969 resultados para DECREASES ARTERIAL-PRESSURE


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1. Angiotensin (Ang)II is involved in responses to hypovolaemia, such as sodium appetite and increase in blood pressure, Target areas subserving these responses for AngII include the cardiovascular system in the periphery and the circumventricular organs in the brain.2. Conflicting data have been reported for the role of systemic versus brain AngII in the mediation of sodium appetite.3. The role for systemic AngII and systemic AngII receptors in the control of blood pressure in hypovolaemia is well established. In contrast with systemic injections, i.c.v injections of AngII non-peptide AT(1) and AT(2) receptor antagonists, such as losartan and PD123319, do not reduce arterial pressure in sodium-depleted (furosemide injection plus removal of ambient sodium for 24 h) rats. Thus, brain AngII receptors are likely not important for cardiovascular responses to hypovolaemia induced by sodium depletion.4. Intracerebroventricular injections of losartan or PD 123319 increase arterial pressure when injected at relatively high doses. This hypertensive effect is unlikely to be an agonist effect on brain AngII receptors, Increases in arterial pressure produced by i.c.v, losartan are attenuated by lesions of the tissue surrounding the anterior third ventricle (AV3V). The hypertensive effect of i.c.v, AngII is abolished by lesions of the AV3V.5. Hypertension induced by AngII receptor antagonists is consistent with hypotension induced by AngII acting in the brain, However, the full physiological significance of this hypotensive effect mediated by brain AngII receptors remains to be determined.

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This study was designed to analyze the impact of diminished renal perfusion pressure due to renal clipping on the rat model of adriamycin nephropathy. Male Wistar rats, divided into four groups (n = 9 per group) were injected with saline as control (C), adriamycin 3 ml/kg (Ad), saline with the left renal artery clipped (Rv), and adriamycin plus clip (AdRv). After 24 weeks mean arterial pressure (MAP), inulin, and p-aminohippurate (PAH) clearances were performed to evaluate renal function. Morphologic analysis included histologic criteria of percentage of glomerulosclerosis and tubulointerstitial lesion index (TILI). The MAP (mm Hg) was similar between Rv (143 +/- 13) and AdRv (154 +/- 20), but higher (P < .05) than C (120 +/- 8) and Ad (124 +/- 11). Inulin clearance (mL/min/100 g) in Ad (0.2 +/- 0.05) was smaller than in C (0.53 +/- 0.17) and Rv (0.4 +/- 0.01) (P < .05), and was at an intermediate level in AdRv (0.33 +/- 0.2). The level of PAH (mL/min/100 g) was normal at 1.76 in C, and diminished more in Ad (0.58) than in Rv (1.06) and AdRv (1.18) (P < .05). Both Ad and the AdRv nonclipped kidneys had the highest degree of glomerulosclerosis (33% and 25%) and TILI (7% and 8%), respectively, compared with C and Rv (both 0%), whereas the clipped kidneys displayed intermediate degrees (9% and 5%) (P < .05 v nonclipped). The data suggest that diminished perfusion pressure of the clipped kidney, by decreasing the intraglomerular pressure, protects the glomerulus from damage and attenuates the evolution of adriamycin nephropathy. Am J Hypertens 1998;11:1124-1128 (C) 1998 American Journal of Hypertension, Ltd.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The cardiovascular effects of dexmedetomidine alone or in combination with atropine were studied in six cats. Cats underwent four treatments in a randomized crossover design as follows: DEX15, saline + dexmedetomidine 15 mu g/kg; DEX30, saline + dexmedetomidine 30 mu g/kg; ADEX15, atropine + dexmedetomidine 15 mu g/kg; ADEX30, atropine + dexmedetomidine 30 mu g/kg. Pulse rate (PR) and systolic arterial pressure (SAP) decreased in DEX15 and DEX30. Premedication with atropine was effective in preventing bradycardia (PR < 100 beats/min) and resulted in a biphasic effect in blood pressure. Hypertension was followed by a gradual decrease in SAP. Rate pressure product decreased in DEX15 and DEX30 whereas in ADEX15 and ADEX30 it remained within baseline values for at least 60 min. Although premedication with atropine in cats sedated with dexmedetomidine prevents bradycardia, it induces hypertension and increases myocardial oxygen consumption. The magnitude of cardiovascular effects produced by dexmedetomidine in cats does not seem to be dose-related. (C) 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.

