Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans.

Transcranial Doppler ultrasound-determined middle (MCA) and anterior (ACA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes (PI) were measured during "no-load" [21, 60, and 102 revolutions/min (rpm)] and loaded cycling (30, 60, and 149 W) at approximately 60 rpm. At rest Vmean MCA was 51 (36-55) cm/s (median and range; n = 10) and Vmean ACA was 41 (36-49) cm/s (n = 7; P < 0.05). With no load on the cycle Vmean MCA increased 4 (2-36), 10 (0-47), and 27% (4-58) (P < 0.05) at the three pedaling frequencies, respectively; arterial PCO2 (PaCO2) remained constant. During loaded cycling the increases were 19 (6-42), 25 (2-45), and 32% (12-67) (P < 0.01), respectively, with only a minimal change in PaCO2. No significant changes were observed in Vmean ACA. Changes in Vmean MCA were similar to those recorded by the initial slope index (ISI) of the 133Xe clearance method (n = 11), which in turn were smaller than increases recorded by the fast-compartment flow. PI ACA followed PI MCA during no-load as well as loaded exercise and increased with work rate, perhaps reflecting an increase in pulse pressure from 56 (48-63) mmHg at rest to 109 (88-123) mmHg at 149 W (P < 0.01). Data demonstrate a graded increase in regional cerebral perfusion during dynamic exercise corresponding to the MCA territory.     

Intra- and extracranial artery blood velocity during a sudden blood pressure decrease in humans

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min⁻¹]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s⁻¹ (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s⁻¹ (P < 0.05) and common carotid artery blood flow (CCAbf ) decreased from 305 (23) to 233 (33) ml min⁻¹ (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s⁻¹], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min⁻¹]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes. Accepted: 8 April 1997     

Effects of dynamic exercise on mean blood velocity and muscle interstitial metabolite responses in humans

We examined the effects of dynamic one-legged knee extension exercise on mean blood velocity (MBV) and muscle interstitial metabolite concentrations in healthy young subjects (n = 7). Femoral MBV (Doppler), mean arterial pressure (MAP) and muscle interstitial metabolite (adenosine, lactate, phosphate, K(+), pH, and H(+); by microdialysis) concentrations were measured during 5 min of exercise at 30 and 60% of maximal work capacity (W(max)). MAP increased (P < 0.05) to a similar extent during the two exercise bouts, whereas the increase in MBV was greater (P < 0.05) during exercise at 60% (77.00 +/- 6.77 cm/s) compared with 30% W(max) (43.71 +/- 3.71 cm/s). The increase in interstitial adenosine from rest to exercise was greater (P < 0.05) during the 60% (0.80 +/- 0.10 microM) compared with the 30% W(max) bout (0.57 +/- 0.10 microM). During exercise at 60% W(max), interstitial K(+) rose at a greater rate than during exercise at 30% W(max) (P < 0.05). However, pH increased (H(+) decreased) at similar rates for the two exercise intensities. During exercise, interstitial lactate and phosphate increased (P < 0.05) with no difference observed between the two intensities. After 5 min of recovery, MBV decreased to baseline levels after exercise at 30% W(max) (4.12 +/- 1.10 cm/s), whereas MBV remained above baseline levels after exercise at 60% W(max) (Delta19.46 +/- 2.61 cm/s; P < 0.05). MAP and interstitial adenosine, K(+), pH, and H(+) returned toward baseline levels. However, interstitial lactate and phosphate continued to increase during the recovery period. Thus an increase in exercise intensity resulted in concomitant changes in MBV and muscle interstitial adenosine and K(+), whereas similar changes were not observed for MAP or muscle interstitial pH, lactate, or phosphate. These data suggest that K(+) and/or adenosine may play an active role in the regulation of skeletal muscle blood flow during exercise.     

