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Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 73 records · Page 4Linked to original sources

Cerebral metabolic response to submaximal exercise.

We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 +/- 3 to 63 +/- 3 and 70 +/- 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 +/- 3 and 25 +/- 3 micromol/l (P < 0. 01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugular-venous (a-v) difference for O(2) decreased at low-intensity exercise (from 3.1 +/- 0.1 to 2. 9 +/- 0.1 mmol/l; P < 0.05) and recovered at moderate exercise (to 3. 3 +/- 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 +/- 0.05 to 0.50 +/- 0.02 mmol/l) and increased during moderate exercise (to 0.64 +/- 0.04 mmol/l; P < 0.05). Thus the molar ratio (a-v difference, O(2) to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 +/- 0.03 to 0.18 +/- 0.04 mmol/l) was taken into account, the O(2)-to-carbohydrate ratio decreased (from 6.1 +/- 0.4 to 4.7 +/- 0.3; P < 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O(2) demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O(2)-to-carbohydrate uptake.

Adult↗

Middle cerebral artery flow velocity and cerebral oxygenation during abdominal aortic surgery.

Cerebral perfusion was evaluated in twelve patients undergoing elective infra-renal abdominal aortic aneurysmectomy by transcranial Doppler ultrasonography-determined middle cerebral artery mean flow velocity, near-infrared spectroscopy-assessed cerebral oxygen saturation and systemic haemodynamic variables. The middle cerebral artery mean flow velocity and cerebral oxygen saturation decreased during cross-clamping of the aorta, and both increased upon declamping of the aorta with the oxygen saturation change lagging behind the change in the flow velocity. The changes in cerebral flow velocity and oxygen saturation paralleled the deviations in cardiac output and end-tidal carbon dioxide tension.

Aged↗

Continuous stroke volume monitoring by modelling flow from non-invasive measurement of arterial pressure in humans under orthostatic stress.

The relationship between aortic flow and pressure is described by a three-element model of the arterial input impedance, including continuous correction for variations in the diameter and the compliance of the aorta (Modelflow). We computed the aortic flow from arterial pressure by this model, and evaluated whether, under orthostatic stress, flow may be derived from both an invasive and a non-invasive determination of arterial pressure. In 10 young adults, Modelflow stroke volume (MFSV) was computed from both intra-brachial arterial pressure (IAP) and non-invasive finger pressure (FINAP) measurements. For comparison, a computer-controlled series of four thermodilution estimates (thermodilution-determined stroke volume; TDSV) were averaged for the following positions: supine, standing, head-down tilt at 20 degrees (HDT20) and head-up tilt at 30 degrees and 70 degrees (HUT30 and HUT70 respectively). Data from one subject were discarded due to malfunctioning thermodilution injections. A total of 155 recordings from 160 series were available for comparison. The supine TDSV of 113+/-13 ml (mean+/-S.D.) dropped by 40% to 68+/-14 ml during standing, by 24% to 86+/-12 ml during HUT30, and by 51% to 55+/-15 ml during HUT70. During HDT20, TDSV was 114+/-13 ml. MFSV for IAP underestimated TDSV during HDT20 (-6+/-6 ml; P<0.05), but that for FINAP did not (-4+/-7 ml; not significant). For HUT70 and standing, MFSV for IAP overestimated TDSV by 11+/-10 ml (HUT70; P<0.01) and 12+/-9 ml (standing; P<0.01). However, the offset of MFSV for FINAP was not significant for either HUT70 (3+/-8 ml) or standing (3+/-9 ml). In conclusion, due to orthostasis, changes in the aortic transmural pressure may lead to an offset in MFSV from IAP. However, Modelflow correctly calculated aortic flow from non-invasively determined finger pressure during orthostasis.

Adult↗

Mesenteric, coeliac and splanchnic blood flow in humans during exercise.

