Impacts of prolonged sitting with mild hypercapnia on vascular and autonomic function in healthy recreationally active adults.

Prolonged sitting, which is known to impair peripheral vascular function, often occurs in spaces (e.g., offices) with mild hypercapnic atmospheres. However, the effects of prolonged sitting in hypercapnic conditions on vascular function are unknown. Therefore, the purpose of this study was to investigate the effects of prolonged sitting in mild hypercapnic conditions on vascular and autonomic function in humans. Twelve healthy young adults participated in two experimental visits that consisted of sitting for 2.5 h in a control condition [normal atmospheric conditions sitting (PSIT)] or a mild hypercapnic condition (HCAP; CO2 = 1,500 ppm). During each visit, heart rate variability (HRV), blood pressure (BP), pulse wave velocity (PWV), augmentation index (AIx), brachial and popliteal artery flow-mediated dilation (FMD), and near-infrared spectroscopy (NIRS) were assessed before and after prolonged sitting. Sitting significantly decreased AIx in both groups (P < 0.05). Brachial and popliteal FMD were reduced with sitting (P < 0.05), and the reduction in popliteal FMD was amplified by HCAP (P < 0.05). Baseline microvascular oxygenation was decreased following sitting in both groups (P < 0.05). However, microvascular reoxygenation upon cuff release was slower only in HCAP (P < 0.05). HRV, HR, BP, and PWV did not significantly change with sitting in either group (P > 0.05). We conclude that prolonged sitting attenuated both brachial and popliteal endothelial function and was associated with perturbed microcirculation. Additionally, mild hypercapnic conditions further impaired peripheral endothelial and microvascular function. Together, these findings suggest that prolonged sitting is accompanied by a host of deleterious effects on the vasculature, which are exacerbated by mild hypercapnia.NEW & NOTEWORTHY The results of this study reveal that prolonged sitting attenuates endothelial function and microvascular function. Additionally, prolonged sitting with mild hypercapnia, which is similar to everyday environments, further exacerbates peripheral endothelial function and microvascular function.

Patterns of Distribution of the Nerves Around the Axillary Artery Evaluated by Ultrasound and Assessed by Nerve Stimulation During Axillary Block.

Our objective was to define the positions of the nerves around the brachial artery and, secondarily, to assess the risk of intraneural injection during dual guided axillary block. Sixty ultrasound-guided axillary blocks were performed. The locations of the musculocutaneous, median, ulnar, and radial nerves relative to the brachial artery were determined. The position of the ulnar nerve was defined in relation to that of the brachial vein, and the position of the musculocutaneous nerve in relation to the coracobrachialis muscle. The locations were confirmed by neurostimulation and injection of local anesthetic was avoided when the current intensities were below 0.3 mA. The incidences of intraneural injection and postblock neurological injury were recorded. The median nerve was located in the upper external quadrant in 89% of cases and the ulnar nerve in the upper internal quadrant (95%), superficial (19%), or deep (81%) to the brachial vein. The radial nerve was located in the lower internal quadrant in 97% of cases, and the musculocutaneous nerve in the lower external quadrant in 85%. Its disposition differed depending on its proximity to the artery (106 ± 26°) or whether it was inside the coracobrachialis muscle (119 ± 15°; P = 0.023). Three intraneural injections were observed (0.5%, one in the median and two in the radial nerves) and no patient had postblock neuropathy. Our study evidences slight anatomical variability among the neural structures in the axillary region and confirms the safety of the axillary technique with double monitoring, using ultrasound to monitor the approach of the needle to the nerve and nerve stimulation at currents > 0.3 mA to reduce the incidence of intraneural injection. Clin. Anat., 2018. © 2018 Wiley Periodicals, Inc. 2018.

Pharmacological assessment of the contribution of the arterial baroreflex to sympathetic discharge patterns in healthy humans.