Effects of age on brachial artery myogenic responses in humans

The myogenic response, the inherent ability of blood vessels to rapidly respond to changes in transmural pressure, is involved in local blood flow autoregulation. Animal studies suggest that aging impairs the myogenic response. The purpose of this study was to compare the effects of changes in transmural pressure on mean blood velocity (MBV, cm/s) in young and older subjects. Twelve younger men and women (25 +/- 1 yr) were gender and body composition matched to twelve older men and women (65 +/- 1 yr). A specially designed tank raised or lowered forearm pressure by 50 mmHg within 0.2 s. Brachial artery MBV was measured directly above the site of forearm pressure change using Doppler methods. In response to increasing transmural pressure (i.e., release of +50 mmHg), older subjects compared with younger subjects had significantly lower peak MBV (Delta 12.43 +/- 1.16 vs. Delta 17.97 +/- 2.01 cm/s; P < 0.05), reduced rates in the dynamic fall of MBV after peak values were achieved (vasoconstriction) (-1.88 +/- 0.17 vs. -2.90 +/- 0.28 cm.s(-1).s(-1); P < 0.05), and lower MBV values with sustained suction. In response to decreasing transmural pressure (i.e., change to +50 mmHg), there was a significantly greater increase in MBV (Delta peak flow from trough 7.71 +/- 1.32 vs. 4.38 +/- 0.71 cm/s; P < 0.05) and a trend toward a greater rate of rise in MBV (vasodilation; 1.61 +/- 0.29 vs. 0.96 +/- 0.21 cm.s(-1).s(-1); P = 0.08) in the older subjects. Older subjects compared with the younger subjects exhibited decreased dynamic vasoconstriction, enhanced steady-state constriction, as well as evidence for enhanced dynamic vasodilation responses to sustained alterations in forearm transmural pressure.     

Regulation of middle cerebral artery blood velocity during recovery from dynamic exercise in humans.

We sought to examine the regulation of cerebral blood flow during 10 min of recovery from mild, moderate, and heavy cycling exercise by measuring middle cerebral artery blood velocity (MCA V). Transfer function analyses between changes in arterial blood pressure and MCA V were used to assess the frequency components of dynamic cerebral autoregulation (CA). After mild and moderate exercise, the decreases in mean arterial pressure (MAP) and mean MCA V (MCA Vm) were small. However, following heavy exercise, MAP was rapidly and markedly reduced, whereas MCA Vm decreased slowly (-23 +/- 4 mmHg and -4 +/- 1 cm/s after 1 min for MAP and MCA Vm, respectively; means +/- SE). Importantly, for each workload, the normalized low-frequency transfer function gain between MAP and MCA Vm remained unchanged from rest to exercise and during recovery, indicating a maintained dynamic CA. Similar results were found for the systolic blood pressure and systolic MCA V relationship. In contrast, the normalized low-frequency transfer function gain between diastolic blood pressure and diastolic MCA V (MCA Vd) increased from rest to exercise and remained elevated in the recovery period (P < 0.05). However, MCA Vd was quite stable on the cessation of exercise. These findings suggest that MCA V is well maintained following mild to heavy dynamic exercise. However, the increased transfer function gain between diastolic blood pressure and MCA Vd suggests that dynamic CA becomes less effective in response to rapid decreases in blood pressure during the initial 10 min of recovery from dynamic exercise.     

Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans

Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V(s)), diastolic (V(d)). and mean (V(m)) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P < 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V(m) and V(s) (P < 0.05) but tended to decrease MCA V(d) (P = 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V(m) and between SBP and MCA V(s) remained unchanged from rest to exercise, whereas that between DBP and MCA V(d) increased from rest to heavy exercise (P < 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V(m), even during high-intensity exercise.     

Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans.

Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of central command, mechanoreceptors, and/or muscle metaboreceptors on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.     

Regulation of middle cerebral artery blood velocity during dynamic exercise in humans: influence of aging.

