1000 resultados para CARDIOVASCULAR DRIFT


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The modal and nonmodal linear properties of the Hasegawa-Wakatani system are examined. This linear model for plasma drift waves is nonnormal in the sense of not having a complete set of orthogonal eigenvectors. A consequence of nonnormality is that finite-time nonmodal growth rates can be larger than modal growth rates. In this system, the nonmodal time-dependent behavior depends strongly on the adiabatic parameter and the time scale of interest. For small values of the adiabatic parameter and short time scales, the nonmodal growth rates, wave number, and phase shifts (between the density and potential fluctuations) are time dependent and differ from those obtained by normal mode analysis. On a given time scale, when the adiabatic parameter is less than a critical value, the drift waves are dominated by nonmodal effects while for values of the adiabatic parameter greater than the critical value, the behavior is that given by normal mode analysis. The critical adiabatic parameter decreases with time and modal behavior eventually dominates. The nonmodal linear properties of the Hasegawa-Wakatani system may help to explain features of the full system previously attributed to nonlinearity.

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Both acute (1 day) lesions of the commissural nucleus of the solitary tract (commNTS) and aortic baroreceptor denervation increase pressor responses to bilateral common carotid occlusion (BCO) during a 60-second period in conscious rats. In this study, we investigated the following: (1) the effects of commNTS lesions on basal mean arterial pressure (MAP) and heart rate (HR) of aortic denervated (ADNx) rats; (2) the effects of acute commNTS lesions on pressor responses to BCO in ADNx rats; and (3) the effects of chronic (10 days) commNTS lesions on the pressor response to BCO. ADNx increased basal MAP and HR in sham-lesioned rats. Acute commNTS lesions abolished the MAP and HR increases observed in ADNx rats. Acute commNTS lesions increased the pressor responses to BCO in rats with intact- baroreceptor innervation but produced no additional change in the pressor response to BCO in ADNx rats. Chronic commNTS lesions did not change the pressor responses to BCO in rats with intact-baroreceptor innervation. The data show that acute commNTS lesions abolish the MAP increase produced by aortic baroreceptor denervation. They also suggest that acute commNTS lesions enhance the pressor response to BCO by partial withdrawal of aortic baroreceptor inputs into the NTS. Chronically, reorganization in the remaining aortic baroreceptor or in the baroreflex function as a whole might produce normalization of the cardiovascular responses to BCO.

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The linear properties of an electromagnetic drift-wave model are examined. The linear system is non-normal in that its eigenvectors are not orthogonal with respect to the energy inner product. The non-normality of the linear evolution operator can lead to enhanced finite-time growth rates compared to modal growth rates. Previous work with an electrostatic drift-wave model found that nonmodal behavior is important in the hydrodynamic limit. Here, similar behavior is seen in the hydrodynamic regime even with the addition of magnetic fluctuations. However, unlike the results for the electrostatic drift-wave model, nonmodal behavior is also important in the adiabatic regime with moderate to strong magnetic fluctuations. © 2000 American Institute of Physics.

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A new topology for a LVLP variable-gain CMOS amplifier is presented. Input- and load-stage are built around triode-transconductors so that voltage-gain is fully defined by a linear relationship involving only device-geometries and biases. Excellent gain-accuracy, temperature-insensitivity; and wide range of programmability, are thus achieved. Moreover, adaptative biasing improves the common-mode voltage stability upon gain-adjusting. As an example, a 0-40dB programmablegain audio-amplifier is designed. Its performance is supported by a range of simulations. For VDD=1.8V and 20dB-nominal gain, one has Av=19.97dB, f3db=770KHz and quiescent dissipation of 378μW. Over temperatures from -25°C to 125°C, the 0. ldB-bandwidth is 52KHz. Dynamic-range is optimized to 57.2dB and 42.6dB for gains of 20dB and 40dB, respectively. THD figures correspond to -60.6dB@Vout= 1Vpp and -79.7dB@Vout= 0.5 Vpp. A nearly constant bandwidth for different gains is also attained.