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

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Objective To evaluate the cardiorespiratory and behavioural effects of epidural xylazine (XYL) or clonidine (CLO) in horses.Study design Blinded, randomized experimental study.Twelve healthy Arabian yearling horses weighing 117-204 kg were randomly allocated into two groups: XYL (n = 6) and CLO (n = 6).Methods An epidural catheter was inserted and a facial arterial catheter was placed and the next day the horses were restrained in stocks. Baseline values for heart (HR) and respiratory (RR) rates, arterial pressure and behavioural responses were evaluated before (TO) and 10, 20, 30, 45, 60, 90 and 120 minutes after epidural injection (T10-T120). The horses received 0.2 mg kg(-1) of XYL or 5 mu g kg(-1) CLO; adjusted to (3.4 + (body weight in kg x 0.013) mL with saline. Data were analysed by the Kolmogorov-Smirnov test, one-way ANOVA with repeated measures, and one-way ANOVA followed by a Student-Newman-Keuls test or Fisher's exact test, as necessary. Significance was set at p <= 0.05.Results Sedation and ataxia were seen at T10, persisting until T120 in four and three horses, respectively, in XYL and all horses in CLO respectively. Two XYL and one CLO horses became recumbent at T45 and T25 respectively. Penile prolapse occurred in four of five males at T30 and T45, in the XYL and CLO groups, respectively, resolving by T120. Tail relaxation was present from T10 to T120 in all horses in XYL and in four horses in CLO. Head drop was observed from T20 to T60 and from T10 to T120 in XYL and CLO respectively. Respiratory rate decreased significantly only at T45 in the CLO group. Heart rate and arterial blood pressure remained stable.Conclusions and clinical relevance Epidural CLO and XYL produce similar cardiorespiratory and behavioural changes but neither would be safe to use clinically at the doses used in this study.

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In order to test if the maximal velocity of shortening (V(max)TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V(max)TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V(max)TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.

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In 18 dogs, previously anesthetized with sodium pentobarbital for the surgical preparation, catheterism and monitoring, the action of sodium pentobarbital (7.5 mg/kg) and enflurane (1.5 - 2%) in the liver circulation was studied. Measurements of the following parameters were made in four different times, before and 15, 30 and 60 min after the drug administration. By direct determination: hepatic artery flow, portal vein flow, mean pressure of the abdominal aorta, peripheral arterial pressure (mean), pressure in the caudal cava vein, portal pressure; and by indirect determination: total flow, arterial-cava gradient, portal-cava gradient, resistance in the hepatic artery territory, resistance in the territory of the portal vein, and total resistance. Based on the results, it is concluded that in the experiment's conditions: sodium pentobarbital doesn't change significantly the hepatic circulation, and enflurance produces a fall in the total hepatic flow, by reducing the portal flow, without alterations of the hepatic arterial flow. It diminishes the total hepatic resistance by diminishing the arterial resistance without alterations of the portal resistance; it diminishes the arterial-cava gradient in consequence of the reduction of the abdominal aorta pressure and of the portal pressure, but it seems that the caudal cava pressure is not altered. It also occurs a fall in the peripheral mean pressure.

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In six dogs, previously anesthetized with sodium pentobarbital (30 mg/kg) for surgical preparation, catheterism and monitoring, the action of sodium pentobarbital (7,5 mg/kg) on renal flow was studied. Determinations of mean arterial pressure, venous pressure, cardiac rate, arterio-cava pressure gradient and renal arterial resistance were made. Pentobarbital doesn't change significantly the renal blood flow or any of the other parameters studied, with the exception of venous pressure in the inferior caval vein where the drug produces a significant fall.

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In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the dipsogenic, natriuretic, kaliuretic and pressor responses elicited by intracerebroventricular (i.c.v.) injection of the cholinergic agonist carbachol. Freely moving rats with sham or MSA lesion (1-7 days and 14-18 days) and a stainless steel cannula implanted into the lateral ventricle were studied. In sham rats, i.c.v. injection of carbachol (7.5 nmol) produced an increase in water intake (10.2 ± 1.5 ml/h), mean arterial pressure (MAP) (35 ± 5 mmHg) and urinary Na+ and K+ excretion (551 ± 83 and 170 ± 17 μEq 120 min, resp.). The pressor (18 ± 3 and 14 ± 4 mmHg, resp.) and natriuretic responses (178 ± 58 and 172 ± 38 μEq 120 min) produced by i.c.v. carbachol in acute or chronic MSA-lesioned rats were reduced. No change was observed in urinary K+ excretion and a reduced water intake (5 ± 1.3 ml/h) was observed only in acute MSA-lesioned rats. These results suggest that the MSA plays an important role for the pressor and natriuretic responses induced by central cholinergic activation in rats. A small influence of this structure on water intake may also be suggested. © 1991.

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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.

