Effect of ingesting a meal and orthostasis on the regulation of splanchnic and systemic hemodynamics and the responsiveness of cardiovascular α1-adrenoceptors.

Postprandial orthostasis activates mechanisms of cardiovascular homeostasis to maintain normal blood pressure (BP) and adequate blood flow to vital organs. The underlying mechanisms of cardiovascular homeostasis in postprandial orthostasis still require elucidation. Fourteen healthy volunteers were recruited to investigate the effect of an orthostatic challenge (60°-head-up-tilt for 20 min) on splanchnic and systemic hemodynamics before and after ingesting an 800-kcal composite meal. The splanchnic circulation was assessed by ultrasonography of the superior mesenteric and hepatic arteries and portal vein. Systemic hemodynamics were assessed noninvasively by continuous monitoring of BP, heart rate (HR), cardiac output (CO), and the pressor response to an intravenous infusion on increasing doses of phenylephrine, an α1-adrenoceptor agonist. Neurohumoral regulation was assessed by spectral analysis of HR and BP, plasma catecholamine and aldosterone levels and plasma renin activity. Postprandial mesenteric hyperemia was associated with an increase in CO, a decrease in SVR and cardiac vagal tone, and reduction in baroreflex sensitivity with no change in sympathetic tone. Arterial α1-adrenoceptor responsiveness was preserved and reduced in hepatic sinusoids. Postprandial orthostasis was associated with a shift of 500 mL of blood from mesenteric to systemic circulation with preserved sympathetic-mediated vasoconstriction. Meal ingestion provokes cardiovascular hyperdynamism, cardiac vagolysis, and resetting of the baroreflex without activation of the sympathetic nervous system. Meal ingestion also alters α1-adrenoceptor responsiveness in the hepatic sinusoids and participates in the redistribution of blood volume from the mesenteric to the systemic circulation to maintain a normal BP during orthostasis.NEW & NOTEWORTHY A unique integrated investigation on the effect of meal on neurohumoral mechanisms and blood flow redistribution of the mesenteric circulation during orthostasis was investigated. Food ingestion results in cardiovascular hyperdynamism, reduction in cardiac vagal tone, and baroreflex sensitivity and causes a decrease in α1-adrenoceptor responsiveness only in the venous intrahepatic sinusoids. About 500-mL blood shifts from the mesenteric to the systemic circulation during orthostasis. Accordingly, the orthostatic homeostatic mechanisms are better understood.

Understanding the neurotropic characteristics of SARS-CoV-2: from neurological manifestations of COVID-19 to potential neurotropic mechanisms.

Coronavirus disease 2019 (COVID-19), a disease caused by the novel betacoronavirus (SARS-CoV-2), has become a global pandemic threat. The potential involvement of COVID-19 in central nervous system (CNS) has attracted considerable attention due to neurological manifestations presented throughout the disease process. In addition, SARS-CoV-2 is structurally similar to SARS-CoV, and both bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. Thus, cells expressing ACE2, such as neurons and glial cells may act as targets and are thus vulnerable to SARS-CoV-2 infection. Here, we have reviewed the neurological characteristics of COVID-19 and summarized possible mechanisms of SARS-CoV-2 invasion of the CNS. COVID-19 patients have presented with a number of different neurological symptoms such as headache, dizziness, hyposmia, and hypogeusia during the course of illness. It has also been reported recently that some cases of COVID-19 have presented with concurrent acute cerebrovascular disease (acute ischemic stroke, cerebral venous sinus thrombosis, cerebral hemorrhage, subarachnoid hemorrhage), meningitis/encephalitis, acute necrotizing hemorrhagic encephalopathy, and acute Guillain-Barré syndrome. Furthermore, SARS-CoV-2 RNA detected in a cerebrospinal fluid specimen of a patient with COVID-19 have provided direct evidence to support the theory of neurotropic involvement of SARS-CoV-2. However, the underlying neurotropic mechanisms of SARS-CoV-2 are yet to be established. SARS-CoV-2 may affect CNS through two direct mechanisms (hematogenous dissemination or neuronal retrograde dissemination) or via indirect routes. The underlying mechanisms require further elucidation in the future.