1. Exercise reduces splanchnic blood flow, but the mesenteric contribution to this response is uncertain. 2. In nineteen humans, superior mesenteric and coeliac artery flows were determined by duplex ultrasonography during fasting and postprandial submaximal cycling and compared with the splanchnic blood flow as assessed by the Indocyanine Green dye-elimination technique. 3. Cycling increased arterial pressure, heart rate and cardiac output, while it reduced total vascular resistance. These responses were not altered in the postprandial state. During fasting, cycling increased mesenteric, coeliac and splanchnic resistances by 76, 165 and 126 %, respectively, and it reduced corresponding blood flows by 32, 50 and 43 % (by 0.18 +/- 0.04, 0.42 +/- 0.03 and 0.60 +/- 0.04 l min-1). Postprandially, mesenteric and splanchnic vascular resistances decreased, thereby elevating regional blood flow, while the coeliac circulation was not influenced. Postprandial cycling did not influence the mesenteric resistance significantly, but its blood flow decreased by 22 % (0.46 +/- 0.28 l min-1). Coeliac and splanchnic resistance increased by 150 and 63 %, respectively, and the corresponding regional blood flow decreased by 51 and 31 % (0.49 +/- 0.07 and 0.96 +/- 0.28 l min-1). Splanchnic blood flow values assessed by duplex ultrasound and by dye-elimination techniques were correlated (r = 0.70; P < 0.01). 4. During submaximal exercise in humans, splanchnic resistance increases and blood flow is reduced following a 50 % reduction in the hepato-splenic and a 25 % reduction in the mesenteric blood flow.

Adult↗

The influence of PaO2, pH and SaO2 on maximal oxygen uptake.

Influence of arterial oxygen pressure (PaO2) and pH on haemoglobin saturation (SaO2) and in turn on O2 uptake (VO2) was evaluated during ergometer rowing (156, 276 and 376 W; VO2max, 5.0 L min-1; n = 11). During low intensity exercise, neither pH nor SaO2 were affected significantly. In response to the higher work intensities, ventilations (VE) of 129 +/- 10 and 155 +/- 8 L min-1 enhanced the end tidal PO2 (PETO2) to the same extent (117 +/- 2 mmHg), but PaO2 became reduced (from 102 +/- 2 to 78 +/- 2 and 81 +/- 3 mmHg, respectively). As pH decreased during maximal exercise (7.14 +/- 0.02 vs. 7.30 +/- 0.02), SaO2 also became lower (92.9 +/- 0.7 vs. 95.1 +/- 0.1%) and arterial O2 content (CaO2) was 202 +/- 3 mL L-1. An inspired O2 fraction (F1O2) of 0.30 (n = 8) did not affect VE, but increased PETO2 and PaO2 to 175 +/- 4 and 164 +/- 5 mmHg and the PETO2-PaO2 difference was reduced (21 +/- 4 vs. 36 +/- 4 mmHg). pH did not change when compared with normoxia and SaO2 remained within 1% of the level at rest in hyperoxia (99 +/- 0.1%). Thus, CaO2 and VO2max increased to 212 +/- 3 mL L-1 and 5.7 +/- 0.2 L min-1, respectively. The reduced PaO2 became of importance for SaO2 when a low pH inhibited the affinity of O2 to haemoglobin. An increased F1O2 reduced the gradient over the alveolar-arterial membrane, maintained haemoglobin saturation despite the reduction in pH and resulted in increases of the arterial oxygen content and uptake.

Adult↗

Contribution of pH, diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip.

The relative importance of pH, diprotonated phosphate (H2PO4-) and potassium (K+) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 +/- 1 to 103 +/- 2 mmHg, [K+] from 4.1 +/- 0.1 to 5.1 +/- 0.1 mmol L-1, while the intracellular (7.00 +/- 0.01 to 6.80 +/- 0.06) and venous pH fell (7.39 +/- 0.01 to 7.30 +/- 0.01) (P < 0.05). The intracellular [H2PO4-] increased 8.4 +/- 2 mmol kg-1 and the venous [H2PO4-] from 0.14 +/- 0.01 to 0.16 +/- 0.01 mmol L-1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H2PO4-] as well as a low intracellular and venous pH. However, venous [K+] and [H2PO4-] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 +/- 3 mmHg, [K+] to 5.8 +/- 0.2 mmol L-1, the intracellular and extracellular [H2PO4-] by 20 +/- 5 mmol kg-1 and to 0.20 +/- 0.02 mmol L-1, respectively, while the intracellular (6.33 +/- 0.06) and venous pH fell (7.23 +/- 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.

