial artery obtained by echo Doppler imaging using a 7.5-MHz probe in B-mode (model SSH-140A, Toshiba; Toshigi-Ken, Japan). Placement of the echo Doppler probe was just proximal to the pulsed Doppler probe to avoid accoustic interference. An optimal signal through the center of the artery was determined as the clearest image of the anterior and posterior walls (28). The pulsed Doppler 4-MHz probe was fixed above the brachial artery proximal to the cubital fossa. The signal was directed 45° relative to the skin, and the ultrasound gate was adjusted to the total width of the artery. Arterial diameter was obtained from frozen screen images during the same phase of the cardiac cycle (diastole) by placing three pairs of markers on the trailing edge of the anterior wall to the leading edge of the posterior wall (25, 26). Shear rate was calculated as 8 x MBV/D (21), where MBV is the mean blood velocity over each cardiac cycle and D is the corresponding diameter for that cycle estimated as described in Blood flow analysis. Forearm volume was measured by water displacement, allowing blood flow measures to be expressed as milliliters per minute per 100 ml of tissue.
Blood flow analysis. Brachial artery diameter measurements were taken as the average of three measurements every 15 s during baseline, every 30 s during occlusion, and every 10 s after cuff release for the first 2 min and then every 30 s until the end of the 5-min recovery period. The individual diameter values were then fit by a nonlinear model that minimized the residual sum of squares and reduced any effect of random error to obtain the best estimate of arterial diameter before the determination of cross-sectional area, forearm blood flow, and shear rate. Forearm blood flow and diameter measures are presented as average values for 15-s intervals during the final phase of the baseline and occlusion periods and every 5 s after cuff deflation (during reactive hyperemia). Peak forearm blood flow and peak shear rate were defined as the average of the first 15 s after cuff release, similar to other investigations (7, 11). Total reactive hyperemia during the 5-min observation period was defined as the difference between forearm blood flow during the postocclusion period compared with baseline.
Circulatory arrest. Brachial artery blood flow was altered by rapidly inflating a standard blood pressure cuff with a tank of compressed air (E-20 Rapid Cuff Inflator, D. E. Hokanson). Cuff inflation was always to suprasystolic levels (200 mmHg) to prevent arterial blood inflow. We used three different occluding cuff positions. The cuff was placed on the upper arm proximal to the Doppler probes for the proximal occlusion condition, just distal the cubital fossa for the forearm occlusion condition and at the wrist (ulnar and radial styloid processes) for wrist occlusion. The forearm occlusion and wrist occlusion were distal to the site of measurement and caused reduced brachial artery blood flow but had little influence on distending pressure. The upper arm proximal position completely prevented flow at the measurement site and caused a great reduction in distending pressure.
Protocol. Subjects reported to the laboratory on 2 separate days separated by no more than 2 wk. After the subjects rested quietly in the supine position for 15–20 min, all signals were monitored to ensure a stable baseline before the collection of 1 min of resting data. The cuff inflated rapidly to 200 mmHg for 5 min (circulatory arrest) and deflated for 5 min of recovery (reactive hyperemia). The three different occlusion cuff positions with no exercise, proximal, forearm, and wrist, were performed on each test day in a random order, with at least 15 min between tests. Subsequent trials began only after all variables had returned to the stable preocclusion baseline values. On one day, forearm occlusion with handgrip exercise followed the no-exercise trials. On the other day, wrist occlusion with finger flexion exercise followed the no-exercise trials. For each of these exercise trials, circulation was occluded for 1 min with no exercise followed by 3 min with exercise and a further 1 min without exercise for a total 5-min occlusion. Exercise was conducted with a 1-s contraction, 2-s rest duty cycle. Finger flexion exercise required lifting small weights attached to the end of each finger while trying to isolate the lumbrical muscles rather than the whole hand in performing the exercise to minimize the work of the forearm flexor muscles. The subjects lifted a 5-kg weight during handgrip exercise.
The goal of these five different conditions was to achieve different levels of hyperemia, providing a broader spectrum to assess FMD. It was expected that forearm occlusion plus handgrip exercise would result in significantly greater and more prolonged hyperemia than all other conditions and that the wrist occlusion with finger exercise would create a level of hyperemia that would be between that of wrist and forearm occlusion alone.