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The main purpose of this study was to analyze the effect of the pedaling cadence (500 × 100 rpm) on the heart rate (HR) and the blood lactate response during incremental and constant workload exercises in active individuals. Nine active male individuals (20.9 ± 2.9 years old; 73.9 ± 6.5 kg; 1.79 ± 0.9 m) were submitted to two incremental tests, and to 6-8 constant workload tests to determine the intensity corresponding to the maximal steady state lactate (MLSSintens) in both cadences. The maximal power (Pmax) attained during the incremental test, and the MLSSintens were significantly lower at 100 rpm (240.9 ± 12.6 W; 148.1 ± 154.W) compared to 50 rpm (263.9 ± 18.6 W; 186.1 ± 21.2 W), respectively. The HRmax did not change between cadences (50 rpm = 191.1 ± 8.8 bpm; 100 rpm = 192.6 ± 9.9 bpm). Regardless the cadence, the HRmax percentage (70, 80, 90, and 100%) determined the same lactate concentrations during the incremental test. However, when the intensity was expressed in Pmax percentage or in absolute power, the lactate and the HR values were always higher at highest cadences. The HR corresponding to MLSSintens was similar between cadences (50 rpm = 162.5 ± 9.1 bpm; 100 rpm = 160.4 ± 9.2 bpm). Based on these results, it can be conclude that regardless the cadence employed (50 × 100 rpm), the use of the HR to individualize the exercise intensity indicates similar blood lactate responses, and this relationship is also kept in the exercise of constant intensity performed at MLSSintens. On the other hand, the use of the Pmax percentages depend on the cadence used, indicating different physiological responses to a same percentage.

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The maintenance of the arterial pressure in normal levels is important for the homeostasis of body fluids. The central nervous system regulating sympathetic and parasympathetic autonomic efferent can adjust arterial pressure which allows animals or human to face different daily activities with the best performance. Different central areas are responsible for the control of autonomic discharges to cardiovascular system and many of them are also involved in the control of fluid electrolyte balance. One of these areas is the tissue surrounding the anteroventral third ventricle (AV3V region) localized in the forebrain and a main central site for angiotensin II receptors and osmoreceptors. The AV3V lesions impair the development of many models of experimental hypertension in rats and the pressor responses to different stimuli. Lesions of the AV3V region also reduce dipsogenic responses to angiotensin II, central cholinergic activation, water deprivation and increase in plasma osmolarity, atrial natriuretic peptide secretion produced by body fluid expansion and the increase in renal excretion to central cholinergic activation. Recent evidence also suggests the participation of AV3V region in pressor responses produced by the activation of medullary mechanisms.

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Scorpionism is a common problem that occurs in tropical and subtropical countries and assumes great medical-sanitary importance due to its fatal effect on sensitive individuals, being able to lead children and aged people to death. The envenomation lethal potential is responsible for the serious cardiopulmonary alterations the scorpion toxin produces in its victims. The present research evaluated the effects of Tityus serrulatus venom on dogs, using two distinct doses: a dose that simulates natural envenomation (0.4 mg/total dose), and an experimental dose (0.25 mg/kg). General clinical signs were observed at different moments after envenomation, and specific data related to the cardiopulmonary system were evaluated by systemic arterial pressure measurement, CK-MB enzymatic activity dosage, and radiographic, electrocardiographic and echocardiographic examinations. Results demonstrated that the scorpion venom, in experimental doses, was able to cause acute and reversible cardiac injury in few days, and, in the dose that simulated natural accident, it produced clinical signs of light envenomation, such as local pain, hyperesthesia, sialorrhea, vomiting, diarrhea, sneeze and prostration.

