Interaction between areas of the central nervous system in the control of water intake and arterial pressure in rats

1. Water intake induced by injection of 0.2 M-NaCl into the lateral preoptic area was increased by the injection of angiotensin II into the subfornical organ of rats. The injection of hypertonic saline solution into the subfornical organ increased water intake. However, the increase was lower than when the solution was injected into the lateral preoptic area. The injection of 4 μg angiotensin II into the lateral preoptic area further augmented this effect. 2. Injection of angiotensin II into the subfornical organ caused a rise in blood pressure which preceded the thirst-inducing effect. The injection of 0.2 M NaCl into the subfornical organ caused no changes in blood pressure, whereas the injection of angiotensin II into the lateral preoptic area caused some increase. 3. Dehydration of the lateral preoptic area by means of 0.2 M NaCl in combination with intravenous infusion of angiotensin II caused a summation of effects in terms of the water intake, without changing cardiovascular alterations induced by the infusion of angiotensin II. A summation of effects in the water intake, but not in blood pressure, was also observed when 0.5 M NaCl was infused intravenously in combination with the injection of angiotensin II into the subfornical organ and into the lateral preoptic area. 4. The results indicate that there are interactions between the subfornical organ and lateral preoptic area in the regulation of cardiovascular and thirst mechanisms.

Different effects on rat arterial pressure and heart rate when losartan is injected into the third or fourth ventricle

Cardiovascular responses to central losartan (LOS), a non-peptide angiotensin II (ANG II) receptor antagonist, were investigated by comparing the effects of LOS injection into the 3rd and 4th cerebral ventricles (3rdV, 4thV) on mean arterial pressure (MAP) and heart rate (HR). Adult male Holtzman rats were used (N=6 animals per group). Average basal MAP and HR were 114±3 mmHg and 343±9 bpm (N=23), respectively. LOS (50, 100 or 200 nmol/2 μl) injected into the 3rdV induced pressor (peak of 25±3 mmHg) and tachycardic (peak of 60±25 bpm) responses. LOS injected into the 4thV had no effect on MAP, but it induced bradycardia (peak of -35±15 bpm). KCl (200 nmol/2 μl) injected into the 3rdV or into the 4thV had no effect on either MAP or HR compared to 0.9% saline injection. The results indicate that LOS injected into the third ventricle acts on forebrain structures to induce its pressor and tachycardic effects and that bradycardia, likely dependent on hindbrain structures, is obtained when LOS is injected into the fourth ventricle.

Effects of intracerebroventricular injections of losartan or PD123319 on arterial pressure and heart rate of sodium replete and sodium deplete rats

Angiotensin II (Ang II) non-peptide antagonists were injected i.c.v. (6.25-200 nmol, n = 5-8 rats/group): In sodium replete rats, losartan (AT1 receptor antagonist) induced an increase in mean arterial pressure (MAP) and in heart rate (HR) by 3rd ventricular (3rdV) injection, and a weaker pressor response and bradycardia by 4th ventricular (4thV) injection. PD123319 (AT2 receptor antagonist) induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and no alteration in HR by 4thV injection. In sodium deplete (furosemide plus removal of ambient sodium for 24 h) rats, losartan induced an increase in MAP and no alteration in HR by 3rdV injection, and no alteration in MAP and bradycardia by 4thV injection. PD123319 induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and bradycardia by 4thV injection. Thus, there was no fall in MAP by central injections of Ang II antagonists. Intravenous injection of losartan, but not of PD123319, induced a fall in MAP in both sodium replete and sodium deplete animals. Therefore, losartan and PD123319 can have similar effects on MAP and HR when injected intracerebroventricularly, although some differences are also present. The bradycardia is consistent with an withdrawal of Ang II inhibitory action on baroreflex.

Functional evidence that the central renin-angiotensin system plays a role in the pressor response induced by central injection of carbachol

We investigated the effects of losartan, an AT 1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/l μl) into the LV blocked the pressor response induced by ANG II (12 ng/l μl) and carbachol (2 nmol/l μl). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 ± 1 and 28 ± 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 ± 1 and 5 ± 2 mmHg, respectively). The injection of ramipril (12 ng/l μl) prior to carbachol blocked the pressor effect of carbachol to 7 ± 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure.