The Effects of Viewing Smart Devices on Static Balance, Oculomotor Function, and Dizziness in Healthy Adults.

BACKGROUND The number of people using smart devices such as smartphones (SPs) or virtual reality head-mounted displays (HMDs) is rapidly increasing. This study aimed to investigate the effects of viewing smart devices, including SPs and HMDs, on postural balance and the development of dizziness in healthy individuals. MATERIAL AND METHODS Twenty-six healthy adults underwent static balance measurements at baseline, and after 5, 10, and 20 minutes of viewing the SP and HMD display. Measurements were taken using a force plate and Wii Balance Board (WBB) and included the parameters of postural sway velocity, path length, and postural sway area. A modified Simulator Sickness Questionnaire (SSQ) evaluated oculomotor function and dizziness twice for each device, after 5 and 20 minutes of use. RESULTS Compared with baseline, the use of smart devices for 20 minutes had significantly increased effects on balance, oculomotor function, and dizziness than shorter use for 10 minutes or 5 minutes in healthy adults. Postural sway velocity and path length were significantly increased after 20 minutes of use of the HMD and SP when compared 5-minute use and baseline measurements (p<0.05). Postural sway area after 20-minute use of the HMD was significantly increased compared with the baseline and 5-minute and 10-minute use of the SP and 5-minute use of the HMD (p<0.05). The SSQ showed that dizziness was significantly increased after 20-minute use compared with 5-minute use of the HMD and SP (p<0.05). CONCLUSIONS Longer use of smart devices affected static balance, oculomotor function, and dizziness in healthy adults.

Oxidative Stress in Cerebral Small Vessel Disease Dizziness Patients, Basally and After Polyphenol Compound Supplementation.

BACKGROUND: Leukoaraiosis (LA) is a common radiological finding in elderly, frequently associated with several clinical disorders, including unexplained dizziness. The pathogenesis of LA is multifactorial, with a dysfunction of cerebral microcirculation resulting in chronic hypoperfusion and tissue loss, with oxidative stress involved in this cascade. OBJECTIVE: The aim of this study was to analyse some oxidative stress biomarkers in a cohort of LA patients. METHOD: Fifty-five consecutive patients (33 males, median age 75 years) with LA were recruited. In a subgroup of 33 patients with LA and unexplained dizziness, we have then performed an open study to evaluate if 60-day supplementation with a polyphenol compound may modify these biomarkers and influence quality of life, analysed with the Dizziness Handicap Inventory (DHI) scale. RESULTS: At baseline, blood oxidative stress parameters values were outside normal ranges and compared to matched healthy controls. After the two months supplementation, we observed a significant decrement of advanced oxidation protein products values and a significant improvement of DHI. CONCLUSION: Oxidative stress biomarkers may be useful to detect redox imbalance in LA and to provide non-invasive tools to monitor disease status and response to therapy.

The cerebrovascular response to lower-body negative pressure vs. head-up tilt.

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (-50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBFv) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT (P ≤ 0.020). Mean CBFv initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller (P ≤ 0.029) during LBNP. The reduction in end-tidal Pco2 partial pressure (PetCO2 ) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT (P = 0.008). We consider the larger decrease in CBFv during HUT vs. LBNP attributable to the pronounced reduction in PetCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality.NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.

In vivo neurometabolic profiling in orthostatic tremor.

