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Background: Maintenance of euvolemia and cerebral perfusion are recommended for the prevention of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). We conducted a pilot randomized controlled study to assess the feasibility and efficacy of goal-directed therapy (GDT) to correct fluid and hemodynamic derangements during endovascular coiling in patients with aSAH., Methods: This study was conducted between November 2015 and February 2019 at a single tertiary center in Canada. Adult patients with aSAH within 5 days of aneurysm rupture were randomly assigned to receive either GDT or standard therapy during endovascular coiling. The incidence of dehydration at presentation and the efficacy of GDT were evaluated., Results: Forty patients were allocated to receive GDT (n=21) or standard therapy (n=19). Sixty percent of all patients were found to have dehydration before the coiling procedure commenced. Compared with standard therapy, GDT reduced the duration of intraoperative hypovolemia (mean difference 37.6 [95% confidence interval, 6.2-37.4] min, P=0.006) and low cardiac index (mean difference 30.7 [95% confidence interval, 9.5-56.9] min, P=0.035). There were no differences between the 2 treatment groups with respect to the incidence of vasospasm, stroke, death, and other complications up to postoperative day 90., Conclusions: A high proportion of aSAH patients presented at the coiling procedure with dehydration and a low cardiac output state; these derangements were more likely to be corrected if the GDT algorithm was used. Compared with standard therapy, use of the GDT algorithm resulted in earlier recognition and more consistent treatment of dehydration and hemodynamic derangement during endovascular coiling., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Aim: This study tested the hypothesis that non-α-adrenergic mechanisms contribute to systemic vascular conductance (SVC) in a reflex-specific manner during the sympathoexcitatory manoeuvres., Methods: Twelve healthy subjects underwent lower-body negative pressure (LBNP, -40 mmHg) as well as static handgrip exercise (HG, 20% of maximal force) followed by post-exercise forearm circulatory occlusion (PECO, 5 min each) with and without α-adrenergic blockade induced by phentolamine (PHE). Aortic blood flow, finger blood pressure and superficial femoral artery blood flow were measured to calculate cardiac output, SVC and leg vascular conductance (LVC) during the last minute of each intervention., Results: Mean arterial pressure (MAP) decreased more during LBNP with PHE compared with saline (-7 ± 7 vs. -2 ± 5%, P = 0.016). PHE did not alter the MAP response to HG (+20 ± 12 and +24 ± 16%, respectively, for PHE and saline) but decreased the change in MAP during PECO (+12 ± 7 vs. +21 ± 14%, P = 0.005). The decrease in SVC and LVC with LBNP did not differ between saline and PHE trials (-13 ± 10 vs. -17 ± 10%, respectively, for SVC, P = 0.379). In contrast, the SVC response to HG increased from -9 ± 12 with saline to + 5 ± 15% with PHE (P = 0.002) and from -16 ± 15 with saline to +1 ± 16% with PHE during PECO (P = 0.003). LVC responses to HG or PECO were not different from saline with PHE., Conclusions: Non-α-adrenergic vasoconstriction was present during LBNP. The systemic vasoconstriction during static exercise and isolated muscle metaboreflex activation, in the absence of leg vasoconstriction, was explained by an α-adrenergic mechanism. Therefore, non-α-adrenergic vasoconstriction is more emphasized during baroreflex, but not metaboreflex-mediated sympathetic activation., (© 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.)

This study tested the hypothesis that the compliance (C) and viscoelasticity (K) of the forearm vascular bed are controlled by myogenic and/or α-adrenergic receptor (αAR) activation. Heart rate (HR) and waveforms of brachial artery blood pressure (Finometer) and forearm blood flow (Doppler ultrasound) were measured in baseline conditions and during infusion of noradrenaline (NA; αAR agonist), with and without phentolamine (αAR antagonist; n = 10; 6 men and 4 women). These baseline and αAR-agonist-based measures were repeated when the arm was positioned above or below the heart to modify the myogenic stimulus. A lumped Windkessel model was used to quantify the values of forearm C and K in each set of conditions. Baseline forearm C was inversely, and K directly, related to the myogenic load (P < 0.001). Compared with saline infusion, C was increased, but K was unaffected, with phentolanine, but only in the 'above' position. Compliance was reduced (P < 0.001) and K increased (P = 0.06) with NA infusion (main effects of NA) across arm positions; phentolamine minimized these NA-induced changes in C and K for both arm positions. Examination of conditions with and without NA infusion at similar forearm intravascular pressures indicated that the NA-induced changes in C and K were due largely to the concurrent changes in blood pressure. Therefore, within the range of arm positions used, it was concluded that vascular stiffness and vessel wall viscoelastic properties are acutely affected by myogenic stimuli. Additionally, forearm vascular compliance is sensitive to baseline levels of αAR activation when transmural pressure is low.