A lung computed tomographic assessment of positive end-expiratory pressure-induced lung overdistension

The aim of this study was to assess positive end-expiratory pressure (PEEP)-induced lung overdistension and alveolar recruitment in six patients with acute lung injury (ALI) using a computed tomographic (CT) scan method. Lung overdistension was first determined in six healthy volunteers in whom CT sections were obtained at FRC and at TLC with a positive airway pressure of 30 cm H2O. In patients, lung volumes were quantified by the analysis of the frequency distribution of CT numbers on the entire lung at zero end-expiratory pressure (ZEEP) and PEEP. In healthy volunteers at FRC, the distribution of the density histograms was monophasic with a peak at -791 ± 12 Hounsfield units (HU). The lowest CT number observed was -912 HU. At TLC, lung volume increased by 79 ± 35% and the peak CT number decreased to -886 ± 26 HU. More than 70% of the increase in lung volume was located below -900 HU, suggesting that this value can be considered as the threshold separating normal aeration from overdistension. In patients with ALI, at ZEEP the distribution of density histograms was either monophasic (n = 3) or biphasic (n = 3). The mean CT number was -319 ± 34 HU. At PEEP 13 ± 3 cm H2O, lung volume increased by 47 ± 19% whereas mean CT number decreased to -538 ± 171 HU. PEEP induced a mean alveolar recruitment of 320 ± 160 ml and a mean lung overdistension of 238 ± 320 ml. In conclusion, overdistended lung parenchyma of healthy volunteers is characterized by a CT number below -900 HU. This threshold can be used in patients with ALI for differentiating PEEP-induced alveolar recruitment from lung overdistension.

Transient flow of the oil-refrigerant mixture through the radial clearance in rolling piston compressors

Unsteady flow of oil and refrigerant gas through radial clearance in rolling piston compressors has been modeled as a heterogeneous mixture, where the properties are determined from the species conservation transport equation coupled with momentum and energy equations. Time variations of pressure, tangential velocity of the rolling piston and radial clearance due to pump setting have been included in the mixture flow model. Those variables have been obtained by modeling the compression process, rolling piston dynamics and by using geometric characteristics of the pump, respectively. An important conclusion concerning this work is the large variation of refrigerant concentration in the oil-filled radial clearance during the compression cycle. That is particularly true for large values of mass flow rates, and for those cases the flow mixture cannot be considered as having uniform concentration. In presence of low mass flow rates homogeneous flow prevail and the mixture tend to have a uniform concentration. In general, it was observed that for calculating the refrigerant mass flow rate using the difference in refrigerant concentration between compression and suction chambers, a time average value for the gas concentration should be used at the clearance inlet.

A two phase flow nonlinear parameter estimation for capillary tube-suction line heat exchanger

Here we present two-phase flow nonlinear parameter estimation for HFC's flow through capillary tube-suction line heat exchangers, commonly used as expansion devices in small refrigeration systems. The simplifying assumptions adopted are: steady state, pure refrigerant, one-dimensional flow, negligible axial heat conduction in the fluid, capillary tube and suction line walls. Additionally, it is considered that the refrigerant is free from oil and both phases are assumed to be at the same pressure, that is, surface tension effects are neglected. Metastable flow effects are also disregarded, and the vapor is assumed to be saturated at the local pressure. The so-called homogeneous model, involving three, first order, ordinary differential equations is applied to analyze the two-phase flow region. Comparison is done with experimental measurements of the mass flow rate and temperature distribution along capillary tubes working with refrigerant HFC-134a in different operating conditions.

Flow evolution of a metallic slurry during thixoextrusion of an automotive valve

The aim of this work is to characterize a metallic slurry (Al-4.5%Cu) flow during thixoforming of an automotive valve. The necessary globular structure was obtained by first inoculating the alloy with TIBAL (5%Ti, 1%B, Al - rest) at 750.0°C, and then reheating to a state between liquidus and solidus prior to thixoforming. Two metallic slurries, with a solid phase of approximately 86.1 and 78.2 percent, were used to generate different experimental flow patterns during the thixoforming process. The flow of the material into the die was observed for total, and partial displacement (2.7, 5.4, 7.5mm) of the punch. The first displacement shows formation of the valve rod. The patterns at each step of displacement of the punch were preserved by quenching in water, thus revealing the profile of the die fill and microstructural evolution. Degeneration of the globular phase was observed along the piece thixoextruded. Thixoextrusion forces versus time curves were generated for partial and full displacement of the punch. Porosity was visible along the billet prior to thixoforming. However, some areas show that the porosity gradually decreased to zero as the thixoextrusion pressure increased. Turbulent, transient and laminar flow are analyzed in this work.