Although cerebral autoregulation (CA) appears well maintained during mild to moderate intensity dynamic exercise in young subjects, it is presently unclear how aging influences the regulation of cerebral blood flow during physical activity. Therefore, to address this question, middle cerebral artery blood velocity (MCAV), mean arterial pressure (MAP), and the partial pressure of arterial carbon dioxide (Pa(CO(2))) were assessed at rest and during steady-state cycling at 30% and 50% heart rate reserve (HRR) in 9 young (24 +/- 3 yr; mean +/- SD) and 10 older middle-aged (57 +/- 7 yr) subjects. Transfer function analysis between changes in MAP and mean MCAV (MCAV(mean)) in the low-frequency (LF) range were used to assess dynamic CA. No age-group differences were found in Pa(CO(2)) at rest or during cycling. Exercise-induced increases in MAP were greater in older subjects, while changes in MCAV(mean) were similar between groups. The cerebral vascular conductance index (MCAV(mean)/MAP) was not different at rest (young 0.66 +/- 0.04 cm x s(-1) x mmHg(-1) vs. older 0.67 +/- 0.03 cm x s(-1) x mmHg(-1); mean +/- SE) or during 30% HRR cycling between groups but was reduced in older subjects during 50% HRR cycling (young 0.67 +/- 0.03 cm x s(-1) x mmHg(-1) vs. older 0.56 +/- 0.02 cm x s(-1) x mmHg(-1); P < 0.05). LF transfer function gain and phase between MAP and MCAV(mean) was not different between groups at rest (LF gain: young 0.95 +/- 0.05 cm x s(-1) x mmHg(-1) vs. older 0.88 +/- 0.06 cm x s(-1) x mmHg(-1); P > 0.05) or during exercise (LF gain: young 0.80 +/- 0.05 cm x s(-1) x mmHg(-1) vs. older 0.72 +/- 0.07 cm x s(-1) x mmHg(-1) at 50% HRR; P > 0.05). We conclude that despite greater increases in MAP, the regulation of MCAV(mean) is well maintained during dynamic exercise in healthy older middle-aged subjects.     

Abnormal systolic blood pressure during treadmill test and brachial artery flow-mediated vasodilatation impairment

The aim of the study was to assess the relationship between systolic blood pressure during maximal treadmill test (SBP9mtt)) and flow-mediated vasodilation (FMD). Abnormal rise of SBP(mtt) is the phenomenon more frequent in hypertensive persons but it could be found in normotensive subjects too. 199 subjects referred to treadmill test were enrolled in the study. Four groups were formed: hypertensives with abnormal SBP(mtt) (group A), hypertensives with normal SBP(mtt) (group B), normotensives with abnormal SBP(mtt) (group C) and normotensives with normal SBP(mtt) (group D). Rise of SBP(mtt) above 200 mmHg was considered abnormal reaction. Simple linear regression analysis showed significant inverse relationship between SBP(mtt) and FMD (F = 20.2036, p < 0.001, R2 = 0.0956). Mean FMD index was worst in hypertensive subjects with abnormal SBP(mtt) (group A), followed by normotensives with abnormal SBP(mtt) (group C), hypertensives with normal SBP(mtt) (group B) and the best was in normotensives with normal SBP(mtt) (3.56 +/- 5.17, 4.19 +/- 5.14, 6.81 +/- 8.43 and 10.92 +/- 7.48%, respectively). In multivariate regression analysis FMD showed significant association with abnormal SBP(mtt) (p < 0.001) along with brachial artery diameter (p < 0.001), male gender (p < 0.001), but not with hypertension (p = 0.073), BMI (p = 0.137) and total cholesterol (p = 0.23) (coefficients: -0.26, -0.40, -0.27, -0.13, -0.11 and -0.07, respectively). There was a significant inverse relationship between SBP(mtt) and FMD. An impairment of FMD exists in normotensive subjects with abnormal SBP(mtt). In hypertensives with abnormal SBP(mtt) an additional impairment of FMD exists when compared to hypertensives with normal SBP(mtt). Abnormal SBP(mtt) should be taken into account in global cardiovascular risk assessment.     

Impact of controlling shear rate on flow-mediated dilation responses in the brachial artery of humans.

The reactive hyperemia test (RHtest) evokes a transient increase in shear stress as a stimulus for endothelial-dependent flow-mediated vasodilation (EDFMD). We developed a noninvasive method to create controlled elevations in brachial artery (BA) shear rate (SR, estimate of shear stress), controlled hyperemia test (CHtest), and assessed the impact of this vs. the RHtest approach on EDFMD. Eight healthy subjects participated in two trials of each test on 3 separate days. For the CHtest, SR was step increased from 8 to 50 s(-1), created by controlled release of BA compression during forearm heating. For the RHtest, transient increases in SR were achieved after 5 min of forearm occlusion. BA diameter and blood flow velocity (ultrasound) were measured upstream of compression and occlusion sites. Both tests elicited significant dilation (RHtest: 6.33 +/- 3.12%; CHtest: 3.00 +/- 1.05%). The CHtest resulted in 1) reduced between-subject SR and EDFMD variability vs. the RHtest [SR coefficient of variation (CV): 4.9% vs. 36.6%; EDFMD CV: 36.16% vs. 51.80%] and 2) virtual elimination of the impact of BA diameter on the peak EDFMD response (peak EDFMD vs. baseline diameter for RHtest, r(2) = 0.64, P < 0.01, vs. CHtest, r(2) = 0.14, P < 0.01). Normalization of the RHtest EDFMD response to the magnitude of the SR stimulus eliminated test differences in between-subject response variability. Reductions in trial-to-trial and day-to-day SR variability with the CHtest did not reduce EDFMD variability. Between-subject SR variability contributes to EDFMD variability with the RHtest. SR controls with the CHtest or RHtest response normalization are essential for examining EDFMD between groups differing in baseline arterial diameter.     