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The median preoptic nucleus (MnPO) is one of most important site of the lamina terminalis implicated in the regulation of hydro electrolytic and cardiovascular balance. The purpose of this study was to determine the effect of L-Type calcium channel antagonist, nifedipine, on the increase of median arterial blood pressure (MAP) induce by angiotensin II (ANG II) injected into the MnPO. The influence of nitric oxide (NO) on nifedipine antipressor action has also been studied by utilizing N W-nitro-L-arginine methyl ester (L-NAME) (40 μg 0.2 μL -1) a NO synthase inhibitor (NOSI), 7-nitroindazole (7-NIT) (40 μg 0.2 μL -1), a specific neuronal NO synthase inhibitor (nNOSI) and sodium nitroprusside (SNP) (20 μg 0.2 μL -1) a NO donor agent. We have also investigated the central role of losartan and PD123349 (20 nmol 0.2 μL -1), AT 1 and AT 2, respectively (selective non peptide ANG II receptor antagonists), in the pressor effect of ANG II (25 pmol 0.2 μL -1) injected into the MnPO. Male Wistar rats weighting 200-250 g, with cannulae implanted into the MnPO were utilized. Losartan injected into the MnPO, prior to ANG II, blocked the pressor effect of ANGII. PD 123319 only decreased the pressor effect of ANG II. Rats pre-treated with either 50 μg 0.2 μL -1 or 100 μg 0.2 μL -1 of nifedipine, followed by 25 pmol 0.2 μL -1 of ANG II, decreased ANG II-pressor effect. L-NAME potentiated the pressor effect of ANG II. 7-NIT injected prior to ANG II into the MnPO also potentiated the pressor effect of ANGII but with less intensity than that of L-NAME. SNP injected prior to ANG II blocked the pressor effect of ANG II. The potentiation action of L-NAME and 7-NIT on ANG II-pressor effect was blocked by prior injection of nifedipine. The results described in this study provide evidence that calcium channels play important roles in central ANG II-induced pressor effect. The structures containing NO in the brain, such as MnPO, include both endothelial and neuronal cells, which might be responsible for the influence of nifedipine on the pressor effect of ANG II. These data have shown the functional relationship between L-Type calcium channel and a free radical gas NO in the MnPO, on the control of ANG II-induced pressor effect acting in AT 1 and AT 2 receptors.

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Reactive oxygen species (ROS) have been shown to modulate neuronal synaptic transmission and may play a role on the autonomic control of the cardiovascular system. In this study we investigated the effects produced by hydrogen peroxide (H 2O 2) injected alone or combined with the anti-oxidant agent N-acetil-l-cysteine (NAC) or catalase into the fourth brain ventricle (4th V) on mean arterial pressure and heart rate of conscious rats. Moreover the involvement of the autonomic nervous system on the cardiovascular responses to H 2O 2 into the 4th V was also investigated. Male Holtzman rats (280-320 g) with a stainless steel cannula implanted into the 4th V and polyethylene cannulas inserted into the femoral artery and vein were used. Injections of H 2O 2 (0.5, 1.0 and 1.5 μmol/0.2 μL, n = 6) into the 4th V produced transient (for 10 min) dose-dependent pressor responses. The 1.0 and 1.5 μmol doses of H 2O 2 also produced a long lasting bradycardia (at least 24 h with the high dose of H 2O 2). Prior injection of N-acetyl-l-cysteine (250 nmol/1 μL/rat) into the 4th V blockade the pressor response and attenuated the bradycardic response to H 2O 2 (1 μmol/0.5 μL/rat, n = 7) into the 4th V. Intravenous (i.v.) atropine methyl bromide (1.0 mg/kg, n = 11) abolished the bradycardia but did not affect the pressor response to H 2O 2. Prazosin hydrochloride (1.0 mg/kg, n = 6) i.v. abolished the pressor response but did not affect the bradycardia. The increase in the catalase activity (500 UEA/1 μL/rat injected into the 4th V) also abolished both, pressor and bradycardic responses to H 2O 2. The results suggest that increased ROS availability into 4th V simultaneously activate sympathetic and parasympathetic outflow inducing pressor and bradycardic responses. © 2006 Elsevier Inc. All rights reserved.

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Equatorial F region vertical plasma drifts, spread F and anomaly responses, in the south American longitude sector during the superstorm of 30 October 2003, are analyzed using data from an array of instruments consisting of Digisondes, a VHF radar, GPS TEC and scintillation receivers in Brazil, and a Digisonde and a magnetometer in Jicamarca, Peru. Prompt penetrating eastward electric field of abnormally large intensity drove the F layer plasma up at a velocity ∼1200 ms -1 during post dusk hours in the eastern sector over Brazil. The equatorial anomaly was intensified and expanded poleward while the development of spread F/plasma bubble irregularities and GPS signal scintillations were weaker than their quiet time intensity. Significantly weaker F region response over Jicamarca presented a striking difference in the intensity of prompt penetration electric field between Peru and eastern longitudes of Brazil. The enhanced post dusk sector vertical drift over Brazil is attributed to electro-dynamics effects arising energetic particle precipitation in the South Atlantic Magnetic Anomaly (SAMA). These extraordinary results and their longitudinal differences are presented and discussed in this paper. Copyright 2008 by the American Geophysical Union.