The pathogenesis of orthostatic tremor (OT) remains unclear, although some evidence points to dysfunction in the brainstem or cerebellum. We used single voxel proton magnetic resonance spectroscopy (1H-MRS) (3 T) to investigate whether neurochemical changes underlie abnormal cerebellar or cortical function in OT. Fourteen OT patients and 14 healthy controls underwent 1H-MRS studies with voxels placed in midparietal gray matter and cerebellum (vermis and central white matter). Spectral analysis was analyzed using the software package LCModel (version 6.3). The absolute metabolite concentrations and ratios of total N-acetylaspartate + N-acetylaspartyl glutamate (NAA), choline-containing compounds, myoinositol, and glutamate + glutamine to creatine were calculated. In midparietal gray matter spectra, we found a significant decrease in the absolute concentration of NAA in OT patients versus healthy controls (7.76 ±â€Š0.25 vs 8.11 ±â€Š0.45, P = 0.017). A similar decrease in NAA was seen in the cerebellar vermis (7.33 ±â€Š0.61 vs 8.55 ±â€Š1.54, P = 0.014) and cerebellar white matter (8.54 ±â€Š0.79 vs 9.95 ±â€Š1.57, P = 0.010). No differences in the other metabolites or their ratios were observed. Reductions in both cerebral cortical and cerebellar NAA suggest that there is neuronal damage or loss in OT, raising the intriguing question as to whether OT is a neurodegenerative disease. Along with clinical history and electrophysio0logical examination, 1H-MRS could serve as a useful diagnostic aid for OT.

Occupancy of Dopamine D3 and D2 Receptors by Buspirone: A [11C]-(+)-PHNO PET Study in Humans.

There is considerable interest in blocking the dopamine D3 receptor (DRD3) versus the D2 receptor (DRD2) to treat drug addiction. However, there are currently no selective DRD3 antagonists available in the clinic. The anxiolytic drug buspirone has been proposed as a potential strategy as findings suggest that this drug has high in vitro affinity for DRD3, binds to DRD3 in brain of living non-human primate, and also disrupts psychostimulant self-administration in preclinical models. No study has explored the occupancy of DRD3 by buspirone in humans. Here, we used positron emission tomography (PET) and the D3-preferring probe, [(11)C]-(+)-PHNO, to test the hypothesis that buspirone will occupy (decreases [(11)C]-(+)-PHNO binding) the DRD3 more readily than the DRD2. Eight healthy participants underwent [(11)C]-(+)-PHNO scans after single oral dose administration of placebo and 30, 60, and 120 mg of buspirone in a single-blind within-subjects design. [(11)C]-(+)-PHNO binding in DRD2- and DRD3-rich areas was decreased by the highest (60-120 mg), but not the lowest (30 mg), doses of buspirone. The maximal occupancy obtained was ~25% in both areas. Plasma levels of prolactin (a DRD2 marker) correlated with percentage occupancy after orally administered buspirone. Self-reported dizziness and drowsiness increased after buspirone but that did not correlate with receptor occupancy in any region. Overall, the modest occupancy of DRD2 and DRD3 even at high acute doses of buspirone, yielding high levels of metabolites, suggests that buspirone may not be a good drug to preferentially block DRD3 in humans.

Stroke risk stratification in acute dizziness presentations: A prospective imaging-based study.

OBJECTIVE: To estimate the ability of bedside information to risk stratify stroke in acute dizziness presentations. METHODS: Surveillance methods were used to identify patients with acute dizziness and nystagmus or imbalance, excluding those with benign paroxysmal positional vertigo, medical causes, or moderate to severe neurologic deficits. Stroke was defined as acute infarction or intracerebral hemorrhage on a clinical or research MRI performed within 14 days of dizziness onset. Bedside information comprised history of stroke, the ABCD(2) score (age, blood pressure, clinical features, duration, and diabetes), an ocular motor (OM)-based assessment (head impulse test, nystagmus pattern [central vs other], test of skew), and a general neurologic examination for other CNS features. Multivariable logistic regression was used to determine the association of the bedside information with stroke. Model calibration was assessed using low (<5%), intermediate (5% to <10%), and high (≥10%) predicted probability risk categories. RESULTS: Acute stroke was identified in 29 of 272 patients (10.7%). Associations with stroke were as follows: ABCD(2) score (continuous) (odds ratio [OR] 1.74; 95% confidence interval [CI] 1.20-2.51), any other CNS features (OR 2.54; 95% CI 1.06-6.08), OM assessment (OR 2.82; 95% CI 0.96-8.30), and prior stroke (OR 0.48; 95% CI 0.05-4.57). No stroke cases were in the model's low-risk probability category (0/86, 0%), whereas 9 were in the moderate-risk category (9/94, 9.6%) and 20 were in the high-risk category (20/92, 21.7%). CONCLUSION: In acute dizziness presentations, the combination of ABCD(2) score, general neurologic examination, and a specialized OM examination has the capacity to risk-stratify acute stroke on MRI.