The present study was designed to address the contribution of α-adrenergic modulation to the genesis of low-frequency (LF; 0.04-0.15 Hz) oscillations in R-R interval (RRi), blood pressure (BP) and muscle sympathetic nerve activity (MSNA) during different sympathetic stimuli. Blood pressure and RRi were measured continuously in 12 healthy subjects during 5 min periods each of lower body negative pressure (LBNP; -40 mmHg), static handgrip exercise (HG; 20% of maximal force) and postexercise forearm circulatory occlusion (PECO) with and without α-adrenergic blockade by phentolamine. Muscle sympathetic nerve activity was recorded in five subjects during LBNP and in six subjects during HG and PECO. Low-frequency powers and median frequencies of BP, RRi and MSNA were calculated from power spectra. Low-frequency power during LBNP was lower with phentolamine versus without for both BP and RRi oscillations (1.6 ± 0.6 versus 1.2 ± 0.7 ln mmHg(2), P = 0.049; and 6.9 ± 0.8 versus 5.4 ± 0.9 ln ms(2), P = 0.001, respectively). In contrast, the LBNP with phentolamine increased the power of high-frequency oscillations (0.15-0.4 Hz) in BP and MSNA (P < 0.01 for both), which was not observed during saline infusion. Phentolamine also blunted the increases in the LBNP-induced increase in frequency of LF oscillations in BP and RRi. Phentolamine decreased the LF power of RRi during HG (P = 0.015) but induced no other changes in LF powers or frequencies during HG. Phentolamine resulted in decreased frequency of LF oscillations in RRi (P = 0.004) during PECO, and a similar tendency was observed in BP and MSNA. The power of LF oscillation in MSNA did not change during any intervention. We conclude that α-adrenergic modulation contributes to LF oscillations in BP and RRi during baroreceptor unloading (LBNP) but not during static exercise. Also, α-adrenergic modulation partly explains the shift to a higher frequency of LF oscillations during baroreceptor unloading and muscle metaboreflex activation.

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.

Longitudinal changes in height, weight and physical performance were studied in 33 Flemish male youth soccer players from the Ghent Youth Soccer Project. The players' ages at the start of the study ranged from 10.4 to 13.7 years, with a mean age of 12.2 +/- 0.7 years. Longitudinal changes were studied over a 5 year period. Peak height velocity and peak weight velocity were determined using non-smoothed polynomials. The estimations of peak height velocity, peak weight velocity and age at peak height velocity were 9.7 +/- 1.5 cm x year-1, 8.4 +/- 3.0 kg x year-1 and 13.8 +/- 0.8 years, respectively. Peak weight velocity occurred, on average, at the same age as peak height velocity. Balance, speed of limb movement, trunk strength, upper-body muscular endurance, explosive strength, running speed and agility, cardiorespiratory endurance and anaerobic capacity showed peak development at peak height velocity. A plateau in the velocity curves was observed after peak height velocity for upper-body muscular endurance, explosive strength and running speed. Flexibility exhibited peak development during the tear after peak height velocity. Trainers and coaches should be aware of the individual characteristics of the adolescent growth spurt and the training load should also be individualized at this time.

Unlabelled: We compared the effects of desflurane and isoflurane on cerebral perfusion pressure (CPP), lumbar cerebrospinal fluid pressure (LCSFP), and mean arterial blood pressure (MAP) in patients anesthetized with desflurane or isoflurane undergoing craniotomy for supratentorial mass lesions. Additionally, emergence from anesthesia was examined to determine if neurologic function could be assessed earlier after isoflurane or desflurane anesthesia. Thirty-six patients were randomized to receive either desflurane or isoflurane for maintenance of anesthesia at 1.2 minimum alveolar concentration (MAC). Patients were hyperventilated (PaCO(2), 30 +/- 2 mm Hg) after baseline LCSFP was obtained via the subarachnoid catheter. At a MAC of 1.2, mean LCSFP was not statistically different between the two study groups either before or after hyperventilation. Additionally, CPP was not significantly different between the two groups. Finally, patient's time to respond to commands was 50% shorter in the desflurane group (30 +/- 36 min) (mean +/- SD) when compared with the isoflurane group (72 +/- 126 min); however, this was not significant (P = 0.17). In patients undergoing craniotomy for supratentorial mass lesions, desflurane and isoflurane have similar effects on CPP and MAP. Additionally, desflurane in the setting of hyperventilation does not cause significant changes in LCSFP., Implications: This is the largest study to date comparing the effects of desflurane and isoflurane on patients undergoing craniotomy for supratentorial mass lesion with evidence of midline shift or edema. Neither desflurane nor isoflurane significantly altered lumbar cerebrospinal fluid pressure when moderate hypocapnia was maintained.