To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside (NTP) and phenylephrine (PE) and measured action potential (AP) patterns with wavelet-based methodology. We hypothesized that 1) baroreflex unloading (NTP) would increase firing of low-threshold axons and recruitment of latent axons and 2) baroreflex loading (PE) would decrease firing of low-threshold axons. Heart rate (HR, ECG), arterial blood pressure (BP, brachial catheter), and muscle sympathetic nerve activity (MSNA, microneurography of peroneal nerve) were measured at baseline and during steady-state systemic, intravenous NTP (0.5-1.2 µg·kg-1·min-1, n = 13) or PE (0.2-1.0 µg·kg-1·min-1, n = 9) infusion. BP decreased and HR and integrated MSNA increased with NTP ( P < 0.01). AP incidence (326 ± 66 to 579 ± 129 APs/100 heartbeats) and AP content per integrated burst (8 ± 1 to 11 ± 2 APs/burst) increased with NTP ( P < 0.05). The firing probability of low-threshold axons increased with NTP, and recruitment of high-threshold axons was observed (22 ± 3 to 24 ± 3 max cluster number, 9 ± 1 to 11 ± 1 clusters/burst; P < 0.05). BP increased and HR and integrated MSNA decreased with PE ( P < 0.05). PE decreased AP incidence (406 ± 128 to 166 ± 42 APs/100 heartbeats) and resulted in fewer unique clusters (15 ± 2 to 9 ± 1 max cluster number, P < 0.05); components of an integrated burst (APs or clusters per burst) were not altered ( P > 0.05). These data support a hierarchical pattern of sympathetic neural activation during manipulation of baroreceptor afferent activity, with rate coding of active neurons playing the predominant role and recruitment/derecruitment of higher-threshold units occurring with steady-state hypotensive stress. NEW & NOTEWORTHY To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside and phenylephrine and measured sympathetic outflow with wavelet-based methodology. Baroreflex unloading increased sympathetic activity by increasing firing probability of low-threshold axons (rate coding) and recruiting new populations of high-threshold axons. Baroreflex loading decreased sympathetic activity by decreasing the firing probability of larger axons (derecruitment); however, the components of an integrated burst were unaffected.

Impact of sympathetic nervous system activity on post-exercise flow-mediated dilatation in humans.

Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 ± 5 years) undertook two 30 min sessions of cycle exercise at 75% HR(max). Prior to exercise, individuals ingested either a placebo or an α1-adrenoreceptor blocker (prazosin; 0.05 mg kg(-1)). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test, P = 0.03). In contrast, FMD increased (37%) immediately following exercise in the prazosin condition (t-test, P = 0.004, interaction effect P = 0.01). Post-exercise FMD remained different between conditions after correction for baseline diameters preceding cuff deflation and also post-deflation SR. No differences in FMD or other variables were evident 60 min following recovery. Our results indicate that sympathetic vasoconstriction competes with endothelium-dependent dilator activity to determine post-exercise arterial function. These findings have implications for understanding the chronic impacts of interventions, such as exercise training, which affect both sympathetic activity and arterial shear stress.

Impact of shear rate pattern on upper and lower limb conduit artery endothelial function in both spinal cord-injured and able-bodied men.

NEW FINDINGS: What is the central question of this study? This study addresses the following two central questions. (i) What is the impact of vascular deconditioning after spinal cord injury (SCI) on shear rate patterns and endothelial function? (ii) What is the impact of acutely altered shear rate on endothelial function in both SCI and able-bodied control subjects? What is the main finding and its importance? Two main findings in the present study were as follows: (i) reduced superficial femoral artery endothelial function in the SCI group; and (ii) acutely altered shear rate decreased endothelial function in both SCI and able-bodied control subjects. These findings may shed some light on future interventions taking into account these regulatory mechanisms. Spinal cord injury (SCI) induces vascular deconditioning below the level of the lesion and disrupts sympathetic innervation of blood vessels. It is unclear how these changes affect shear rate (SR) profiles and endothelial function when compared with able-bodied (AB) persons. Recent evidence suggests that periods of increased retrograde SR are associated with acute decreases in endothelial function, but is unknown how modified SR patterns influence sublesional vasculature in SCI. The present study examined the acute and chronic effects of altered SR patterns and oscillatory shear index on endothelial function via relative flow-mediated dilatation (FMD%) in both the brachial and superficial femoral arteries (BA and SFA, respectively) of eight individuals with SCI and eight matched AB control subjects. Baseline BA SR patterns and FMD% were similar between groups, while SFA anterograde SR was higher (P < 0.01) and FMD% lower (P = 0.04) in SCI versus AB subjects. Shear rate patterns were then acutely altered through the BA and SFA using a subsystolic cuff-inflation model. Bilateral FMD assessments were conducted before and after 30 min of unilateral inflation of a forearm or thigh blood pressure cuff to 75 mmHg. Cuff inflation resulted in concomitant increases in both anterograde (P < 0.05) and retrograde SR (P < 0.05), as well as acute decreases in FMD% (P < 0.05) in the BA and SFA in both groups. These results highlight that brief manipulation of SR patterns can acutely impair FMD% in conditions of both normal and altered sympathetic innervation and arterial remodelling. This information is crucial when designing strategies to combat impaired vascular function in both healthy and clinical populations.