Tramadol hydrochloride: pharmacokinetics, pharmacodynamics, adverse side effects, co-administration of drugs and new drug delivery systems.

Tramadol hydrochloride (TrHC) is a synthetic analgesic drug exhibiting opioid and non-opioid properties, acting mainly on the central nervous system. It has been mostly used to treat pain, although its use to treat anxiety and depression has also been documented. These properties arise from the fact that they inhibit serotonin (5-HT) reuptake augmenting 5-HT concentration on the synaptic cleft. Despite this, TrHC has also been described to have several side effects which are mainly due to its fast metabolization and excretion which in turn requires multiple doses per day. To surpass this limitation, new pharmaceutical formulations are being developed intending the protection, target and sustained delivery as well as a reduction on daily dose aiming a reduction on the side effects. In the present work we have revised the efficacy, safety, biological and adverse effects of TrHC, and the added value of developing a novel drug delivery system for topical administration.

Effect of orthostasis on endothelial function: a gender comparative study.

As the vascular endothelium has multiple functions, including regulation of vascular tone, it may play a role in the pathophysiology of orthostatic intolerance. We investigated the effect of orthostasis on endothelial function using EndoPAT®, a non-invasive and user-independent method, and across gender. As sex steroid hormones are known to affect endothelial function, this study examined the potential effect of these hormones on the endothelial response to orthostasis by including females at different phases of the menstrual cycle (follicular and luteal-where the hormone balance differs), and females taking an oral contraceptive. A total of 31 subjects took part in this study (11 males, 11 females having normal menstrual cycles and 9 females taking oral contraceptive). Each subject made two visits for testing; in the case of females having normal menstrual cycles the first session was conducted either 1-7 (follicular) or 14-21 days (luteal) after the start of menstruation, and the second session two weeks later, i.e., during the other phase, respectively. Endothelial function was assessed at baseline and following a 20-min orthostatic challenge (active standing). The EndoPAT® index increased from 1.71 ± 0.09 (mean ± SEM) at baseline to 2.07 ± 0.09 following orthostasis in females (p<0.001). In males, the index increased from 1.60 ± 0.08 to 1.94 ± 0.13 following orthostasis (p<0.001). There were no significant differences, however, in the endothelial response to orthostasis between females and males, menstrual cycle phases and the usage of oral contraceptive. Our results suggest an increased vasodilatatory endothelial response following orthostasis in both females and males. The effect of gender and sex hormones on the endothelial response to orthostasis appears limited. Further studies are needed to determine the potential role of this post orthostasis endothelial response in the pathophysiology of orthostatic intolerance.

First-time-in-human study with GSK1018921, a selective GlyT1 inhibitor: relationship between exposure and dizziness.