Differential sensitivities of cerebral and brachial blood flow to hypercapnia in humans.

Although it is known that the vasculatures of the brain and the forearm are sensitive to changes in arterial Pco(2), previous investigations have not made direct comparisons of the sensitivities of cerebral blood flow (CBF) (middle cerebral artery blood velocity associated with maximum frequency of Doppler shift; Vp) and brachial blood flow (BBF) to hypercapnia. We compared the sensitivities of Vp and BBF to hypercapnia in humans. On the basis of the critical importance of the brain for the survival of the organism, we hypothesized that Vp would be more sensitive than BBF to hypercapnia. Nine healthy males (30.1 +/- 5.2 yr, mean +/- SD) participated. Euoxic hypercapnia (end-tidal Po(2) = 88 Torr, end-tidal Pco(2) = 9 Torr above resting) was achieved by using the technique of dynamic end-tidal forcing. Vp was measured by transcranial Doppler ultrasound as an index of CBF, whereas BBF was measured in the brachial artery by echo Doppler. Vp and BBF were measured during two 60-min trials of hypercapnia, each trial separated by 60 min. Since no differences in the responses were found between trials, data from both trials were averaged to make comparisons between Vp and BBF. During hypercapnia, Vp and BBF increased by 34 +/- 8 and 14 +/- 8%, respectively. Vp remained elevated throughout the hypercapnic period, but BBF returned to baseline levels by 60 min. The Vp CO(2) sensitivity was greater than BBF (4 +/- 1 vs. 2 +/- 1%/Torr; P < 0.05). Our findings confirm that Vp has a greater sensitivity than BBF in response to hypercapnia and show an adaptive response of BBF that is not evident in Vp.     

Mean aortic pressure is the geometric mean of systolic and diastolic aortic pressure in resting humans.

The aim of our study was twofold: 1) to establish a mathematical link between mean aortic pressure (MAP) and systolic (SAP) and diastolic aortic pressures (DAP) by testing the hypothesis that either the geometric mean or the harmonic mean of SAP and DAP were reliable MAP estimates; and 2) to critically evaluate three empirical formulas recently proposed to estimate MAP. High-fidelity pressures were recorded at rest at the aortic root level in controls (n = 31) and in subjects with various forms of cardiovascular diseases (n = 108). The time-averaged MAP and the pulse pressure (PP = SAP - DAP) were calculated. The MAP ranged from 66 to 160 mmHg [mean = 107.9 mmHg (SD 18.2)]. The geometric mean, i.e., the square root of the product of SAP and DAP, furnished a reliable estimate of MAP [mean bias = 0.3 mmHg (SD 2.7)]. The harmonic mean was inaccurate. The following MAP formulas were also tested: DAP + 0.412 PP (Meaney E, Alva F, Meaney A, Alva J, and Webel R. Heart 84: 64, 2000), DAP + 0.33 PP + 5 mmHg [Chemla D, Hébert JL, Aptecar E, Mazoit JX, Zamani K, Frank R, Fontaine G, Nitenberg A, and Lecarpentier Y. Clin Sci (Lond) 103: 7-13, 2002], and DAP + [0.33 + (heart rate x 0.0012)] PP (Razminia M, Trivedi A, Molnar J, Elbzour M, Guerrero M, Salem Y, Ahmed A, Khosla S, Lubell DL. Catheter Cardiovasc Interv 63: 419-425, 2004). They all provided accurate and precise estimates of MAP [mean bias = -0.2 (SD 2.9), -0.3 (SD 2.7), and 0.1 mmHg (SD 2.9), respectively]. The implications of the geometric mean pressure strictly pertained to the central (not peripheral) level. It was demonstrated that the fractional systolic (SAP/MAP) and diastolic (DAP/MAP) pressures were reciprocal estimates of aortic pulsatility and that the SAP times DAP product matched the total peripheral resistance times cardiac power product. In conclusion, although the previously described thumb-rules applied, the "geometric MAP" appears more valuable as it established a simple mathematical link between the steady and pulsatile component of aortic pressure.     