Asymmetric bilateral variations in the musculocutaneous and median nerves with high branching of brachial artery.

Brachial Plexus is formed by the union of the anterior rami of cervical 5, 6, 7, 8 and thoracic 1 nerves. These nerves unite and divide to form the key nerves innervating the upper limb. Variations in the course of these nerves are clinically important to anesthetists, neurologists and orthopedicians. We report bilateral variations in the arterial and neural structures in the upper limb of a 65 year old cadaver. The muscles of the arm on one side were innervated by the median nerve with absence ofmusculocutaneous. While on the other side the musculocutaneous nerve contributed to the formation of the median nerve. There was a presence of high bifurcation of brachial artery on both sides. Knowledge of such variations in the innervations of muscles and the arterial supply of the limbs are important to remember before performing any reconstructive procedures or interventions on the limb.

[The efficacy of hand desimpatization after sympatectomy by complex regional pain syndrome].

64 patients operated on the reason of complex regional hand pain syndrome were examined with the use of laser spectral Doppler flowmetry and thermography. 33 patients had thoracoscopic Th3 ganglion clipation; 16 patients had brachial artery and vein perivascular sympathectomy; 15 patients periarterial sympathectomy on the level of brachial artery. Desympathisation (microcirculatory hemodynamic improvement and trophotropic microcirculation regulatory changes) was mostly apparent after thoracoscopic clipation and perivascular desympatisation in comparison with isolated periarterial sympatectomy.

Changes in electrocardiogram parameters during acute nonshivering cold exposure and associations with brown adipose tissue activity, plasma catecholamine levels, and brachial blood pressure in healthy adults.

BACKGROUND: Sympathetic activity causes changes in electrocardiogram (ECG) during cold exposure and the changes have been studied mostly during hypothermia and less during mild acute nonshivering cold exposure. Cold-induced sympathetic activity also activates brown adipose tissue (BAT) and increases arterial blood pressure (BP) and plasma catecholamine levels. We examined changes in ECG parameters during acute nonshivering cold exposure and their associations with markers of sympathetic activity during cold exposure: brachial blood pressure (BP), plasma catecholamine levels, and BAT activity measured by positron emission tomography (PET). METHODS AND RESULTS: Healthy subjects (M/F = 13/24, aged 20-55 years) were imaged with [15 O]H2 O (perfusion, N = 37) and [18 F]FTHA to measure plasma nonesterified fatty acid uptake (NEFA uptake, N = 37) during 2-h nonshivering cold exposure. 12-lead ECG (N = 37), plasma catecholamine levels (N = 17), and brachial BP (N = 31) were measured at rest in room temperature (RT) and re-measured after a 2-h nonshivering cold exposure. There were significant differences between RT and cold exposure in P axis (35.6 ± 26.4 vs. 50.8 ± 22.7 degrees, p = 0.005), PR interval (177.7 ± 24.6 ms vs.163.0 ± 28.7 ms, p = 0.001), QRS axis (42.1 ± 31.3 vs. 56.9 ± 24.1, p = 0.003), and QT (411.7 ± 25.5 ms vs. 434.5 ± 39.3 ms, p = 0.001). There was no significant change in HR, QRS duration, QTc, JTc, and T axis during cold exposure. Systolic BP (127.2 ± 15.7 vs. 131.8 ± 17.9 mmHg, p = 0.008), diastolic BP (81.7 ± 12.0 vs. 85.4 ± 13.0 mmHg, p = 0.02), and plasma noradrenaline level increased during cold exposure (1.97 ± 0.61 vs. 5.07 ± 1.32 µmol/L, p = 0.001). Cold-induced changes in ECG parameters did not correlate with changes in BAT activity, brachial BP, plasma catecholamines, or skin temperature. CONCLUSIONS: During short-term nonshivering cold exposure, there were increases in P axis, PR interval, QRS axis, and QT compared to RT in healthy adults. Cold-induced changes in ECG parameters did not correlate with BAT activity, brachial BP, or plasma catecholamine levels which were used as markers of cold-induced sympathetic activity.