The pharmacokinetics (PK), safety, and tolerability of GSK1018921, a glycine transporter 1 (GlyT-1) inhibitor, were assessed in this first-time-in-human (FTIH) study. Single oral doses ranging from 0.5 to 280 mg and placebo were administered to 25 healthy subjects in a five-period, two-cohort, crossover study. GSK1018921 showed dose-proportional PK with a terminal half-life of ~17 h. The subjects reported dizziness with a dose-dependent frequency of 22-88% at doses of 70-280 mg. The time course of the dizziness paralleled the PK of the drug, with peak response at 2 h after the dose, consistent with time to maximum plasma concentration (T(max)). The dizziness was resolved by 10-12 h in all subjects. A Markov-chain logistic regression model was implemented in NONMEM to determine the probability of developing dizziness as a function of the plasma concentration of the compound. Frequency, onset (<1 h), and offset (4 h) were well described by the model. Exposure resulting in 80% receptor occupancy is predicted to be well tolerated.

Evidence for modulation of opioidergic activity in central vestibular processing: A [(18)F] diprenorphine PET study.

Animal and functional imaging studies had identified cortical structures such as the parieto-insular vestibular cortex, the retro-insular cortex, or the anterior cingulate cortex belonging to a vestibular cortical network. Basic animal studies revealed that endorphins might be important transmitters involved in cerebral vestibular processing. The aim of the present study was therefore to analyse whether the opioid system is involved in vestibular neurotransmission of humans or not. Changes in opioid receptor availability during caloric air stimulation of the right ear were studied with [(18)F] Fluoroethyl-diprenorphine ([(18)F]FEDPN) PET scans in 10 right-handed healthy volunteers and compared to a control condition. Decrease in receptor availability to [(18)F]FEDPN during vestibular stimulation in comparison to the control condition was significant at the right posterior insular cortex and the postcentral region indicating more endogenous opioidergic binding in these regions during stimulation. These data give evidence that the opioidergic system plays a role in the right hemispheric dominance of the vestibular cortical system in right-handers.

Reduced adverse event profile of orally inhaled DHE (MAP0004) vs IV DHE: potential mechanism.

BACKGROUND: MAP0004 is a novel orally inhaled formulation of dihydroergotamine mesylate (DHE) currently in development that has been clinically observed to provide rapid ( approximately 10 minutes) therapeutic levels of DHE but with lower rates of adverse effects (dizziness, nausea, and paresthesia) compared with intravenous (IV) dosing. Receptor-based mechanistic studies were conducted to determine if differences between IV DHE and inhaled DHE (MAP0004) binding and functional activity were responsible for the improved adverse event profile. METHODS: Radioligand competitive binding assays were performed at adrenergic (alpha1 [non-specific], alpha2A, alpha2B, alpha2C, beta), dopaminergic (D; D(1), D(2), D(3)), and at serotonergic (5-HT; 5-HT(1A), 5-HT(1B), 5-HT(1D), 5-HT(2A), 5-HT(2C), 5-HT(3), 5-HT(4), 5-HT(5A), 5-HT(6), 5-HT(7)) receptors. Binding assays were also conducted for the major metabolite of DHE, 8'-hydroxy-DHE (8'-OH-DHE). Subsequent functional receptor assays were also performed at 5-HT(1B), 5-HT(1D), 5-HT(2A), 5-HT(2C), 5-HT(3), D(2), alpha1A, alpha2A, alpha2B, beta1, and beta2 and muscarinic receptors to ensure that observed receptor binding translated into potential functional response. RESULTS: For competitive binding studies, DHE demonstrated extensive activity at IV C(max) for all 5-HT receptors tested, except 5-HT(3) and 5-HT(4), and alpha1, alpha2A, alpha2B, alpha2C, and D(3) receptors. DHE concentrations used in the studies were equal to the peak plasma concentrations (C(max)) observed in human subjects following IV DHE 1.0 mg (the standard approved dose), and 2 and 4 inhalations MAP0004 which, respectively, produced systemic circulation levels of DHE equivalent to 0.44 mg and 0.88 mg administered IV. MAP0004 binding activity at the C(max) concentrations was lower than IV DHE and no binding was observed for the 8'-OH-DHE metabolite. However, MAP0004 preserved potent agonist action at key anti-migraine 5-HT(1B) and 5-HT(1D) receptors, even at the lower C(max )concentrations. Functional binding studies displayed similar results whereby IV DHE C(max) concentrations invoked strong agonist/antagonist responses, for instance at adrenergic and 5-HT(2C) receptors, which could have been responsible for dizziness. Conversely, at C(max) concentrations of MAP0004, inhaled DHE achieved a significantly lower response or no response at the adrenergic and 5-HT(2C) receptors. CONCLUSIONS: The mechanism by which nausea was experienced with IV DHE--yet not with MAP0004--was not associated with classic nausea pathways/targets (dopamine, 5-HT(3), or muscarinic receptors) or with peripheral action in the intestine via enterochromaffin cells. Importantly, the maximum DHE concentrations following MAP0004 administration were insufficient to interact with receptors implicated in cardiovascular (5-HT(2B) and beta(1)) and pulmonary effects (beta(2), adenosine, muscarinic, and leukotriene).