Adult↗

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass.

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective beta 1 adrenergic blockade (0.15 mg kg-1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 +/- 13 vs. 260 +/- 16%), heart rate (114 +/- 3 vs. 135 +/- 7 beats min-1) and mean arterial pressure (103 +/- 3 vs. 112 +/- 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 +/- 3 to 66 +/- 3 vs. 60 +/- 2 to 72 +/- 3 cm s-1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest: -4.8 +/- 1.8 vs. 1.2 +/- 1.7 mumol L-1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.

Adrenergic beta-1 Receptor Antagonists↗

Near-infrared spectrophotometry determined brain oxygenation during fainting.

During orthostatic hypotension we evaluated whether presyncopal symptoms relate to a reduced brain oxygenation. Nine subjects performed 50 degrees head-up tilt for 1 h and eight subjects were followed during 2 h of supine rest and during 1 h of 10 degrees head-down tilt. Cerebral perfusion was assessed by transcranial Doppler determined middle cerebral artery blood velocity (MCA vmean), while brain blood oxygenation was assessed by near-infrared spectrophotometry determined concentration changes for oxygenated (delta HbO2) and deoxygenated haemoglobin and brain cell oxygenation by the oxidized cytochrome c concentration (delta CytO2). During head-up tilt, six volunteers developed presyncopal symptoms and mean arterial pressure (88 (78-103) to 68 (57-79) mmHg; median and range), heart rate (96 (72-111) to 65 (50-107) beats min-1), MCA vmean (59 (51-82) to 41 (29-56) cm s-1), delta HbO2 (by -5.3 (-3.0 to -14.8) mumol l-1) and delta CytO2 were reduced (by -0.2 (-0.1 to -0.4) mumol l-1; P < 0.05). During tilt down the cardiovascular variables recovered immediately and delta HbO2 increased to 2.2 (-0.9-12.0) mmol L-1 above the resting value and also delta CytO2 recovered. In the nonsyncopal head-up tilted subjects as in the controls, blood pressure, heart rate, MCA vmean and brain oxygenation indices remained stable. The results suggest that during orthostasis, presyncopal symptoms relate not only to cerebral hypoperfusion but also to reduced brain oxygenation.

Adult↗

Lower leg electrical impedance after distal bypass surgery.

Electrical impedance was determined in 13 patients following distal bypass surgery to evaluate lower leg oedema as reflected by its circumference. Tissue injury was assessed by the plasma concentration of muscle enzymes. After surgery, the volume of the control lower leg increased from 1250 (816-2373) to 1384 (874-2345) ml (median and range; P < 0.05), where the impedance did not change significantly from 140 (92-181) ohms. The volume of the operated leg increased more [from 1129 (824-2373) to 1600 (1090-2837) ml], and the decrease in electrical impedance was also pronounced [137 (125-169) to 83 (69-104) ohms (P < 0.001)]. Tissue injury after surgery was indicated by an increase in total creatine kinase (n = 17) and MB isoenzyme of creatine kinase (n = 8) (P < 0.05). Myoglobin (n = 8) had increased already during surgery (P < 0.05), whereas there was no significant change in the plasma concentration of troponin I (n = 8). In conclusion, tissue injury was reflected by increases in muscle enzymes in plasma. We found an inverse correlation between lower leg electrical impedance and volume, but the deviation in electrical impedance was approximately twice that of the leg volume. Electrical impedance appears to be a useful method for the evaluation of lower leg oedema after distal bypass surgery.

Adult↗

Cholinergic blockade and the mesenteric artery response to head-up tilt-induced central hypovolaemia.