Alterations in the peripheral circulation in COPD patients.

RATIONALE: Although various factors influence peripheral circulation in chronic obstructive pulmonary disease (COPD) patients, little is known about the vasomotor changes in these subjects. OBJECTIVES: The present study was designed to assess alterations in the brachial circulation of COPD patients. METHODS: Twenty-five COPD patients and 25 healthy subjects were studied. Brachial artery (BA) blood flow and indices of BA stiffness were investigated by two-dimensional ultrasonography and pulsed Doppler. Cardiac dimensions, left ventricular (LV) function and cardiac output were assessed by pulsed Doppler echocardiography. MAIN RESULTS: A significant increase in LV mass was observed in the COPD group despite normal arterial pressure. Total arterial compliance and BA compliance were significantly decreased in COPD patients in comparison with healthy subjects. Heart rate was increased in COPD patients and was inversely correlated with PaO(2) and forced expiratory volume in the first second (FEV(1)). A decrease in LV preload was expressed by a reduction in LV diastolic diameters and LV stroke volume. Patients with severe COPD have a lower BA surface area than patients with moderate COPD. FEV(1) and PaO(2) were significantly related to BA compliance. CONCLUSION: In COPD patients, significant alterations in the peripheral circulation were observed. Moreover, the magnitude of changes in the peripheral circulation was related to the severity of COPD.

A case of spinal cord stimulation in Raynaud's Phenomenon: can subthreshold sensory stimulation have an effect?

Spinal cord stimulation is currently used to treat a variety of chronic intractable painful conditions. We report a case of severe Raynaud's phenomenon in the hands refractory to conservative treatment and responsive to diagnostic stellate ganglion block that was effectively treated with a spinal cord stimulator placed in the cervical epidural space. After capturing the affected areas with paresthesias, blood flow in the left hand and fingers significantly improved as evidenced by an increase in skin temperature, a change from cyanotic to pink appearance and concomitant reduction in pain. Moreover, the patient reported that limb ischemia and pain could be managed overnight with stimulation intensities that were below sensory perception thresholds. Thus it seems, at least in the overnight period, paresthesias were not required to maintain pain relief. This case presents a potential divergence between a requirement for paresthesias and pain relief in spinal cord stimulation therapy for the treatment of Raynaud's phenomenon. The possible role of the sympathetic nervous system in this relationship is also discussed.

Immunohistochemical and biochemical evidence for the presence of serotonin-containing neurons and nerve fibers in the octopus arm.

The octopus arm contains a tridimensional array of muscles with a massive sensory-motor system. We herein provide the first evidence for the existence of serotonin (5-HT) in the octopus arm nervous system and investigated its distribution using immunohistochemistry. 5-HT-like immunoreactive (5-HT-lir) nerve cell bodies were exclusively localized in the cellular layer of the axial nerve cord. Those cell bodies emitted 5-HT-lir nerve fibers in the direction of the sucker, the intramuscular nerves cords, the ganglion of the sucker, and the intrinsic musculature. Others 5-HT-lir nerve fibers were observed in various tissues, including the cerebrobrachial tract, the skin, and the blood vessels. 5-HT was detected by high-performance liquid chromatography in various regions of the octopus arm at levels matching the density of 5-HT-lir staining. The absence of 5-HT-lir interconnections between the cerebrobrachial tract and the other components of the axial nerve cord suggests that two types of 5-HT-lir innervation exist in the arm. One type, which originates from the brain, may innervate the periphery through the cerebrobrachial tract. Another type, which originates in the cellular layer of the axial nerve cord, may form an intrinsic network in the arm. In addition, 5-HT-lir fibers likely emitted from the neuropil of the axial nerve cord were found to project into cells showing staining for peripheral choline acetyltransferase, a marker of sensory cells of the sucker. Taken together, these observations suggest that intrinsic 5-HT-lir innervation may participate in the sensory transmission in the octopus arm.

The reliability of a single protocol to determine endothelial, microvascular and autonomic functions in adolescents.