Statistical analysis. All analyses from the occlusion only tests were based on the mean value of the two repetitions. The effects of occlusion position and time (from rest through cuff inflation, hyperemia, and recovery) on blood flow, brachial artery diameter, and mean arterial pressure were evaluated by two-way repeated-measures ANOVA. A probability of P < 0.05 was accepted as statistically significant, and any differences were then analyzed with the Student-Newman-Keuls post hoc test. A least-squares regression was performed to determine the Pearson product-moment correlation coefficient for the relationships between the magnitude of hyperemia or shear rate and the magnitude of FMD. Data are presented as means ± SE.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Forearm blood flow during the occlusion period (Fig. 1) was reduced during wrist occlusion (–23%), increased for wrist occlusion plus exercise (+61%), and reduced for forearm occlusion (–78%), proximal occlusion (–100%), and forearm occlusion plus exercise (–61%), all P < 0.05. Upon release of the circulatory arrest, forearm blood flow increased above baseline levels for all conditions (Fig. 1 and Table 1). The peak increase above baseline was smallest for wrist occlusion alone (568%). Wrist occlusion plus exercise caused a significantly greater increase (808%). The next greatest increases in flow were observed in forearm occlusion (1,353%) and proximal occlusion (1,394%), but these were not different from each other. The increase above baseline after forearm occlusion plus exercise (1,769%) was significantly greater than all other conditions.
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Brachial artery diameter during the occlusion period was reduced significantly (P < 0.05) from baseline only in the proximal occlusion condition (–9.1%), with all other conditions having a <1% change from baseline (Fig. 2). During the period of reactive hyperemia, brachial artery diameter was not significantly different from baseline for wrist occlusion and wrist occlusion plus exercise, but it was different for the other conditions (Fig. 2 and Table 1). The increase in brachial artery diameter above baseline after forearm occlusion (0.15 ± 0.03 mm, 3.4% above baseline) was different from all other conditions (P < 0.05). Brachial artery diameter was further increased after proximal occlusion (0.28 ± 0.06 mm, 6.6% above baseline even though it started below baseline) and forearm occlusion plus exercise (0.31 ± 0.03 mm, 7.0% above baseline) compared with all other conditions (P < 0.05), but these two conditions were not different from each other.
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There were no differences between conditions for the time for the artery to reach peak diameter after the increase in blood flow, although mean values ranged from 50 to 72 s (Table 1 and Fig. 2). When data were considered across all five different conditions, there were modest but significant correlations for the peak change in brachial artery diameter as a function of peak change in forearm blood flow (r = 0.59, P < 0.001; Fig. 3), peak shear rate (r = 0.49, P < 0.002; Fig. 4), and total reactive hyperemia (r = 0.52, P < 0.001; Fig. 5). It should be noted that the total hyperemia after forearm occlusion plus exercise was underestimated as recording was stopped at 5 min while blood flow was still elevated (Fig. 1). Continuing to measure hyperemia would have further dissociated the response of forearm occlusion plus exercise from the other conditions.
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Mean arterial blood pressure was significantly greater during the occlusion period than during baseline (P < 0.001) but was not different within 15 s after the release of occlusion (Table 2).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Three different comparisons provide additional insight into the mechanisms and nature of FMD. First, with a five- to eightfold increase in brachial artery blood flow after wrist occlusion and wrist occlusion plus exercise conditions, the small 1–2% FMD of the brachial artery was not significant. Second, when there was a similar 13- to 14-fold increase in forearm blood flow as well as a similar time course of recovery in each of the forearm occlusion and the proximal occlusion conditions, the magnitude and duration of FMD were greater with proximal occlusion (6.6%) compared with forearm occlusion (3.4%). Third, there was a somewhat greater peak (17-fold) and markedly prolonged increase in forearm blood flow after the forearm occlusion plus exercise condition, yet the magnitude and duration of FMD was similar to that of the proximal occlusion condition.
Proximal versus distal circulatory occlusion. An important finding of the present study was that proximal occlusion of arterial inflow caused a FMD response that was qualitatively and quantitatively different from the response to distal occlusion. This occurred even though the forearm blood flow was similar in the two conditions, as would be expected because the volume of ischemic tissue distal to the measurement site was similar in the two occlusion models. These findings extend the results of previous investigations (1, 4, 9, 10) and strongly suggest that FMD with proximal occlusion is a consequence of different or additional mechanisms. Agewall et al. (1) found significantly greater FMD after upper arm (proximal) occlusion but did not report the prolonged FMD that we observed. These researchers also reported greater FMD of the radial artery than observed in the brachial artery, but this could be explained by both the finding of greater percent dilatation in smaller arteries (7) as well as the fact that the radial artery was distal to the site of occlusion. Berry et al. (4) also noted a more prolonged FMD response after proximal compared with distal occlusion. Doshi et al. (10) found a greater magnitude of FMD after proximal compared with distal occlusion, but the two protocols caused a similar time course of change in diameter. Overall, these results are important because they could serve to explain some differences between various research groups that have used exclusively distal (16, 28) or proximal (9, 27) occlusion.