The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head-up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.v. glycopyrron. During supine rest, cholinergic blockade increased heart rate from 58 +/- 3 to 106 +/- 6 beats min-1 (mean +/- SE) and mean arterial pressure from 81 +/- 3 to 97 +/- 4 mmHg (P < 0.01) and it reduced the cardiac stroke volume from 89 +/- 6 to 59 +/- 7 ml (P < 0.01) with no significant effect on the SMA diameter and blood flow velocities. HUT provoked a further increase in heart rate to 134 +/- 5 beats min-1 (P < 0.01) and a reduction in stroke volume to 45 +/- 4 ml (P < 0.01). The early diastolic velocity increased from -51 +/- 4 to 6 +/- 8 cm s-1 during the normotensive stage of HUT and further to 21 +/- 9 cm s-1 during the hypotensive stage with a reduction in mean arterial pressure from 97 +/- 4 to 73 +/- 7 mmHg (P < 0.01) but, in contrast to control HUT (without cholinergic blockade), the end-diastolic velocity did not change significantly. Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance. Likewise, during hypovolaemia, a glycopyrron-induced inhibition in diastolic velocity supports an increase in SMA impedance. The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.

Adult↗

Glycogen depletion and lactate accumulation in human intercostal muscles after administration of succinylcholine.

I.m. glycogen content, lactate concentration and staining intensity for glycogen in slow- (ST) and fast-twitch (FTa and FTb) fibres were determined in the external and internal intercostal muscles after thoracotomy. Thirteen patients received a precurarizing dose of a non-depolarizing neuromuscular blocking agent followed by the depolarizing agent, succinylcholine, to facilitate intubation of the trachea (succinylcholine group). Nine patients received pancuronium or gallamine (control group). There were no significant differences in ventilatory functional capacity between the two groups. In the external intercostal muscles, lower i.m. glycogen content was observed in the succinylcholine compared with the control group (P < 0.05). I.m. glycogen was depleted from the FT fibres and in particular from FTb fibres, while little depletion was noted in ST fibres. In both the external and internal intercostal muscles, a higher lactate concentration was observed in the succinylcholine than in the control group (P < 0.05). The results indicate that the use of succinylcholine for tracheal intubation stimulated breakdown of i.m. glycogen, particularly in fast-twitch muscle fibres, and caused accumulation of lactate in intercostal muscles.

Adult↗

N-acetylcysteine does not affect the lymphocyte proliferation and natural killer cell activity responses to exercise.

This study evaluated whether N-acetylcysteine (NAC) attenuates the reduced lymphocyte proliferation and natural killer (NK) cell activity responses to exercise in humans. Fourteen oarsmen were double-blind randomized to either NAC (6 g daily for 3 days) or placebo groups. During 6-min "all-out" ergometer rowing, the concentration of lymphocytes in the peripheral blood increased, with no significant difference between NAC and placebo as reflected in lymphocyte subsets: CD4(+), CD8(+), CD16(+), and CD19(+) cells. The phytohemagglutinin-stimulated lymphocyte proliferation decreased from 9,112 +/- 2,865 to 5,851 +/- 1,588 cpm (P < 0.05), but it was not affected by NAC. During exercise, the NK cell activity was elevated from 17 +/- 3 to 38 +/- 4% and it decreased to 7 +/- 1% below the resting value 2 h into recovery. Yet, when evaluated as lytic units per CD16(+) cell, the NK cell activity decreased during and after exercise without a significant effect of NAC. We conclude that NAC does not attenuate the reduction in lymphocyte proliferation and NK cell activity associated with intense exercise.

Acetylcysteine↗

Tolerance to head-up tilt and suspension with elevated legs.