BACKGROUND: Impairments in macrovascular, microvascular and autonomic function are present in asymptomatic youths with clustered cardiovascular disease risk factors. This study determines the within-day reliability and between-day reliability of a single protocol to non-invasively assess these outcomes in adolescents. METHODS: Forty 12- to 15-year-old adolescents (20 boys) visited the laboratory in a fasted state on two occasions, approximately 1 week apart. One hour after a standardized cereal breakfast, macrovascular function was determined via flow-mediated dilation (FMD). Heart rate variability (root mean square of successive R-R intervals; RMSSD) was determined from the ECG-gated ultrasound images acquired during the FMD protocol prior to cuff occlusion. Microvascular function was simultaneously quantified as the peak (PRH) and total (TRH) hyperaemic response to occlusion in the cutaneous circulation of the forearm via laser Doppler imaging. To address within-day reliability, a subset of twenty adolescents (10 boys) repeated these measures 90 min afterwards on one occasion. RESULTS: The within-day typical error and between-day typical error expressed as a coefficient of variation of these outcomes are as follows: ratio-scaled FMD, 5·1% and 10·6%; allometrically scaled FMD, 4·4% and 9·4%; PRH, 11% and 13·3%; TRH, 29·9% and 23·1%; and RMSSD, 17·6% and 17·6%. The within- and between-day test-retest correlation coefficients for these outcomes were all significant (r > 0·54 for all). CONCLUSION: Macrovascular, microvascular and autonomic functions can be simultaneously and non-invasively determined in adolescents using a single protocol with an appropriate degree of reproducibility. Determining these outcomes may provide greater understanding of the progression of cardiovascular disease and aid early intervention.

[Preclinical assessment of disturbances of vascular and vegetative reactivity of peripheral blood circulation in young men (students) with risk factors of atherosclerosis].

Hemodynamics of forearm and neurovegetative status were studied in 142 clinically healthy male students with risk factors of atherosclerosis and in 54 male students without risk factors of atherosclerosis at rest and during test with reactive hyperemia. Rheovasography of forearm, cardiointervalography, Doppler examination of brachial artery, and test with reactive hyperemia were undertaken in all subjects. The results testify to the fact that endothelial dysfunction leads to spastic state of regional hemodynamics and hyperactivity of sympathetic nervous system at rest as well as during reactive hyperemia which has a "delayed" character.

Vasopressin facilitates presynaptic sympathetic nerve activity in humans.

OBJECTIVE: It was the objective of this study to investigate whether a facilitatory role of vasopressin (AVP) on sympathetic nerve activity can be demonstrated in humans at the peripheral level. METHODS: Eight subjects (32 +/- 2.3 years) participated in this study. Forearm blood flow (FABF) was measured using the venous occlusion plethysmography model. Each session was performed in the presence of a continuous infusion (into the brachial artery) of AVP in sub-pressor dosage of 0.008 ng/kg per min, or NaCl 0.9%. Using lower-body negative pressure (LBNP) (-10, -20 and -30 mmHg) the combined pre- and postsynaptic action of AVP on the sympathetic nervous system was investigated. This was followed by a second protocol in which the possible postsynaptic effects of AVP were evaluated with intra-arterial infused norepinephrine (NE). RESULTS: The baseline FABF was 5.2 +/- 0.6 ml/100 ml per min. After infusion of AVP (0.008 ng/kg per min), the FABF remained unchanged at a flow of 5.5 +/- 0.6 ml/100 ml per min (P = 0.26). LBNP caused a pressure-dependent decrease in FABF (25.6 +/- 4.4, 29.0 +/- 6.1 and 38.6 +/- 6.9%, for -10, -20 and -30 mmHg, respectively). AVP significantly enhanced the FABF responses to lower-body negative pressures (38.0 +/- 8.6, 49.3 +/- 5.1 and 58.9 +/- 6.3%, respectively (P = 0.014). NE caused a dose-dependent vasoconstriction by 3.1 +/- 4.6, 17.0 +/- 4.3 and 23.2 +/- 4.9%, at dosages of 10, 20 and 40 pg/min, respectively, unaffected by AVP (P = 0.91). CONCLUSIONS: We conclude that AVP can facilitate vasoconstriction mediated by the peripheral sympathetic nervous system at the presynaptic level in humans.

Flow dependence of forearm noradrenaline overflow, as assessed during mental stress and sodium nitroprusside infusion.