Major factors differ during proximal compared with distal circulatory occlusion. First, with proximal cuff placement the brachial artery was ischemic and might have become hypoxic during the occlusion period, but this is not certain as the oxygen in trapped arterial blood might have been sufficient to supply the arterial smooth muscle. Hypoxia, if it did occur, might directly cause dilation of the conduit arteries (1), although other researchers have suggested that hypoxia could impair vasodilation (4). Hypoxia is also known to impact on cyclooxygenase activity and might alter production of prostaglandin vasodilator or constrictor compounds (33). Second, the intra-arterial pressure is markedly reduced during proximal occlusion, and this could have induced a myogenic dilation (12), although the reactive hyperemia is primarily related to metabolite-induced vasodilation rather than a myogenic response (35). On release of the occlusion cuff, the increase in forearm blood flow was approximately the same for the proximal and forearm cuff positions and peak shear rate was only slightly higher after proximal occlusion due to the initial 9% reduction in diameter. The marked increase in arterial distending pressure on release of occlusion in the proximal cuff position might have evoked a myogenic response that would tend to constrict the brachial artery. However, Doshi et al. (10) speculated that myogenic tone might not be regained within 5 min after release of occlusion and that this could contribute to the greater FMD after proximal occlusion. Shear stress-induced release of NO dominates over the myogenic response at least at the arteriolar level (22). An additional factor to consider is the rate of onset of shear. In isolated rat first-order arterioles, a rapid attainment of a given shear rate caused greater dilation than a slower onset to the same shear rate (6). In the proximal occlusion condition, there would have been a somewhat steeper onset, although the peak shear rate (see Fig. 5) was not markedly different between proximal and forearm occlusions. Whether flow was turbulent at the onset of hyperemia is uncertain. A Reynolds' number can be calculated (5) for the peak flow using a velocity of 50 cm/s, which was typical of the average value over a beat in the postforearm occlusion plus exercise condition according to the following equation: Reynolds' number = (velocity x density x radius)/(viscosity) = 50 x 1 x 0.22/0.04 = 275. This value is considerably below the value of 1,000 for the onset of turbulence in a long straight tube but is above the value of 150 found in some arterial models (5), especially if one were to consider the peak flow during systole. In any case, velocity quickly dropped so even if there were turbulence it should have been transient, but it might have contributed to the stimulated release of NO and other vasoactive compounds.
There is agreement that the primary mechanism responsible for FMD in humans is the increase in NO release with the stimulation of the endothelial cells by increased shear rate (10, 16, 17, 19). However, there is no agreement on the mechanism for the difference in FMD for proximal versus distal circulatory occlusion models. Recently, Doshi et al. (10) suggested that NO was the exclusive mediator of FMD in the brachial artery during reactive hyperemia that followed distal occlusion but that some other factor might be involved with proximal occlusion. Joannides et al. (16) observed that inhibition of NO synthase was actually associated with constriction of the radial artery after release of distal (wrist) occlusion. The latter results might have been due to an endothelium-derived vasoconstrictor that is inhibited by aspirin (15). Although animal experimentation supports a role for the vasodilator prostacyclin in FMD (17), research with healthy humans suggests no important role for this dilator compound in FMD (20). The more complex mechanisms responsible for FMD after proximal occlusion might include a direct effect of hypoxia on the arterial smooth muscle, altered myogenic response, or altered release of NO or some other dilator or constrictor compound in response to slightly higher shear rate immediately after cuff release. It is worth noting that the increase in shear rate after proximal occlusion was transient and that overall the forearm blood flow profile was similar in the proximal and forearm occlusion conditions, but the FMD was sustained through the 5-min recording period only for the proximal condition. NO has a relatively short biological half-life (30), although processes initiated in the signaling pathway that result in vasodilatation might have a longer-lasting time course (23).