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The purpose of this randomized study was to evaluate EMG spectral, subjective and cardiovascular recovery parameters after isometric lumbar extension contractions. Ten healthy women performed isometric lumbar extensions until exhaustion with 5%, 10%, 15% and 20% of maximal voluntary isometric contraction on 4 different days (random order). One baseline five second contraction was performed before the fatiguing task which was followed by eight submaximal five second extension contractions (until 20 minutes after the end of the fatiguing task) at the same intensity as the trial to evaluate muscle recovery. EMG (Median Frequency, Peak Power, Peak Power Frequency, Total Power and Zero-crossing Rate) and cardiovascular variables did not demonstrate any statistical difference between the 5-second contractions (p > 0.05) performed before and after the fatiguing task, showing a quick EMG recovery. However, the data analysis showed that the perceived effort variable had not recovered even 10 minutes after the fatigue contraction (p < 0.05). Our results represent a data basis for future comparisons and since subjective felling can affect performance, this study shows the importance of its analysis, since the subjective effort rate was not fully recovered after 10 minutes the end of the exhaustion contraction. © 2008 IOS Press. All rights reserved.

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Introduction: The present study examines cardiovascular risk factor profiles and 24-month mortality in patients with symptomatic peripheral arterial disease. Design Study: Prospective observational study including 75 consecutive patients with PAD (67 ± 9.7 years of age; 52 men and 23 women) hospitalized for planned peripheral vascular reconstruction. Doppler echocardiograms were performed before surgery in 54 cases. Univariate analyses were performed using Student's t-test or Fisher's exact test. Survival analysis at 24-month follow-up was performed using the Cox regression model and Kaplan-Meier method including age and chronic use of aspirin as covariates. Survival curves were compared using the log-rank test. Results: Hypertension and smoking were the most frequent risk factors (52 cases and 51 cases, respectively), followed by diabetes (32 cases). Undertreated dyslipidemia was found in 26 cases. Fasting glycine levels (131 ± 69.1 mg/dl) were elevated in 29 cases. Myocardial hypertrophy was found in 18 out of 54 patients. Thirty-four patients had been treated with aspirin. Overall mortality over 24 months was 24% and was associated with age (HR: 0.064; CI95: 0.014-0.115; p=0.013) and lack of use of aspirin, as no deaths occurred among those using this drug (p<0.001). No association was found between cardiovascular death (11 cases) and the other risk factors. Conclusion: There is a high prevalence of uncontrolled (treated or untreated) cardiovascular risk factors in patients undergoing planned peripheral vascular reconstruction, and chronic use of aspirin is associated with reduced all-cause mortality in these patients.

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Coronary heart disease (CHD) is the most common cause of death in many developed countries. The major risk factors for CHD are smoking, high blood pressure, diabetes, high cholesterol levels, and lack of physical activity. Importantly, passive smoke also increases the risk for CHD. The mechanisms involved in the effects of passive smoke in CHD are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Recently, several studies have shown that exposure to tobacco smoke can result in cardiac remodeling and compromised cardiac function. Potential mechanisms for these alterations are neurohumoral activation, oxidative stress, and MAPK activation. Although the vascular effects of cigarette smoke exposure are well known, the effects of tobacco smoking on the heart have received less attention. Therefore, this review will focus on the recent findings as to the effects of passive smoking in acute and chronic phases of vascular and cardiac remodeling. © 2009 Bentham Science Publishers Ltd.

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Angiotensin is an important peptide of renin-angiotensin-aldosterone system. This peptide has an important function on arterial blood pressure regulation and body fluid homeostasis. However, its action on abnormal conditions causes deleterious effects on the cardiovascular system. Vascular resistance, hypertension, vascular and myocytes hipertrophy, production of free radicals and pro-inflammatory substances are some of the actions of angiotensin II that can result on cardiovascular remodeling. Angiotensinconverting enzyme (ACE) inhibitors, angiotensin receptors antagonists, antiinflammatories and antioxidants are used clinically and/or experimentally to prevent or reduce the effects of angiotensin II. The purpose of this work is to review the actions and interactions of angiotensin II on the cardiovascular system, as well as the therapeutic measures employed for the control of these effects.

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The performance of the Local Trigger based on the drift-tube system of the CMS experiment has been studied using muons from cosmic ray events collected during the commissioning of the detector in 2008. The properties of the system are extensively tested and compared with the simulation. The effect of the random arrival time of the cosmic rays on the trigger performance is reported, and the results are compared with the design expectations for proton-proton collisions and with previous measurements obtained with muon beams. © 2010 IOP Publishing Ltd and SISSA.