OBJECTIVE: To evaluate the influence of blood flow on measurements of regional sympathetic nerve activity by radiotracer methodology ([3H]noradrenaline). DESIGN: Ten healthy men were studied under two conditions of elevated forearm blood flow: mental stress (Stroop colour word conflict test) and an intra-arterial infusion of sodium nitroprusside. METHODS: Arterial blood pressure was measured invasively and forearm blood flow with strain-gauge plethysmography. Arterial and venous plasma adrenaline and noradrenaline were measured with high-performance liquid chromatography, and regional and total noradrenaline spillover were calculated. RESULTS: During mental stress, mean arterial pressure increased by 17%, heart rate by 16 beats/min, forearm blood flow by 117%, while forearm vascular resistance decreased by 44% (P < 0.001 for all). Sodium nitroprusside increased forearm blood flow dose-dependently, but elicited only minor effects on systemic haemodynamics. Mental stress increased arterial plasma noradrenaline by 52% (P < 0.001), and total body noradrenaline spillover by 75% (P < 0.001). During sodium nitroprusside infusion, arterial plasma noradrenaline increased only slightly and total body noradrenaline spillover was unaffected Forearm noradrenaline overflow increased from 5.4 +/- 0.9 to 16.9 +/- 2.6 pmol/min per I (P < 0.001) during mental stress and from 6.6 +/- 0.8 to 16.9 +/- 3.7 pmol/min per I (P < 0.001) during the second dose-step of sodium nitroprusside infusion. By intra-individual comparisons of forearm noradrenaline overflow increases during mental stress and during sodium nitroprusside infusion, with similar forearm blood flow increases, the flow dependence of forearm noradrenaline overflow was estimated. During mental stress, about 60% (median value, range 29-112%) of the increase in forearm noradrenaline overflow was attributed to the increase in forearm blood flow, whereas 40% was considered to reflect increased sympathetic nerve activity. CONCLUSIONS: There seems to be a considerable flow dependence of the regional overflow of noradrenaline, that is, a component of simple wash-out of noradrenaline from the forearm tissues during vasodilation. However, the present results still indicate that sympathetic nerve activity in the forearm is increased during mental stress, justifying the radiotracer technique for semiquantitative measurements, also during vasodilation.

Removal of a Norplant implant located near a major nerve using interventional radiology-digital subtraction fluoroscopy.

Norplant implants can be removed easily, if inserted properly. When they are inserted deeply and can not be palpated, or if they are located close to the neurovascular structures of the upper arm, radiological guidance may be needed to locate and remove the implants without causing injury to the surrounding vital structures. Digital subtraction fluoroscopic guidance is helpful in removing deeply located contraceptive implants and those that are close to the neurovascular structures, where blind removal may result in injury to those structures. We describe a case in which an implant that was located close to a major nerve near the axilla was removed under digital subtraction fluoroscopic guidance.

PIP: When Norplant implants are inserted too deeply and cannot be palpated, or if they are located close to the neurovascular structures of the upper arm, radiologic guidance may be needed to locate and remove the implants without injury to surrounding structures. This paper describes a case in which digital subtraction fluoroscopic guidance was helpful in removing an implant located close to a major nerve near the axilla. This technique enables both localization and direct image-guided removal. The patient, a 36-year-old US woman, requested implant removal 18 months after insertion because she desired pregnancy. At removal of the sixth capsule, the patient reported pain suggestive of nerve stimulation. Soft tissue x-ray indicated the capsule was located deep in the tissues near the area of the brachial artery and nerve. Fluoroscopic-guided removal was successful in removing this capsule in 30 minutes.

[Anatomical organization, organogenesis and innervation of the arteries of the hand]. / Notions d'organisation anatomique, organogenèse et innervation des artères de la main.

The authors sum up the anatomical aspects of the arteries of the hand. They emphasise the fact that, by the side of the classical description; there is a lot of variations. These can be explained by organogenesis, showing that hand arteries pass over several stages, before reaching the terminal one. Generally, it seems that the classical diagram correspond to the majority of cases, and that there is a main flow for hand's arteries: this are the superficial and deep arches, which give common and proper digital arteries. About the innervation, this structures are very richly innervated, but this sympathetic innervation is not so precisely delimited in its topography, and for that reason, its seems to be difficult to give an clear diagram of its origin and distribution. That can explain surgical treatment's failure in vasomotor syndromes of upper limbs.

[Hypothalamic mechanisms of regulating blood circulation in the coronary and brachial artery systems]. / Gipotalamicheskie mekhanizmy reguliatsii krovoobrashcheniia v sistemakh koronarnoi i plechovoi arterii.