Blood flow and FMD with distal occlusions. In general, the data support the hypothesis that the magnitude of FMD would be dependent on the anticipated stimuli of peak blood flow, peak shear rate, or total reactive hyperemia (Figs. 3, 4, 5). There are, however, some specific deviations that should be noted. For our smallest changes in blood flow, there was no reduction in diameter noted during the period of lower flow during the occlusion, and there was no FMD associated with the hyperemia in either the wrist occlusion or the wrist occlusion plus exercise conditions. These observations suggest that there might have been a threshold for an effect and that our analysis with a simple linear model might not be appropriate. We suggest caution concerning our inclusion of the two wrist occlusion conditions in the overall analysis; however, given that there are insufficient data to justify fitting a more complex model, we present the results here for a linear model analysis. As considered above, the proximal occlusion caused a qualitatively different FMD than the other distal occlusion conditions; therefore, we recalculated the correlation coefficients, omitting the proximal condition. In each case, the correlation coefficient for the peak change in diameter as a function of peak blood flow (Fig. 3), peak shear rate (Fig. 4), and 5-min total hyperemia (Fig. 5) increased slightly (r = 0.65, 0.58, and 0.77, respectively, all P < 0.002) compared with the data set including proximal occlusion. Thus these data are consistent with other research that investigated different magnitude of reactive hyperemia and the impact on FMD (2, 8, 9). Close examination of Fig. 5 shows that the magnitude of FMD expressed as the peak change in diameter of the brachial artery is largely independent of the total 5-min reactive hyperemia. Thus it appears that peak blood flow, which is of course tightly linked to peak shear rate (r = 0.88 for n = 8 subjects and 5 conditions), is a major determinant of the extent of FMD, and peak shear rate probably reflects the rate of onset of shear rate that has been demonstrated to be an important determinant in the magnitude of FMD (6).
In the present study, brachial artery diameter was measured every 10 s through the first 2 min after occlusion cuff release and then every 30 s to the end of the 5-min observation period. For each individual test, we then fit these diameter data by a nonlinear regression that minimized the random error and provided an estimate of the full time course for FMD, which was then used to calculate the peak diameter change and the time at which peak diameter occurred. Observations of the peak diameter at time points that varied between conditions from 50 to 72 s were consistent with recent guidelines (8) and argue against measurement at specific time points (2, 9, 18). The continuous estimate of brachial artery diameter from the regression equation allowed calculation of beat-to-beat forearm blood flow. As expected by using regression analysis to reduce the effects of random measurement error, our curve fit method gave a slight underestimate of the magnitude of FMD compared with the use of only the maximum diameter value. If we had used the peak value, the percent change in FMD for each condition would have been 2.5% rather than 1.1% for wrist occlusion, 3.4% rather than 2.1% for wrist occlusion plus exercise, 4.4% rather than 3.4% for forearm occlusion, 7.8% rather than 7.0% for forearm occlusion plus exercise, and 7.4% rather than 6.6% for proximal occlusion.
Our use of the fitted curve for brachial artery diameter rather than the maximum measured FMD probably contributed to our reported FMD being at the lower end of values reported such as an 18% FMD of the brachial artery (3) or 3.7% FMD of the radial artery (16) after a threefold increase in peak blood flow. Our findings support the concept that it is advantageous to increase the magnitude of reactive hyperemia to achieve greater FMD (2, 20). Our subjects experienced circulatory occlusion for 5 min with exercise added in the middle 3 min of this occlusion period. This resulted in an increase in peak forearm blood flow from 44.3 ml·min–1·100 ml–1 (
13-fold increase above baseline) after occlusion alone to 59.3 ml·min–1·100 ml–1 (17-fold increase above baseline) after occlusion plus exercise. There was an increase in mean arterial blood pressure during the occlusion periods, and the increase was quantitatively greater in the occlusion plus exercise conditions, suggesting activation of the muscle chemoreflex pressor response (24). It has been suggested that FMD might be impaired during sustained activation of the sympathetic nervous system with lower body negative pressure (14) or that FMD is enhanced with sympathetic activation by mental stress (13). Our observation that mean arterial pressure rapidly decreased after release of circulatory occlusion plus the finding of marked FMD in the forearm occlusion plus exercise condition argue against any negative effect of activating the muscle chemoreflex.
In conclusion, the present experiments demonstrated that there are important between-method differences in the FMD response of the brachial artery. These differences are due in part to the magnitude of the peak increase in blood flow or shear rate after release of the occlusion cuff. An important observation was that similar increases in peak forearm blood flow for the forearm versus proximal arm occlusion sites were followed by significantly greater and more prolonged FMD for the proximal occlusion condition. Furthermore, a greater peak and more prolonged increase in forearm blood flow after forearm occlusion with exercise caused approximately equivalent magnitude and duration of FMD as observed for proximal occlusion without exercise. Taken together, these results indicate that the mechanism(s) for FMD is different with proximal occlusion compared with distal occlusion models. Given uncertainties about the roles of reduced arterial pressure and ischemia during proximal occlusion that might interfere with myogenic responses or production and action of vasoactive compounds, it is recommended that distal occlusion be used to study endothelial function, that a period of exercise during the occlusion will enhance the reactive hyperemia and FMD responses, and, furthermore, that the increase in mean arterial pressure during the occlusion plus exercise condition was transient and did not appear to have any noticeable effect on FMD.
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ACKNOWLEDGMENTS |
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GRANTS
This research was supported the Natural Sciences and Engineering Research Council of Canada.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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