863 resultados para Heart-rate Changes


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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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The effects of carotid occlusion on parasympathetic activity were studied in anesthetized dogs submitted to beta adrenergic blockade. Modifications of the heart rate, before and after administration of atropine, were utilized for assessment of vagal changes. When vagal activity was intact there was elevation of the heart rate. After parasympathetic blockade carotid occlusion did not cause heart rate modifications. The data suggest that carotid occlusion produced vagal inhibition.

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1. 1. The mechanisms behind cardiac control were investigated in the South American lungfish, Lepidosiren paradoxa, using fish with chronically implanted cannulae and electromagnetic flow probes. In addition, a preliminary study was made of the cardiovascular events associated with air breathing. 2. 2. The study suggests that the heart of Lepidosiren is controlled by cholinergic vagal fibres which, in some animals, exert a tonic influence in the resting fish. Cyclic changes in heart rate in association with air breaths is due to modulation of this cholinergic tonus. 3. 3. In addition to the variable cholinergic tonus, there appears to be a relatively stable adrenergic tonus on the heart, which causes an elevated heart rate. The adrenergic tonus is likely to be due to local release of catecholamines from endogenous chromaffin cells within the atrium. 4. 4. Preliminary results suggest that pulmonary arterial flow increases by about 50% immediately following an air breath. The mechanism behind this increase probably involves both an elevation of the heart rate and a redistribution of blood flow into the pulmonary circuit. © 1989.

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The present study investigates the participation and interaction between cholinergic and opiate receptors of the medial septal area (MSA) in the regulation of Na+, K+ and water excretion, drinking and blood pressure regulation. Male Holtzman rats were implanted with stainless steel cannulae opening into the MSA. Na+, K+ and water excretion, water intake and blood pressure were measured after injection of carbachol (cholinergic agonist), FK-33824 (an opiate agonist) + carbachol or naloxone (an opiate antagonist) + carbachol into MSA. Carbachol (0.5 or 2.0 nmol) induced an increase in Na+ and K+ excretion, water intake and blood pressure and reduced the urinary volume. FK-33824 reduced the urinary volume and Na+ and K+ excretion. Previous injection of FK-33824 (100 ng) into the MSA blocked the increases in Na+ and K+ excretion, water intake and blood pressure induced by carbachol. Naloxone (10 μg) produced no changes in the effect of 2.0 nmol carbachol, but potentiated the natriuretic effect induced by 0.5 nmol dose of carbachol. These data show an inhibitory effect of opiate receptors on the changes in cardiovascular, fluid and electrolyte balance induced by cholinergic stimulation of the MSA in rats. © 1992.

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Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of β-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.

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The purpose of the present study was to demonstrate a physiological response to TA2005, a potent β2-adrenoceptor (β2-AR) selective agonist, in right atria isolated from stressed female rats under the influence of the estrous cycle. We obtained concentration-response curves to the agonist in the presence and in the absence of selective antagonists in right atria isolated from female rats submitted to three daily foot-shock sessions (30 min duration, 120 pulses of 1.0 mA, 1.0 s, applied at random intervals of 5- 25 s) and sacrificed at estrus or diestrus. Our results showed that the pD2 values of TA2005 were not influenced by estrous cycle phase or foot-shock stress. However, in right atria from stressed rats sacrificed during diestins, the concentration-response curve to TA2005 was biphasic, with a response being obtained at concentrations of 0.1 nM, whereas during estrus no response was observed at doses lower than 3 nM. ICI118,551, a β2-AR antagonist, abolished the response to nanomolar concentrations of TA2005 in right atria from stressed rats at diestrus, with no changes in agonist pD2 values in right atria from control rats (7.47 ± 0.09, p > 0.05) but a 3-fold decrease in pD2 values of TA2005 in right atria from foot shock stressed rats (7.90 ± 0.07, p ≤ 0.05). Concentration-response curves to TA2005 in the presence of ICI118,551 were best fitted by a one-site model equation. The β1-AR antagonist, CGP20712A, shifted to the right only the second part of the concentration-response curves to the agonist, unmasking the putative β2-AR-mediated response to the agonist in tissues isolated from stressed rats at diestrus. Under this condition, concentration-response curves to the agonist were best fitted by a two-site model equation, pD2 and maximum response of TA2005 interaction with β1- and putative β2-adrenoceptor components were calculated. Schild analyses gave a pK(B) value for CGP20712A that was typical for the interaction with β1-AR in each experimental group, pK(B) values for ICI118,551 could not be obtained in stressed rats sacrificed at diestins since Schild plot slopes were lower than 1.0. In right atria from control rats, ICI118,551 pK(B) values were similar to reported values for the interaction of the antagonist with β1-AR. These results confirm that a heterogenous β1-AR population mediating the chronotropic response to catecholamines can be demonstrated in right atria from foot shock stressed female rats sacrificed at diestins. The stress-induced response seems to be mediated by the β2-AR subtype. Right atria from rats sacrificed during estrus are protected against stress-induced alterations on the homogeneity of β-AR population.