OBJECTIVE: Orthostatic hypotension is usually a benign event. However, some patients are disabled by frequent syncopal events, and vertical transportation during helicopter rescue, for example, may even be fatal. Normal orthostatic tolerance is poorly defined, so we evaluated the response to 50 degrees head-up tilt. Also, the effect of leg elevation was examined in order to establish the influence of venous return, and a fatal accident associated with orthostasis is reported. METHODS: There were 79 volunteers who were subjected to 50 degrees head-up tilt, and 9 subjects performed 1 h of suspension by double strops placed around the thorax and knee bends, respectively. The time to presyncope and changes in BP, heart rate, thoracic electrical impedance, central venous pressure and central venous and muscle oxygen saturations were measured. RESULTS: Head-up tilt resulted in hypotension, bradycardia and presyncopal symptoms in 69 subjects within 1 h (87%; half time 27 min), but during suspension with elevated legs in only one subject (11%; p < 0.02). In presyncopal subjects the central blood volume was reduced as reflected by an elevated thoracic electrical impedance and reduced central venous and muscle oxygen saturations. CONCLUSIONS: During 50 degrees head-up tilt, half of 79 subjects near-fainted within 27 min, whereas elevation of the legs secured venous return to the heart and prevented presyncopal symptoms. The high rate of near-fainting in normal subjects should be taken into account during evaluation of patients with syncope, and it emphasizes the use of a position that secures venous return during transportation.

Adult↗

Lower body impedance for the evaluation of venovenous bypass flow.

Inferior vena cava (IVC) clamping during liver transplantation causes venous congestion in the splanchnic and IVC beds. A venovenous bypass relieves congestion and improves cardiac output (CO), but the bypass flow required for adequate drainage of the vascular beds is controversial. In this study we evaluated the bypass flow necessary to compensate for the IVC clamping. Lower body impedance (BI) is inversely related to tissue fluid content and was used to reflect congestion. A venovenous bypass was successfully applied to 59 of 62 patients. BI was measured across the left buttock and related to bypass flow, CO, bypass flow ratio (bypass flow/CO before IVC clamping; n = 62), and right femoral venous pressure (n = 8). The bypass flow was 1.7 (0.0-3.0) L.min-1 (median and range). BI decreased (delta BI; -2.2 [-10.3-1.1)] omega) as the femoral venous pressure increased (29 [21-49] mm Hg; r = -0.81; P < .05), and the femoral venous pressure correlated inversely to bypass flow (r = -0.35; P < .01). The change in CO at IVC clamping (delta CO; -2.3 [-6.3-1.6] L.min-1) related to bypass flow ratio (0.25 [0-0.51]; r = 0.57, P < .01), whereas delta BI related only minimally to bypass flow or bypass flow ratio (r = 0.37; P < .05). In conclusion the median bypass flow of 1.7 L.min-1 was too small to prevent fluid accumulation in the lower caval region, and extrapolation of data suggests that bypass flow should have approached 3.5 L.min-1 or 50% of CO in order to prevent fluid accumulation in the lower caval region. However the minimal correlation between lower BI and bypass flow indicates that bypass flow per se is not the only determinant of lower body fluid accumulation.

Adult↗

Influence of Naloxone on the cellular immune response to head-up tilt in humans.

To evaluate a possible role for beta-endorphin in the stress-induced modulation of natural killer (NK) cells, immunologically competent blood cells were followed in eight male volunteers administered either Naloxone or saline (control) during head-up tilt maintained until the appearance of presyncopal symptoms (PS). The PS appeared more rapidly with Naloxone compared to control [5.7 (SEM 1.1) vs 22.3 (SEM 5.1) min; P = 0.01]. The NK cell activity increased threefold during PS partly due to an increase in CD16+ and CD56+ NK cells in blood. In support, NK cell activity boosted with interferon-alpha and interleukin 2 rose in parallel with unboosted NK cell activity and NK cell concentration and activities returned to the baseline level after 105 min. The total lymphocyte count and the concentrations of CD3+, CD4+, CD8+, CD16+, and CD56+ cells increased during PS. Head-up tilt also induced an increase in plasma adrenaline concentration during control PS and a rise in plasma cortisol and adrenocorticotropic hormone concentrations up to 30 min thereafter, whereas no significant changes were found in plasma concentrations of noradrenaline, growth hormone, or beta-endorphin. The results would indicate an influence of endorphin on the increase in plasma adrenaline concentration during head-up tilt and at the same time contra-indicate a significant role for adrenaline in the provocation of PS. The influence of head-up tilt on plasma beta-endorphin was too small to influence the modulation of the cellular immune system.