Influence of arginine vasopressin receptor and nitric oxide on the water, sodium intake and arterial blood pressure induce by angiotensin injected into third ventricle of the brain

As several structures of the central nervous system are involved in the control of hydromineral and cardiovascular balance we investigated whether the natriorhexigenic and pressor response induced by the injection of ANG II into the 3rd V could be mediated by vasopressinergic and nitrergic system. Male Holtzman rats weighing 200-250 g with cannulae implanted into the 3rd V were used. The drugs were injected in 0.5 μL over 30-60 sec. Controls were injected with a similar volume of 0.15 M NaCl. ANGII increased the water intake vs control. AVPA injected into 3rd V prior to ANGII decreased the dipsogenic effect of ANGII. L-arginine also decreased the water intake induced by ANGII. AVPA plus L-arginine inhibit the water intake induced by ANGII. 7NIT injected prior to ANGII potentiated the dipsogenic effect of ANGII. Pre-treatment with ANGII increased the sodium ingestion vs control. AVPA decreased the ANGII effect in sodium intake. L-arginine also decreased the natriorhexigenic effect of ANGII. The combination of L-arginine and AVPA inhibit the sodium intake induced by ANGII. 7NIT injected prior to ANGII potentiated the sodium intake induced by ANGII. ANGII induced an increase in Mean Arterial Pressure (MAP) vs control. AVPA and L-arginine induced a decreased in the pressor effect of ANGII. The combination of L-arginine and AVPA inhibit the pressor effect of ANGII. 7NIT injected prior to ANGII into 3rd V potentiated the pressor effect of ANGII. These data suggest that arginine vasopressin V 1 receptors and Nitric Oxide (NO) within the circumventricular structures may be involved in sodium intake and pressor response induced by the activation of ANGII receptors within the circumventricular neurons. These studies revealed the involvement of sodium appetite by utilizing the angiotensinergic, vasopressinergic and nitrergic system in the central regulation of blood pressure. © 2006 Asian Network for Scientific Information.

Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats

Microinjection of S-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia, and vasoconstriction in the renal, mesenteric, and hindquarter vascular beds. In the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses >5 pmol/100 nl. To test the hypothesis that this vasodilation is caused by activation of a nitroxidergic pathway in the NTS, we examined the effect of pretreatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10 nmol/100 nl, microinjected into the NTS) on changes in mean arterial pressure, heart rate, and regional vascular conductance (VC) induced by microinjection of AMPA (10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 ± 4%, but after pretreatment with L-NAME, AMPA reduced hindquarter VC by 16 ± 7% and 17 ± 9% (5 and 15 min after pretreatment, P < 0.05 compared with before pretreatment). Pretreatment with L-NAME reduced AMPA-induced bradycardia from 122 ± 40 to 92 ± 32 beats/min but did not alter the hypertension induced by AMPA (35 ± 5 mmHg before pretreatment, 43 ± 6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values or the response to AMPA. The present study shows that stimulation of AMPA receptors in the NTS activates both vasodilatatory and vasoconstrictor mechanisms and that the vasodilatatory mechanism depends on production of nitric oxide in the NTS. Copyright © 2006 the American Physiological Society.

Central nifedipine-induced alterations in salivary flow and compounds: Role of nitric oxide

The aim of this study was to examine the role of nifedipine and Nitric Oxide (NO) on salivary flow and compounds (salivary amylase, saliva total proteins, saliva calcium, sodium and potassium). Male Holtzman rats weighting 200-250 g were anesthetized with zoletil 50 mg kg -1 (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle and stainless steel cannulas were implanted into their lateral ventricle of the brain (LV). Animals in divided group were injected with nifedipine (50 μg μL -1) alone and in combination with 7-nitroindazol (7-NIT) (40 μg μL -1), neuronal NO Sinthase Inhibitor (nNOSI) and Sodium Nitroprussate (SNP) (30 μg μL -1) NO donor agent. As a secretory stimuli, pilocarpine dissolved in isotonic was administered intraperitoneally (ip) at a dosage of 10 mg kg -1 body weight. Saliva was collected for 7 min with four cotton balls weighing approximately 20 mg each, two of which were placed on either side of the oral cavity, with the other two placed under the tongue. Nifedipine treatment induced a reduction in saliva secretion rate and concentration of amylase, total protein and calcium without changes in sodium and potassium concentration in comparison with controls. Co-treatment of animals with nifedipine and SNP retained flow rate and concentration of amylase, total protein and calcium in normal levels. Co-treatment of animals with nifedipine and 7-NIT potentiated the effect of nifedipine on the reduction of saliva secretion and concentrations of amylase, total protein and calcium. Nifedipine (dihydroperidine) calcium-channel blocker widely in use is associated with salivary dysfunction acting in the central nervous system structures. NO might be the mechanism for protective effect against the nifedipine-induce salivary dysfunction, acting in the CNS. © 2006 Asian Network for Scientific Information.