In anesthetized curarized cats effects of high frequency stimulation of anterior, ventromedial, and posterior hypothalamus on arterial blood pressure (ABP) and on perfusion pressure of the coronary and brachial arteries were studied. The stimulation induced vasoconstriction of coronary vessels and increased the ABP. In most experiments, especially in case of stimulation of anterior hypothalamus, simultaneously with increase of perfusion pressure of the coronary artery, a decrease of the brachial artery perfusion pressure was revealed. The mechanism of vasodilatation of the brachial artery seems to be related to a direct inhibition of the tonic activity of the vertebral branch of the ganglion stellatum. The descending influence of the hypothalamus in respect to the activity of the inferior cardiac nerve is mainly facilitatory. Mechanisms of neural control of the regional blood flow in coronary and brachial arteries are discussed.

Aging enhances autonomic support of blood pressure in women.

The autonomic nervous system plays a central role in both acute and chronic blood pressure regulation in humans. The activity of the sympathetic branch of the autonomic nervous system is positively associated with peripheral resistance, an important determinant of mean arterial pressure in men. In contrast, there is no association between sympathetic nerve activity and peripheral resistance in women before menopause, yet a positive association after menopause. We hypothesized that autonomic support of blood pressure is higher after menopause in women. We examined the effect of ganglionic blockade on arterial blood pressure and how this relates to baseline muscle sympathetic nerve activity in 12 young (25±1 years) and 12 older postmenopausal (61±2 years) women. The women were studied before and during autonomic blockade using trimethaphan camsylate. At baseline, muscle sympathetic nerve activity burst frequency and burst incidence were higher in the older women (33±3 versus 15±1 bursts/min; 57±5 versus 25±2 bursts/100 heartbeats, respectively; P<0.05). Muscle sympathetic nerve activity bursts were abolished by trimethaphan within minutes. Older women had a greater decrease in mean arterial pressure (-29±2 versus -9±2 mm Hg; P<0.01) and total peripheral resistance (-10±1 versus -5±1 mm Hg/L per minute; P<0.01) during trimethaphan. Baseline muscle sympathetic nerve activity was associated with the decrease in mean arterial pressure during trimethaphan (r=-0.74; P<0.05). In summary, our results suggest that autonomic support of blood pressure is greater in older women compared with young women and that elevated sympathetic nerve activity in older women contributes importantly to the increased incidence of hypertension after menopause.

Sildenafil increases sympathetically mediated vascular tone in humans.

BACKGROUND: Sildenafil, a selective phosphodiesterase-type-5 (PDE-5) inhibitor, produces vasodilation that improves erectile dysfunction and pulmonary hypertension. Sildenafil could also cause baroreflex sympathetic activation that would enhance vascular tone and oppose direct vasodilation. We tested the hypothesis that sildenafil administration increases sympathetically mediated vascular tone in healthy middle-aged men. METHODS: We randomized 9 healthy, middle-aged, male volunteers (mean age 45±2 years) in a double-blind, crossover fashion to receive a single oral dose of sildenafil 100mg or placebo on 2 separate study days. Hemodynamics and forearm blood flow responses were measured at baseline, at 30 and 45 minutes after study drug administration, and then during intra-arterial infusions of vasoactive drugs. After sildenafil and placebo administration, intrabrachial medications were infused to test forearm alpha receptor sensitivity (norepinephrine), cyclic-AMP-mediated vasodilation (isoproterenol), and sympathetically mediated vascular tone (phentolamine) (adenosine was a control vasodilator). Blood samples were taken before and 60 minutes after study drug administration and at the end of the intrabrachial infusions for measurement of plasma norepinephrine concentrations. RESULTS: Forearm vascular responses to norepinephrine, isoproterenol, and adenosine were not different after placebo and sildenafil administration. Percentage reduction in forearm vascular resistance during phentolamine was significantly lower after sildenafil than placebo (-73% ± 3% vs -63% ± 3%; P = 0.0002). Sildenafil significantly increased plasma norepinephrine compared with placebo 60 minutes after study drug administration and at the end of the study session (P = 0.02). CONCLUSIONS: Sildenafil increased sympathetically mediated vascular tone in middle-aged healthy men. Alpha-adrenergic-mediated vasoconstriction may offset vasodilation during PDE-5 inhibition and may explain the significant hypotension observed in patients taking alpha-blockers with sildenafil.