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Increased Heart Rate (increased + heart_rate)
Selected AbstractsEffect of antivenin dose on outcome from crotalid envenomation: 218 dogs (1988,2006)JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 6 2009DACVIM, Jennifer L. McCown DVM Abstract Objective , To determine whether the dose of antivenin administered is associated with a difference in survival of crotalid-envenomated dogs. A secondary objective was to determine whether other covariables affect survival. Design , Retrospective study (1988,2006). Setting , Private referral center and university small animal teaching hospital. Animals , Two hundred and eighteen dogs with evidence of crotalid envenomation and treatment with equine-derived antivenin. Interventions , Administration of antivenin. Measurements and Main Results , Patient signalment, physical and clinicopathologic data at time of presentation, treatments, complications of antivenin therapy, length and cost of hospitalization, and outcome were recorded. Confidence intervals were determined for the difference in median number of vials administered and for median dosage for patients that lived versus died. Penalized logistic regression was performed to evaluate the effect of other covariables on survival. The median age of affected dogs was 3 years (range 6 w,12 y) with a median weight of 25.7 kg (range 1.95,86.4 kg). The median number of antivenin vials administered was 1.0 (range 1.0,10.0). Acute and chronic reactions were reported in 7% (16/218) and 0.9% (2/218) of dogs, respectively. Nine of 218 dogs (4.1%) died. The median number of vials administered to the nonsurvivors and survivors were 2.0 (range 1,5 vials) and 1.0 (range 1,10 vials), respectively. The median number of vials received was significantly different in dogs that died versus those that lived (P<0.05). Increased heart rate (P=0.02) and petechiation (P=0.04) were associated with decreased likelihood of survival, while diphenhydramine (P=0.02) and fluoroquinolone (P=0.046) administration was associated with increased likelihood of survival. The median duration of hospitalization was 1.0 day (range 2 h,22 d). The median cost of hospitalization was US$1592.00 (range US$267.20,US$6738.00). Conclusion , The administration of more vials of antivenin is potentially associated with negative outcome; however, a causal relationship has not been established. Controlled, prospective studies are needed to optimize antivenin administration. [source] Long-term prognostic value of B-type natriuretic peptide in cardiac and non-cardiac causes of acute dyspnoeaEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2007M. Christ Abstract Background, B-type natriuretic peptide (BNP) levels significantly predict increased risk of death in heart failure. The predictive role of BNP levels in patients with non-cardiac causes of acute dyspnoea presenting to the emergency department is not well characterized. Materials and methods, The B-type natriuretic peptide for Acute Shortness of Breath EvaLuation (BASEL) study enrolled consecutive patients with acute dyspnoea. Results, Cumulative mortality was 14·8%, 33·1% and 51·9% in 452 patients (age: 19,97 years; 58% male) within low (< 100 pg mL,1), intermediate (100,500 pg mL,1) and high (> 500 pg mL,1) BNP plasma levels at 18 months of follow-up. BNP classes (point estimate: 1·55, 95%CI: 1·19,2·03, P = 0·001) in addition to age, increased heart rate and diuretic use emerged as significant predictors for long-term mortality in multivariable Cox regression analyses. The BNP concentration alone had an area under the receiver operating characteristic curve of 0·71 (95%CI: 0·66,0·76; P < 0·001) for predicting 18 months mortality. BNP plasma levels independently predicted long-term risk of death in patients with non-cardiac (point estimate: 1·72, 95%CI: 1·16,2·56; P = 0·007) and with cardiac causes of acute dyspnoea (point estimate: 2·21, 95%CI: 1·34,3·64; P = 0·002). Conclusions, BNP levels are strong and independent predictors for long-term mortality in unselected dyspnoeic patients presenting to the emergency department independent from the cause of dyspnoea. [source] Dysautonomia after severe traumatic brain injuryEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2010H. T. Hendricks Background:, Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe TBI, the clinical variables that are associated with dysautonomia, and the functional outcome of patients with dysautonomia. Methods:, A historic cohort study in patients with severe TBI [Glasgow Coma Scale (GCS) , 8 on admission]. Results:, Seventy-six of 119 patients survived and were eligible for follow-up. The incidence of dysautonomia was 11.8%. Episodes of dysautonomia were prevalent during a mean period of 20.1 days (range 3,68) and were often initiated by discomfort. Patients with dysautonomia showed significant longer periods of coma (24.78 vs. 7.99 days) and mechanical ventilation (22.67 vs. 7.21 days). Dysautonomia was associated with diffuse axonal injury (DAI) [relative risk (RR) 20.83, CI 4.92,83.33] and the development of spasticity (RR 16.94, CI 3.96,71.42). Patients with dysautonomia experienced more secondary complications. They tended to have poorer outcome. Conclusions:, Dysautonomia occurs in approximately 10% of patients surviving severe TBI and is associated with DAI and the development of spasticity at follow-up. The initiation of dysautonomia by discomfort supports the Excitatory: Inhibitory Ratio model as pathophysiological mechanism. [source] Validation of a New Noninvasive Device for the Monitoring of Peak Endocardial Acceleration in Pigs: Implications for Optimization of Pacing Site and ConfigurationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008PIERRE BORDACHAR M.D. Introduction: The peak of endocardial acceleration (PEA) is an index of myocardial contractility. We aimed to (1) demonstrate that the PEA measured by the noninvasive cutaneous precordial application of an accelerometer sensor is related to left ventricular (LV) dP/dt max and (2) assess the usefulness of PEA monitoring during graded ischemia and during different configurations of sequential biventricular pacing. Methods and Results: Measurements of invasive LV dP/dt max were compared with measurements of transcutaneous PEA in seven pigs at baseline and during acute drug infusions; increased heart rate; right, left, biventricular and sequential biventricular pacing before and after graded ischemia induced by the constriction of the left anterior descending coronary artery. A consistent PEA signal was obtained in all animals. PEA changes were highly related to LV dP/dt max changes (r= 0.93; P < 0.001). The changes of LV contractility induced by the different pacing configurations were detected by PEA analysis in the absence of ischemia (r= 0.94; P < 0.001) and in the presence of ischemic LV dysfunction (r= 0.91; P < 0.001). Conclusion: Noninvasive PEA measurement allows monitoring of left ventricular contractility and may be a useful tool to detect global effect of ventricular ischemia and to optimize the choice of both pacing site and pacing configuration. [source] Individual Differences in Responses to Ethanol and d-Amphetamine: A Within-Subject StudyALCOHOLISM, Issue 4 2001Louis Holdstock Background: In some individuals, ethanol (EtOH) produces marked stimulant-like subjective effects resembling those of stimulant drugs, like d-amphetamine (AMP). In this study, we examined the neurochemical basis of these individual differences by examining the same subjects' responses to both EtOH and AMP. A positive correlation between subjects' responses to the two drugs may suggest that AMP and EtOH produce their stimulant-like subjective effects by a shared mechanism. Methods: Twenty-seven volunteers (17 male, 10 female), aged 21,35, received beverages or capsules containing EtOH 0.8 g/kg, AMP 10 or 20 mg, or placebo on four separate sessions in random order and under double-blind conditions. Various self-reported and objective drug effects were measured, including measures sensitive to subjective and cognitive stimulant-like effects. Results: EtOH and AMP produced their prototypical subjective and behavioral effects, including increased ratings of stimulant-like subjective effects, increased heart rate and blood pressure, and improved vigilance performance after AMP and increased ratings of sedative-like subjective effects, increased heart rate and blood pressure, and impaired vigilance performance after EtOH. Consistent with previous reports, there was substantial intersubject variability in subjective responses to EtOH: some subjects reported primarily stimulant-like effects, whereas others reported primarily sedative-like effects. To examine the relationship between these responses to EtOH and subjects' responses to AMP, correlations were examined between effects of EtOH and AMP. For all subjects together, there was a significant positive correlation between responses to EtOH and 20 mg AMP on the ARCI A scale (a measure of stimulant-like subjective effects;r= 0.41, p < 0.05). Among only those subjects who reported primarily stimulant-like effects from EtOH, the correlation between EtOH and AMP was 0.64 (p < 0.05). Conclusions: Subjects who experience pronounced stimulant-like effects from EtOH also report greater stimulant effects from AMP, suggesting that these effects may be mediated through similar mechanisms. These correlations between the drugs' effects were not observed on other measures, such as DSST or vigilance task performance or heart rate. This