Multiple coherence of cerebral blood flow velocity in humans

The coherence function has been used in transfer function analysis of dynamic cerebral autoregulation to assess the statistical significance of spectral estimates of gain and phase frequency response. Interpretation of the coherence function and choice of confidence limits has not taken into account the intrinsic nonlinearity represented by changes in cerebrovascular resistance due to vasomotor activity. For small spontaneous changes in arterial blood pressure (ABP), the relationship between ABP and cerebral blood flow velocity (CBFV) can be linearized, showing that corresponding changes in cerebrovascular resistance should be included as a second input variable. In this case, the standard univariate coherence function needs to be replaced by the multiple coherence, which takes into account the contribution of both inputs to explain CBFV variability. With the use of two different indicators of cerebrovascular resistance index [CVRI = ABP/CBFV and the resistance-area product (RAP)], multiple coherences were calculated for 42 healthy control subjects, aged 20 to 40 yr (28 +/- 4.6 yr, mean +/- SD), at rest in the supine position. CBFV was measured in both middle cerebral arteries, and ABP was recorded noninvasively by finger photoplethysmography. Results for the ABP + RAP inputs show that the multiple coherence of CBFV for frequencies <0.05 Hz is significantly higher than the corresponding values obtained for univariate coherence (P < 10(-5)). Corresponding results for the ABP + CVRI inputs confirm the principle of multiple coherence but are less useful due to the interdependence between CVRI, ABP, and CBFV. The main conclusion is that values of univariate coherence between ABP and CBFV should not be used to reject spectral estimates of gain and phase, derived from small fluctuations in ABP, because the true explained power of CBFV in healthy subjects is much higher than what has been usually predicted by the univariate coherence functions.     

Neurogenic-nitric oxide interactions affecting brachial artery mechanics in humans: roles of vessel distensibility vs. diameter

The purpose of this investigation was to assess the interactive influence of sympathetic activation and supplemental nitric oxide (NO) on brachial artery distensibility vs. its diameter. It was hypothesized that 1) sympathetic activation and NO competitively impact muscular conduit artery (brachial artery) mechanics, and 2) neurogenic constrictor input affects conduit vessel stiffness independently of outright changes in conduit vessel diastolic diameter. Lower body negative pressure (LBNP) and a cold pressor stress (CPT) were used to study the changes in conduit vessel mechanics when the increased sympathetic outflow occurred with and without changes in heart rate (LBNP -40 vs. -15 mmHg) and blood pressure (CPT vs. LBNP). These maneuvers were performed in the absence and presence of nitroglycerin. Neither LBNP nor CPT altered brachial artery diastolic diameter; however, distensibility was reduced by 25 to 54% in each reflex (all P < 0.05). This impact of sympathetic activation on brachial artery distensibility was not altered by nitroglycerin supplementation (21-54%; P < 0.05), although baseline diameter was increased by the exogenous NO (P < 0.05). The results indicate that sympathetic excitation can reduce the distensibility of the brachial artery independently of concurrent changes in diastolic diameter, heart rate, and blood pressure. However, exogenous NO did not minimize or reverse brachial stiffening during sympathetic activation. Therefore, sympathetic outflow appears to impact the stiffness of this conduit vessel rather than its diastolic diameter or, by inference, its local resistance to flow.     

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans

We tested the hypothesis that the slowerincrease in alveolar oxygen uptake(O₂) at the onset ofsupine, compared with upright, exercise would be accompanied by aslower rate of increase in leg blood flow (LBF). Seven healthy subjectsperformed transitions from rest to 40-W knee extension exercise in theupright and supine positions. LBF was measured continuously with pulsedand echo Doppler methods, andO₂ was measured breath bybreath at the mouth. At rest, a smaller diameter of thefemoral artery in the supine position(P < 0.05) was compensated by agreater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of6 min of exercise, femoral artery diameter was larger in the uprightposition and there were no differences inO₂, MBV, or LBF betweenupright and supine positions. The rates of increase ofO₂ and LBF in thetransition between rest and 40 W exercise, as evaluated by the meanresponse time (time to 63% of the increase), were slower in the supine[O₂ = 39.7 ± 3.8 (SE) s, LBF = 27.6 ± 3.9 s] than in the uprightpositions (O₂ = 29.3 ± 3.0 s, LBF = 17.3 ± 4.0 s;P < 0.05). These data support ourhypothesis that slower increases in alveolarO₂ at the onset of exercisein the supine position are accompanied by a slower increase in LBF.