Correlation between neurological dysfunction with vitamin E deficiency and gastrectomy.

OBJECTIVE: We previously reported on vitamin E malabsorption after gastrectomy. In this study, we focused on neurological dysfunction due to serum vitamin E decrease during the postgastrectomy period in lager number of patients. METHODS: We examined the type of gastrectomy, type of reconstruction, serum vitamin E level, and neurological status for 96 gastrectomy patients. RESULTS: Low serum vitamin E levels were observed in 20 patients, and 10 of those patients suffered some neurological symptoms, i.e., peripheral neuropathy, limb or truncal ataxia. Vitamin E levels tended to decrease with time after gastrectomy, and the number of patients with low serum vitamin E levels increased at about 50 months after gastrectomy. This relationship was stronger in total gastrectomy patients than in subtotal gastrectomy patients. Ten patients were given oral vitamin E, and serum vitamin E levels normalized in 9 of the patients and neurological abnormalities improved in 8 patients. An oral intake of 300 mg or more of vitamin E was necessary for normalization of vitamin E levels. CONCLUSIONS: Gastrectomy should be considered a risk for vitamin E deficiency and neurological disturbance over the long-term clinical course. An oral vitamin E supply can improve serum vitamin E levels and neurological symptoms.

Cardiovascular dynamics in healthy subjects with differing heart rate responses to tilt.

Orthostatic stress such as head-up tilt (HUT) elicits a wide range of heart rate (HR) and arterial pressure (AP) responses among healthy individuals. In this study, we evaluated cardiovascular dynamics in healthy subjects with different HR responses to HUT, but without autonomic dysfunction. We measured AP (brachial artery) and HR (ECG) during 5 min of 60 degrees HUT in 76 healthy normotensive individuals. We then chose individuals on the basis of the extremes of HR responses to HUT (high = DeltaHR > or = 20 beats/min, and low = DeltaHR < or = 10 beats/min; n = 15 per group). Peak HR during HUT was 87 +/- 10 beats/min in the high and 69 +/- 14 beats/min in the low group (P < 0.05). High HR responders had lower systolic pressure at baseline (121 +/- 9 vs. 129 +/- 11 mmHg, P < 0.05) and during HUT (120 +/- 10 vs. 131 +/- 13 mmHg, P < 0.05), and higher plasma norepinephrine (NE) response to HUT (DeltaNE: 156.9 +/- 17.8 vs. 89.0 +/- 17.2 pg/ml; P < 0.05). DeltaNE during HUT was also significantly correlated with DeltaHR when all 76 subjects were included in a regression analysis (r = 0.39; P < 0.001). Pulse pressure was lower during HUT in high HR responders compared with low HR responders (45 +/- 1 vs. 55 +/- 2 mmHg, P < 0.05). High HR responders also had larger fluctuations in systolic and pulse pressure during HUT (coefficient of variation = 10.7 +/- 0.7 vs. 5.7 +/- 0.3%; 7.9 +/- 0.5 vs. 4.1 +/- 0.4%, respectively, P < 0.05). Sex distribution was different between groups (high: 5 women, 10 men; low: 10 women, 5 men). Higher HR with lower AP during HUT is consistent with normal baroreflex mechanisms of integration. Although interindividual variability appears to be a fundamental part of cardiovascular regulation, the mechanisms of these differences and the sex discrepancy requires further investigation.