A multicommuted flow-based system for hydrogen peroxide determination by chemiluminescence detection using a photodiode

A simple, rapid, and automated assay for hydrogen peroxide in pharmaceutical samples was developed by combining the multicommutation system with a chemiluminescence (CL) detector. The detection was performed using a spiral flow-cell reactor made from polyethylene tubing that was positioned in front of a photodiode. It allows the rapid mixing of CL reagent and analyte and simultaneous detection of the emitted light. The chemiluminescence was based on the reaction of luminol with hydrogen peroxide catalyzed by hexacyanoferrate(III). The feasibility of the flow system was ascertained by analyzing a set of pharmaceutical samples. A linear response within the range of 2.2-210 μmol l-1 H2O2 with a LD of 1.8 μmol l-1 H2O2 and coefficient of variations smaller than 0.8% for 1.0×10-5 mol l-1 and 6.8×10-5 mol l-1 hydrogen peroxide solutions (n=10) were obtained. Reagents consumption of 90 μg of luminol and 0.7 mg of hexacyanoferrate(III) per determination and sampling rate of 200 samples per hour were also achieved. Copyright © Taylor & Francis Group, LLC.

Critical parameter determination of sonic flow controller diamond microtubes and micronozzles

In this article, the authors measure throughput of sonic diamond microtubes and micronozzles that can work as passive gas flow controllers and flow meters under choking conditions. The behavior of the outlet pressure through the microdevices using an experimental setup with constant volume and constant temperature was determined in order to obtain the critical throughput, the critical mass flow rate, and the discharge coefficients of the diamond sonic microdevices. © 2007 American Vacuum Society.

Echocardiographic Doppler estimation of pulmonary artery pressure in critically ill patients with severe hypoxemia

BACKGROUND: In spontaneously breathing cardiac patients, pulmonary artery pressure (PAP) can be accurately estimated from the transthoracic Doppler study of pulmonary artery and tricuspid regurgitation blood flows. In critically ill patients on mechanical ventilation for acute lung injury, the interposition of gas between the probe and the heart renders the transthoracic approach problematic. This study was aimed at determining whether the transesophageal approach could offer an alternative. METHODS: Fifty-one consecutive sedated and ventilated patients with severe hypoxemia (arterial oxygen tension/fraction of inspired oxygen < 300) were prospectively studied. Mean PAP measured from the pulmonary artery catheter was compared with several indices characterizing pulmonary artery blood flow assessed using transesophageal echocardiography: preejection time, acceleration time, ejection duration, preejection time on ejection duration ratio, and acceleration time on ejection duration ratio. In a subgroup of 20 patients, systolic PAP measured from the pulmonary artery catheter immediately before withdrawal was compared with Doppler study of regurgitation tricuspid flow performed immediately after pulmonary artery catheter withdrawal using either the transthoracic or the transesophageal approach. RESULTS: Weak and clinically irrelevant correlations were found between mean PAP and indices of pulmonary artery flow. A statistically significant and clinically relevant correlation was found between systolic PAP and regurgitation tricuspid flow. In 3 patients (14%), pulmonary artery pressure could not be assessed echocardiographically. CONCLUSIONS: In hypoxemic patients on mechanical ventilation, mean PAP cannot be reliably estimated from indices characterizing pulmonary artery blood flow. Systolic PAP can be estimated from regurgitation tricuspid flow using either transthoracic or transesophageal approach. © 2008 American Society of Anesthesiologists, Inc.

Treatment of pulmonary thromboembolism in patients with systemic blood pressure stability and right ventricular dysfunction

Pulmonary thromboembolism (PTE) ranges from incidental, clinically unimportant thromboembolism to massive embolism with sudden death. Its treatment is well established in two groups of patients: heparin for those with normal systemic blood pressure without right ventricular dysfunction (RVD) and thrombolysis for those with RVD and circulatory shock. In an intermediate group of patients with systemic blood pressure stability combined with RVD, which is usually associated with worse outcome, the treatment is controversial. There are authors who strongly suggest thrombolysis while others contraindicate this procedure and recommend anticoagulation with heparin. This is a narrative review that includes clinical trials comparing thrombolysis and heparin for the treatment of PTE patients with systemic blood pressure stability and RVD published since 1973. The results show that there are only four trials on this subject with less than 500 patients. Many PTE patients with systemic blood pressure stability and RVD might benefit from thrombolysis but, on the other hand, the risk for hemorrhagic events may be increased. Large randomized clinical trials are required to clarify this. © 2008 Bentham Science Publishers Ltd.