     

Effects of aging on adipose resistance artery vasoconstriction: possible implications for orthostatic blood pressure regulation.

The purpose of this investigation was to determine mean arterial pressure (MAP) and regional vascular conductance responses in young and aged Fisher-344 rats during orthostatic stress, i.e., 70 degrees head-up tilt (HUT). Both groups demonstrated directionally different changes in MAP during HUT (young, 7% increase; aged, 7% decrease). Vascular conductance during HUT in young rats decreased in most tissues but largely remained unchanged in the aged animals. Based on the higher vascular conductance of white adipose tissue from aged rats during HUT, resistance arteries from white visceral fat were isolated and studied in vitro. There was diminished maximal vasoconstriction to phenylephrine and norepinephrine (NE: young, 42 +/- 5%; old, 18 +/- 6%) in adipose resistance arteries from aged rats. These results demonstrate that aging reduces the ability to maintain MAP during orthostatic stress, and this is associated with a diminished vasoconstriction of adipose resistance arteries.     

Effects of high pressure on nervous conduction velocity in man

The velocities of motor and sensory nervous conduction and of neuro-muscular transmission were measured in four subjects during a simulated dive at 4.6 MPa (46 bars). The results show an increase in motor distal latency in the ulnar nerve, especially during decompression, with reversibility of the effect on return to ambient conditions. The hypothesis of an interaction of dissolved gases with the membranes of ischaemic cells is proposed.     

Effects of hypotension on cutaneous and subcutaneous blood flow in anaesthetized humans.

The aim of this study was to determine the effect of controlled hypotension on subcutaneous and cutaneous haemodynamics in humans. Moderate hypotension was achieved with nitroglycerin (NTG) and sodium nitroprusside (SNP) infusion during narconeuroleptanalgesia in seven patients. Subcutaneous and cutaneous blood flow were measured by a superficial and deep heat clearance (HC) technique. The mean arterial pressure (BPa) decreased by 23%-30% and heart rate (fc) increased but only during NTG infusion (+22%; P less than 0.02). Subcutaneous and cutaneous blood flows remained unchanged despite a significant decrease in calculated cutaneous resistance (NTG: -26%, P less than 0.01; SNP: -34%, P less than 0.02] and subcutaneous vascular resistance changed only with SNP (-31%, P less than 0.02). After hypotension was discontinued the subcutaneous blood flow decreased (-13%, P = 0.05), whereas subcutaneous vascular resistance returned to its control values. An inverse relationship was found between fc and BPa (NTG: r = -0.525, P less than 0.01; SNP: r = -0.622, P less than 0.01) as well as with subcutaneous blood flow (NTG: r = -0.653, P less than 0.001; SNP: r = -0.573, P less than 0.01). In addition, we found oscillatory changes in deep HC values which differed in magnitudes (NTG 0.22 (SEM 0.09) W.m-1.degree C-1 vs SNP 0.42 (SEM 0.1) W.m-1.degrees C-1, P less than 0.01) and frequencies (NTG 0.02 (SEM 0.006) Hz vs SNP 0.01 (SEM 0.002) Hz, P less than 0.01). Despite unchanged blood flow, the effects of controlled hypotension on cutaneous and subcutaneous haemodynamics were different depending on the type of drug. These differences may have been related to counterregulatory responses and/or to direct vascular effects.     

Effects of elements on blood pressure

This article presents a comprehensive review of all known elements involved in blood pressure control. Data source was by computerized literature searches. A total of 28 elements have been documented as being involved in blood pressure control. The individual elements react directly and indirectly in a variety of metabolic and structural activities known to participate in blood pressure regulation. Reports from both experimental animal and human subjects are presented. The role of certain elements in blood pressure control is controversial. Conversely, important established functions of dosage, absorption, storage, and excretion of individual elements are known and are described in relation to blood pressure control. Some elements are pressor, whereas others are depressor in action, and this article demonstrates the important role elements play in the control of blood pressure.