Effect of blood donation on well-being of blood donors.

The demand for blood products steadily increases. Concurrently, blood donor recruitment becomes more and more difficult. This study aimed to investigate effects of blood donation on blood donors, which could be helpful for blood donor recruitment and retention. In addition to cortisol measurements in saliva, three questionnaires quantifying mood (good/bad), vigilance (awake/tired), agitation (calm/nervous), actual strain and asking for donation-related effects perceived were distributed to 110 whole blood donors (DON). Results obtained were compared with 109 control subjects (CON) lacking the blood donation experience. Overall, 216 subjects completed the questionnaires. Sixty-eight percent of DON reported at least one effect perceived with blood donation. Exclusively, positive, negative or mixed effects were described by 26.5%, 23.5% and 17.6%, respectively. Among positive effects (i.e. physical/psychological well-being, feeling satisfied, happy, proud), no significant differences were observed between males and females (P = 0.07), whereas mixed or negative effects (i.e. vertigo, dizziness, tiredness, pain) were significantly (P = 0.03; P = 0.049) more associated with females. DON showed higher levels of well-being than CON as indicated by better mood (P = 0.004), higher vigilance (P = 0.015) and relaxation (P = 0.003). The latter even increased after donation with maximum values after 15 and 30 min. Despite significantly higher initial strain scores (P = 0.008), first-time donors maintained a better mood (P = 0.025) than repeat donors. DON showed a statistically better psychological well-being than CON, although the donation experience was perceived as stressful, especially for first-time donors. The results may facilitate donor recruitment and retention as blood donation may become less frightening and perhaps even attractive.

Model study of the effects of interactions between systemic and peripheral circulation on interstitial fluid balance.

Interstitial fluid balance is severely altered in microgravity, but the mechanisms underlying the fluid shift from lower to upper body are still partially unclear. A lumped parameter model of the arterial tree with active and non linear modulation of peripheral resistances and capillary fluid exchange was adopted to simulate the response of microcirculation to pulsatility and edema. Results suggest that myogenic regulation not only impinges on arteriolar radius, but it also indirectly affects interstitial fluid balance. Non linear dynamics of blood pressure (BP) and flow in capillary beds are influenced by systemic pulsatility, hinting that local activity is involved in the response to peripheral edema as well.

Correlation between dizziness and impaired glucose metabolism.

INTRODUCTION: Impaired glucose metabolism is characterized by conditions of hypo and hyperglycemia. AIM: The objective of the present study was to asses whether or not there is a relationship between impaired glucose metabolism and dizziness. In the clinical laboratory settings, patients were examined using vectoelectronystagmography in association with glycemic levels. METHODS: 33 patients were divided in 3 groups: diabetics; patients with dizziness and a control group. RESULTS: 65% of the patients with dizziness showed impaired glucose metabolism. 40% of the patients with dizziness had alterations in their vectoelectronystagmography results. CONCLUSION: Dizziness is a good indicator of glucose metabolism alterations and these may be a good indicator of alterations in vectoelectronystagmography responses. The study of glycemic levels after glucose overexposure is a good prognosis factor to evaluate dizziness and shows the same results as insulin level studies after glucose overexposure.