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Little research has been done with propofol in relation to renal function. The aim of this study was to evaluate the effects of the continuous infusion of propofol on renal function in dogs. Sixteen dogs, previously anesthetized with pentobarbital sodium (30 mg.kg-1) for surgical preparation, catheterism and monitoring, were studied. The dogs were mechanically ventilated with air and received alcuronium (0.2 mg.kg-1 in bolus and 0.06 mg.kg-1 - maintenance). The following parameters were studied: heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), aortic blood flow (A(o)BF - by electromagnetic flowmeter installed in the ascending aortic), aortic vascular resistance index (A(o)VRI), renal plasma flow (ERPF - by para-aminohipurate clearance), glomerular filtration rate (GFR - by creatinine clearance), effective renal blood flow (ERBF = ERPF/1 - hematocrit), urinary volume (UV), renal vascular resistance (RVR = MAP.80/ERBF.10-3), urinary sodium excretion (UE(Na)), fractionated sodium excretion (FE(Na)), osmolar clearance (C(osm)) and free water clearance (C(H2O)). These parameters were studied at 15 (M1), 30 (M2), 45 (M3) and 60 (M4) min after beginning pentobarbital sodium infusion (5 mg.kg-1.h-1). The dogs were allocated into two groups of eight animals each: G1 (control-pentobarbital sodium) and G2 (propofol). In G1, pentobarbital was given at the four times studied. G2 dogs received the same treatment as G1 dogs at M1 and M2; infusion of pentobarbital was substituted by propofol (3 mg.kg-1 bolus, followed by 12 mg.kg-1.h-1 continuous infusion) at M3 and M4. Profile Analysis was used to analyze the results statistically. In G1 (pentobarbital), there was a significant increase in RVR (M1 < M4) and a decrease in ERPF and ERBF (M1 > M4). In G2 (propofol) there was only a significant increase in A(o)BF (M1 < M2 = M3). In comparison among groups, these was a significant alteration of FE(Na) at M3 (pentobarbital > propofol). It was observed that the continuous infusion of propofol in dogs, at the given doses, did not alter the basic variables of renal function and hemodynamics studied. We concluded that propofol can be one of the drugs of choice to provide base anesthesia in studies of renal function in dogs.

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Purpose - To analyse the influence of mannitol added to Krebs-Henseleit (KH) solution on the myocardium edema and myocardial function. Methods - Isolated rat heart under isovolumetric contractions studied according to Langendorff's technique were perfused with KH solution at constant flow during 90 min. The coronary perfusion pressure, diastolic and systolic pressures were recorded at every 15 min. At the end of the experiment, myocardium water content was measured in hearts perfused with KH solution (group I, n = 9) and in hearts perfused with KH solution plus 8 mM mannitol (group II, n = 8). These results were compared to non-perfused control heart (n = 9). Results - Myocardial water content was statistically higher in group I (80.8 ± 1.3%) compared to group II (78.1 ± 0.7%) and control group (75.5 ± 0.5%). Systolic arterial pressure was statistically higher in group I (86.2 ± 11.5 mmHg) compared to group II (72.7 ± 21.1 mmHg). There was no difference in the diastolic pressure between the two groups. Coronary perfusion pressure (Pp) increased progressively during the experiment in both groups. However, Pp was lower in group II than in group I. Conclusion - Mannitol added to KH solution significantly attenuates the myocardium edema in the isolated perfused rat heart.

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The authors studied the effect of temperature and humidity of inhaled gases on the respiratory tract of dogs submitted to mechanic ventilation. According to these two variables, fourty dogs were divided in five groups: -G1: 22-26°C and 17-20 mg H2O.l-1; G2: 27-31°C and 23-27 mg H2O.l-1; G3: 32-36°C and 30-36 mg H2O.l-1; G4: 37-41°C and 40-49 mg H2O.l-1; G5: 42-46°C and 59-65 mg H2O.l-1. The following parameters were evaluated: medial arterial pressure, cardiac frequency, venous pressure of inferior cava (CVP), endotracheal pressure, arterial pH, PaO2, PaCO2, rectal temperature, and the histology of the tracheobronchial tree. In the groups G1 and G5, the endotracheal pressure and CVP presented a slight raise. In the groups G1, G2 and G3, there was no histological modification or progressive hypothermia. The group G5 presented metabolic acidosis and great histological alteration; in this group the rectal temperature remained stable. The group G4 presented great histological alteration and hypothermia. In conclusion, the temperature and humidity of inhaled gases should not be higher than 36°C and 36 mm H2O.l-1, respectively. However, the stability of body temperature only is achieved when the temperature of the inhaled air is 42°C or higher.