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Background and Objectives - Allopurinol is a drug which inhibits the formation of noxious renal free radicals. The aim of this study was to evaluate the protecting renal effects of allopurinol in ischemic kidneys of dogs. Methods - Sixteen dogs were anesthetized with sodium pentobarbital and submitted to extracellular volume expansion (1.4 ml.kg-1.min-1), to mechanic ventilation with air, to right nephrectomy and to left renal artery clamping. Changes which might occur in renal morphology and function after 30 min of total ischemia and posterior reperfusion were studied in Group 1 (G1), in addition to the action of allopurinol (50 mg.kg-1) on those kidneys, when administered 24 h before the experiment and 1 h before the ischemic procedure in Group 2 (G2). The following parameters: heart rate, inferior vena cava pressure, mean blood pressure, PAH clearance (PAH(c)), renal blood flow (RBF), renal vascular resistance (RVR), creatinine clearance (Cr(c)), filtration fraction, urine output, plasma and urine osmolality, osmolar clearance, free water, sodium and potassium clearance, urine and fractional sodium and potassium excretion, hematocrit, rectal temperature, and left kidney histology were evaluated in four moments: M1 control, and M2, M3, M4 obtained immediately, 15 and 30 min after unclamping of the left renal artery. In G2, M1, M2, M3 and M4 were obtained 45, 90, 105, and 120 min after the second allopurinol dose. Results - Both groups showed the highest values for PAH(c), RBF, and Cr(c), and the lowest values for RVR in M1. Animals were tachycardiac since the beginning of the experiment both in G1 and in G2. The other parameters were not changed. Left kidney histological evaluation showed alterations compatible with acute tubular necrosis in both experimental groups. Conclusions - Alterations found in renal hemodynamics were compatible with the release of vasoconstrictor substances due to renal ischemia. Allopurinol was not effective in preventing renal alterations caused by ischemia and reperfusion.

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There still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) underwent ascending aorta stenosis for 8 weeks (group AAS, n=9). LV performance was assessed by transthoracic echocardiography under light anesthesia. Myocardial function was studied in isolated papillary muscle preparation during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, n=9). LV weight-to-body weight ratio (C: 2.0 ± 0.5 mg/g; AAS: 3.3 ± 0.7 mg/g), LV relative wall thickness (C: 0.19 ± 0.02; AAS; 0.34 ± 0.10), and LV fractional shortening (C: 54 ± 5%; AAS: 70 ± 8%) were increased in the group AAS (p<0.05). Echocardiographic analysis also indicated a significant association (r=0.74; p<0.001) between percent fractional shortening and LV relative wall thickness. The performance of AAS isolated muscle revealed that active tension (C: 6.6 ± 1.7 g/mm 2; AAS: 6.5 ± 1.5 g/mm 2) and maximum rate of tension development (C: 69 ± 21 g/mm 2/s; AAS: 69 ± 18 g/mm 2) were not significantly different from group C (p>0.05). In conclusion: 1) Compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance; 2) The improved LV function might be due to the ventricular remodeling characterized by an increased relative wall thickness. Copyright © 2002 By PJD Publications Limited.

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Objectives: To evaluate the effects of a combination of tiletamine-zolazepam-romifidine-atropine in ocelots. Design: Prospective experimental trial. Animals: Eight captive adult ocelots (three females and five males). Methods: Calculated doses of tiletamine-zolazepam (3.75 mg kg -1), romifidine (50 μg kg-1) and atropine (0.04 mg kg-1) were administered intramuscularly. After immobilization, animals were weighed and the real doses determined. Heart rate, respiratory frequency, noninvasive systolic, diastolic, and mean arterial pressure, arterial oxygen hemoglobin saturation, and rectal temperature were measured. Data were analyzed by means of ANOVA for repeated measures, followed by the Tukey test to compare values over time. Results: Doses administered were 3.4 ± 0.6 mg kg-1 of tiletamine-zolazepam, 0.04 ± 7.0 mg kg-1 of romifidine, and 0.03 ± 0.007 mg kg-1 of atropine. The mean time to recumbency and duration of immobilization were 7.0 ± 4.5 and 109.2 ± 27.9 minutes, respectively. The median times to standing and walking were 52.3 [0-90] and 2.3 [0-69.3] minutes, respectively. A decrease in heart rate was observed 45 minutes following drug administration. Arterial blood pressure was maintained during the study. Conclusions and clinical relevance: This protocol produced good immobilization in ocelots with minimal changes over time in cardiovascular parameters.

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The purpose of this study was to verify the effects of a carbohydrate-electrolyte drink on soccer performance. Twenty soccer players volunteered to participate in the study. Players were allocated to two assigned trials according to their positional roles in the team: CHO group (ingesting a 6% carbohydrate-electrolyte solution at regular 15 minutes intervals) and NCHO (ingesting no fluid) during 75 min on-field soccer game. During the trials, body mass loss, heart rate, time spent running, number of sprints and core temperature were measured. There were statistically significant changes (p < 0.05) in body mass loss (CHO: 1.14 ± 0.37 kg vs. NCHO: 1.75 ± 0.47 kg) and number of sprints performed (CHO: 14.70 ± 4.38 vs. NCHO: 10.70 ± 5.80) between groups. The main finding of the present study indicates that supplementation with a carbohydrate-electrolyte drink during a soccer match is beneficial in helping to prevent deterioration in performance. © Journal of Sports Science and Medicine (2004).