Correlação entre tontura e disfunções do metabolismo da glicose / Correlation between dizziness and impaired glucose metabolism

INTRODUÇÃO: as alterações do metabolismo da glicose são caracterizadas por estados de hipoglicemia e hiperglicemia. OBJETIVO: A proposta deste trabalho é verificar a associação entre as alterações do metabolismo da glicose, por glicemia de jejum e teste de tolerância à glicose e à tontura, avaliada por sua queixa e exames clínicos e subsidiários. MÉTODO: O estudo foi efetivado num grupo de 33 pacientes divididos em 3 subgrupos: pacientes com queixa de tontura, pacientes diabéticos e pacientes assintomáticos. RESULTADOS: O grupo de pacientes com queixa espontânea ou questionada de tontura apresentava alterações no metabolismo da glicose em 65 por cento dos casos. Já entre os pacientes dos 3 grupos sem queixa de tontura, 30 por cento apresentavam alterações do metabolismo da glicose. 40 por cento dos pacientes que apresentaram queixas de tonturas tinham o exame vestibular clínico e a vectoeletronistagmografia alterados, enquanto que entre os assintomáticos 7,5 por cento apresentaram as alterações vestibulares referidas. CONCLUSÃO: A tontura é um bom indicador de alteração do metabolismo da glicose e a alteração do metabolismo da glicose é um bom indicador de alteração do exame vestibular. O estudo do metabolismo da glicose a partir dos níveis glicêmicos é eficaz e tem resultados próximos dos observados nos estudos que mensuram os níveis insulinêmicos.

INTRODUCTION: Impaired glucose metabolism is characterized by conditions of hypo and hyperglycemia. AIM: The objective of the present study was to asses whether or not there is a relationship between impaired glucose metabolism and dizziness. In the clinical laboratory settings, patients were examined using vectoelectronystagmography in association with glycemic levels. METHODS: 33 patients were divided in 3 groups: diabetics; patients with dizziness and a control group. RESULTS: 65 percent of the patients with dizziness showed impaired glucose metabolism. 40 percent of the patients with dizziness had alterations in their vectoelectronystagmography results. CONCLUSION: Dizziness is a good indicator of glucose metabolism alterations and these may be a good indicator of alterations in vectoelectronystagmography responses. The study of glycemic levels after glucose overexposure is a good prognosis factor to evaluate dizziness and shows the same results as insulin level studies after glucose overexposure.

Phase of the menstrual cycle does not affect orthostatic tolerance in healthy women.

Women of child-bearing age have a lower orthostatic tolerance (OT) than older women or men, and women suffering from frequent syncopal episodes often comment that their symptoms occur at certain times of the menstrual cycle. However, it is not known whether, in asymptomatic women, OT varies at different phases of the menstrual cycle. We studied 8 healthy asymptomatic women aged 26.8 +/- 3.4 years. We determined OT using a test of combined head-up tilting and lower body suction. We continuously monitored beat-to-beat blood pressure (Finapres), heart rate (ECG), and cerebral and forearm blood flow velocities (Doppler ultrasound). On each test day we assessed carotid baroreceptor sensitivity from suction/pressure applied to a neck chamber. We also determined estradiol and progesterone levels from a venous blood sample. Tests were performed in early follicular and late luteal phases, and during ovulation. Serum concentrations of estradiol (pmol x l(-1)) and progesterone (nmol x l(-1)) were in follicular phase 464.1 +/- 63 and 6.3 +/- 2.8; ovulation 941.6 +/- 298 and 5.8 +/- 1.2; luteal phase 698 +/- 188 and 32.3 +/- 9.6. Progesterone levels were significantly higher in the luteal phase (p < 0.001). OT was not different on any test day: follicular 31.9 +/- 1.6 min, ovulation 31.3 +/- 0.7 min; luteal 31.1 +/- 2.2 min. Supine and tilted heart rates and blood pressures, the maximum heart rate, and the cerebral autoregulatory and forearm vascular resistance responses to the orthostatic stress were similar during all studies. Both cardiac and vascular resistance carotid baroreceptor sensitivities were also similar on all test days. These results suggest that there is no difference in either OT or cardiovascular control at the tested phases of the menstrual cycle in healthy women.