Adult↗

Near-infrared spectroscopy during peripheral vascular surgery.

Near-infrared spectroscopy was performed perioperatively on the dorsum of the foot in 14 patients who underwent infrainguinal bypass surgery using a prosthesis or the greater saphenous vein. Dual-wavelength continuous light spectroscopy was used to assess changes in tissue saturation before, during and after the operation. Following the use of peripheral vascular grafts an immediate postoperative increase in tissue saturation of median 28 (range -10 to +81) arbitrary units was noted (P < 0.01). Following distal clamping of the common femoral artery, maximal ischaemia corresponding to a median reduction in tissue saturation of 61 (range 6-94) units was reached after 26 (range 8-95) min (P < 0.01). The maximal tissue saturation following declamping was median 27 (range -16 to +100) units higher than the preoperative level (P < 0.01) and was reached after median 42 (range 8-125) min. The results indicate that near-infrared spectroscopy is appropriate for perioperative monitoring during vascular grafting.

Aged↗

Cardiovascular and catecholamine responses to static exercise in partially curarized humans.

Neural control of the circulation was evaluated during static exercise in 19 subjects by the determination of heart rate (HR), mean arterial pressure (MAP), cardiac output (CO) and plasma catecholamines. Influence from central command was evaluated during contractions with weakened muscles following partial curarization and reflex influence from metaboreceptors was assessed by post-exercise muscle ischaemia. Static handgrip increased HR and more so MAP and CO and MAP remained elevated during post-exercise muscle ischaemia. With partial curarization plasma catecholamines were also increased (P < 0.05). Two-leg extension increased all variables and during post-exercise muscle ischaemia elevations of HR, MAP and CO were maintained (P < 0.05). With partial curarization HR, MAP and plasma noradrenaline were even greater during the contraction. With the involvement of both legs during static exercise, reflex influence from the muscles elevated blood pressure by way of HR and CO and the importance of central command was detectable for HR and MAP as plasma catecholamines became elevated. However, the results indicate a separation between a central command influence on HR and CO related to an increase in plasma catecholamines during a handgrip, while the reflex influence on blood pressure was directed towards total peripheral resistance.

Adult↗

Middle cerebral artery blood velocity, arterial diameter and muscle sympathetic nerve activity during post-exercise muscle ischaemia.

During exercise the transcranial Doppler determined mean blood velocity (Vmean) increases in the middle cerebral artery (MCA) and reflects cerebral flood flow when the diameter at the site of investigation remains constant. Sympathetic activation could induce MCA vasoconstriction and in turn elevate Vmean at an unchanged cerebral blood flow. In 12 volunteers we evaluated whether Vmean relates to muscle sympathetic nerve activity (MSNA) in the peroneal nerve during rhythmic handgrip and post-exercise muscle ischaemia (PEMI). The luminal diameter of the dorsalis pedis artery (AD) was taken to reflect the MSNA influence on a peripheral artery. Rhythmic handgrip increased heart rate (HR) from 74 +/- 20 to 92 +/- 21 beats min-1 and mean arterial pressure (MAP) from 87 +/- 7 to 105 +/- 9 mmHg (mean +/- SD; P < 0.05). During PEMI, HR returned to pre-exercise levels while MAP remained elevated (101 +/- 9 mmHg). During handgrip contralateral MCA Vmean increased from 65 +/- 10 to 75 +/- 13 cm s-1 and this was more than on the ipsilateral side (from 63 +/- 10 to 68 +/- 10 cm s-1; P < 0.05). On both sides of the brain Vmean returned to baseline during PEMI. MSNA did not increase significantly during handgrip (from 56 +/- 24 to 116 +/- 39 units) but the elevation became statistically significant during PEMI (135 +/- 86 units, P < 0.05), while AD did not change. Taken together, during exercise and PEMI, Vmean changed independent of an elevation of MSNA by more than 140% and the dorsalis pedis artery diameter was stable. The results provide no evidence for a vasoconstrictive influence of sympathetic nerve activity on medium size arteries of the limbs and the brain during rhythmic handgrip and post-exercise muscle ischaemia.

Adult↗