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BACKGROUND AND OBJECTIVES: Pressure controlled ventilation (PCV) is available in anesthesia machines, but there are no studies on its use during CO 2 pneumoperitoneum (CPP). This study aimed at evaluating pressure-controlled ventilation and hemodynamic and ventilatory changes during CPP, as compared to conventional volume controlled ventilation (VCV). METHODS: This study involved 16 dogs anesthetized with thiopental, fentanyl and pancuronium, which were randomly assigned to two groups: VC - volume controlled ventilation (n=8) and PC - pressure controlled ventilation (n=8). Hemodynamic and ventilatory parameters were monitored and recorded in 4 moments: M1 (before CPP), M2 (30 minutes after CPP = 10 mmHg), M3 (30 minutes after CPP=15 mmHg) and M4 (30 minutes after deflation). RESULTS: With CPP, there has been significant increase in tidal volume in PC group; there has been increase in airway pressures (peak and plateau), decrease in compliance with increase in CPP pressure, increase in heart rate, maintenance of mean blood pressure with higher values in the VC group in all stages; there was also increase in right atrium pressure with significant decrease after deflation, decrease in arterial pH with minor variations in PC group, greater arterial pCO 2 stability in PC group, and no significant changes in arterial pO 2. CONCLUSIONS: There were some differences in hemodynamic and ventilatory data between both ventilation control modes (VC and PC). It is possible to use pressure controlled ventilation during CPP, but the anesthesiologist must monitor and take a close look at alveolar ventilation, adjusting inspiratory pressure to ensure proper CO 2 elimination and oxygenation. © Sociedade Brasileira de Anestesiologia, 2005.

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Many investigations have shown that the coincidence between the ventilatory thresholds and those thresholds using the lactate response does not happen all of the time, suggesting that there is no relationship between the cause-effect between these phenomena. Thus, the present study had as main purpose to compare and correlate the Oxygen consumption (V̇O 2), the power (W), and the heart rate (HR) values attained using protocols to determine the Ventilatory Threshold (VT) and the Individual Anaerobic Threshold (IAT). The sampling was constituted by eight State and National level cyclists (age: 27.88 ± 8.77 years; body mass: 65.19 ± 4.40 kg; height: 169.31 ± 5,77 cm). The IAT was determined starting from a three minutes 50 W warm up with progressive increases of 50 W.3min -1 up to achieving the voluntary exhaustion, when the blood was collected in the last 20 seconds of each phase, and during the recovering period. In order to determine the VT, it was used the same protocol used to determine the IAT, but without performing the blood collection. The VT was identified through the changes in the pulmonary ventilation, as well as of the ventilatory equivalent of the O 2 and CO 2. The t-Student test showed no significant statistical difference in any of the attained variables. The associations found were high and significant. The V̇O 2 (ml.kg -1.min. -1), P (W), and HR (bpm) corresponding to the VT and IAT, as well as the associations between variables were respectively: 48.00 ± 3.82 vs. 48.08 ± 3.71 (r = 0.90); 256.25 ± 32.04 vs. 246.88 ± 33.91 (r = 0.84); 173.75 ± 9.18 vs. 171.25 ± 12.02 (r = 0.97). According to the results attained, it can be concluded that the IAT and the VT produce similar V̇O 2, W, and HR values, favoring the adoption of the VT because it is a non-invasive method to determine the anaerobic threshold in cyclists.

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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.

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Objective - To investigate the effects of buprenorphine on cardiopulmonary variables and on abdominal auscultation scores in horses. Animals - 6 healthy adult horses. Procedures - Horses were restrained in stocks and allocated to 2 treatments in a randomized crossover design, with 1-week intervals between each treatment. Saline (0.9% NaCl) solution was administered IV as a control, whereas buprenorphine (10 μg/kg, IV) was administered to the experimental group. Cardiopulmonary data were collected for 120 minutes after buprenorphine or saline solution administration. Abdominal auscultation scores were monitored for 2 and 12 hours after drug administration in the control and experimental groups, respectively. Results - Following control treatment, horses remained calm while restrained in the stocks and no significant changes in cardiopulmonary variables were observed throughout the study. Buprenorphine administration caused excitatory phenomena (restlessness and head shaking). Heart rate, cardiac index, and arterial blood pressure were significantly increased after buprenorphine administration until the end of the observational period (120 minutes). Minimal changes were found in arterial blood gas tensions. Abdominal auscultation scores decreased significantly from baseline for 4 hours after buprenorphine administration. Conclusions and Clinical Relevance - Buprenorphine induced excitement and hemodynamic stimulation with minimal changes in arterial blood gas tensions. These effects may impact the clinical use of buprenorphine in horses. Further studies are indicated to investigate the effects of buprenorphine on gastrointestinal motility and fecal output.