Is gender crucial for cardiovascular adjustments induced by exercise training in female spontaneously hypertensive rats?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of AV3V lesion on the cardiovascular, fluid, and electrolytic changes induced by activation of the lateral preoptic area

In this study we investigated the effect of the anteroventral third ventricle (AV3V) lesion on the pressor, bradycardic, natriuretic, kaliuretic, and dipsogenic responses induced by the injection of the cholinergic agonist carbachol into the lateral preoptic area (LPOA) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with stainless steel cannula directly into the LPOA. Injection of carbachol (7.5 nmol) into the LPOA of sham rats induced natriuresis (405 ± 66 μEq/120 min), kaliuresis (234 ± 44 μEq/120 min), water intake (9.5 ± 1.7 ml/60 min), bradycardia (-47 ± 11 bpm), and increase in mean arterial pressure (28 ± 3 mmHg). Acute AV3V lesion (1-5 days) reduced the natriuresis (12 ± 4 μEq/120 min), kaliuresis (128 ± 27 μEq/120 min), water intake (1.7 ± 0.9 ml/60 min), and pressor responses (14 ± 4 mmHg) produced by carbachol into the LPOA. Tachycardia instead of bradycardia was also observed. Chronic (14-18 days) AV3V lesion reduced only the pressor response (10 ± 2 mmHg) induced by carbachol. These results showed that acute, but not chronic, AV3V lesion reduced the natriuretic, kaliuretic, and dipsogenic responses to carbachol injection into the LPOA. The pressor response was reduced in acute or chronic AV3V-lesioned rats. The results suggest that the lateral areas may control the fluid and electrolyte balance independently from the AV3V region in chronic AV3V-lesioned rats. © 1992.

EFEIFOS DO SULFATE DE MAGNESIO NA HEMODINAMICA CARDIOVASCULAR DE CAES ANESTESIADOS COM PENTOBARBITAL SODICO

Background and Objectives - A controversy exists in the literature regarding the effects of the acute administration of magnesium on the cardiovascular system of animals and humans. The purpose of this study was to evaluate the effects of hypermagnesemia on the cardiovascular hemodynamics of dogs. Methods - Sixteen mongrel dogs were anesthetized with pentobarbitone 30 mg.kg-1 and submitted to volume expansion with Ringer's solution (0.4 ml.kg-1.min-1 and mechanical ventilation with room air. In this model, the hemodynamic repercussions of the following drugs and doses were studied. pentobarbitone 5 mg.kg-1 Group 1, control - and the association of pentobarbitone and magnesium sulphate (MS), at the dose of 140 mg.kg-1 injected in 15 minutes, followed by an infusion of 80 mg.kg-1.h-1 - Group 2. The parameters studied were: heart rate, blood pressure, inferior vena cava pressure, cardiac index, systolic index and peripheral resistance index, evaluated at 5 different moments: 15(M1), 30(M2), 60(M3) and 75(M4) minutes after the first suppplementary dose of pentobarbitone and 15 minutes (M5) after the second supplementary dose. In Group 2, the moments M3, M4, M5 corresponded to 15, 30 and 60 minutes after the priming dose of magnesium sulphate. Results - Group 1 animals exhibited tachycardia since the beginning of the experiment. There was a decrease in the cardiac index, in the systolic index and an increase in the inferior vena cava pressure. Group 2 animals also exhibited tachycardia, but heart rate decreased after MS infusion. The blood pressure and the peripheral resistance index decreased. The systolic index increased and the cardiac index decreased only at the end of the experiment. Conclusions: The antiadrenergic effects of MS could have been responsible for the decrease in heart rate. The vasodilating effects of the magnesium induced the decrease in the peripheral resistance index. The systolic index increased, showing that myocardial depression did not occur.

Preoptic-periventricular tissue (AV3V): central cholinergic-induced hydromineral and cardiovascular responses, and salt intake.

The periventricular tissue of the anterior ventral portion of the third ventricle (AV3V) is an important area for the control of hydromineral balance and of cardiovascular function. The present work discusses the importance of the integrity of the AV3V for multiple responses to central cholinergic activation (water intake, hypertension, natriuresis, salivation) and for the control of salt intake.

Nonmodal energetics of resistive drift waves

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.

Commissural NTS lesions and cardiovascular responses in aortic baroreceptor-denervated rats

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.

Nonmodal energetics of electromagnetic drift waves

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.

A low-voltage programmable-gain CMOS amplifier with very-low temperature-drift

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.

Efeito da cadência de pedalada sobre as respostas metabólica e cardiovascular durante o exercício incremental e de carga constante em indivíduos ativos

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.

Importância da região anteroventral do terceiro ventrículo (AV3V) no controle cardiovascular e do equilíbrio hidroeletrolítico

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.

Clinical and cardiovascular alterations produced by scorpion envenomation in dogs

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.

Nitrergic pathways and L-type calcium channel of MnPO influencing cardiovascular homeostasis

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.

Cardiovascular responses produced by central injection of hydrogen peroxide in conscious rats

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.

Abnormal evening vertical plasma drift and effects on ESF and EIA over Brazil-South Atlantic sector during the 30 October 2003 superstorm

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.