may indicate that these other effects are mediated by separate mechanisms. The study illustrates a novel approach to studying the neurochemical basis of drug effects. [source] The peri-microvascular edema in hippocampal CA1 area in a rat model of sepsisNEUROPATHOLOGY, Issue 3 2007Ilker Mustafa Kafa Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham-operated and not operated control groups. Significantly more peri-microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri-microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham-operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics. [source] Physiological and behavioral effects of social introduction on adult male rhesus macaquesAMERICAN JOURNAL OF PRIMATOLOGY, Issue 6 2008Lara A. Doyle Abstract Pair housing of laboratory macaques is widely considered to lead to positive changes in well-being, yet the process of introduction is viewed as potentially stressful and risk-prone. Behavioral and physiological data were collected on eight adult male rhesus macaques before, during, and after the process of introduction, in order to measure the initial stress of introduction as well as long-term changes in well-being. Socially experienced subjects, all implanted with biotelemetry devices, were studied in five successive phases: baseline (singly housed), 1 day each of protected contact and full contact introduction, post-introduction (1,3 weeks after introduction), and settled pairs (,20 weeks after introduction). One hundred and seventy-six hours of behavioral data and 672,hr of heart rate data were analyzed. Fecal cortisol was also measured for the baseline, post-introduction, and settled pair phases. All introductions were successful and subjects showed no physiological or behavioral signs of stress, such as increased heart rate, abnormal behavior, or psychological indices of distress (depressive/anxiety-related behavior). Agonism was minimal throughout the introduction process and over the subsequent months; only one wound was incurred over the course of the study. Levels of abnormal behaviors, psychological indices of distress, locomotion, inactivity, and affiliation showed improvements within several weeks after introduction; these changes were still present 5,9 months later for the latter two categories. Heart rates during introduction fell significantly in the settled pair phase, and also varied predictably with time of day. Fecal cortisol levels were lower in settled pairs than in single housing. The fact that reductions in abnormal behavior did not persist over the long term may have been confounded by increasing duration of time spent caged. The results of this study may be of practical use for designing and monitoring social introductions and suggest that managers should not dismiss the feasibility of successful pairing of adult male rhesus macaques. Am. J. Primatol. 70:542,550, 2008. © 2008 Wiley-Liss, Inc. [source] Hemodynamic Changes in a Model of Chronic Heart Failure Induced by Multiple Sequential Coronary Microembolization in SheepARTIFICIAL ORGANS, Issue 11 2009Jan Dieter Schmitto Abstract Although a large variety of animal models for acute ischemia and acute heart failure exist, valuable models for studies on the effect of ventricular assist devices in chronic heart failure are scarce. We established a stable and reproducible animal model of chronic heart failure in sheep and aimed to investigate the hemodynamic changes of this animal model of chronic heart failure in sheep. In five sheep (n = 5, 77 ± 2 kg), chronic heart failure was induced under flouroscopic guidance by multiple sequential microembolization through bolus injection of polysterol microspheres (90 µm, n = 25.000) into the left main coronary artery. Coronary microembolization (CME) was repeated up to three times in 2 to 3-week intervals until animals started to develop stable signs of heart failure. During each operation, hemodynamic monitoring was performed through implantation of central venous catheter (central venous pressure [CVP]), arterial pressure line (mean arterial pressure [MAP]), implantation of a right heart catheter {Swan-Ganz catheter (mean pulmonary arterial pressure [PAPmean])}, pulmonary capillary wedge pressure (PCWP), and cardiac output [CO]) as well as pre- and postoperative clinical investigations. All animals were followed for 3 months after first microembolization and then sacrificed for histological examination. All animals developed clinical signs of heart failure as indicated by increased heart rate (HR) at rest (68 ± 4 bpm [base] to 93 ± 5 bpm [3 mo][P < 0.05]), increased respiratory rate (RR) at rest (28 ± 5 [base] to 38 ± 7 [3 mo][P < 0.05]), and increased body weight 77 ± 2 kg to 81 ± 2 kg (P < 0.05) due to pleural effusion, peripheral edema, and ascites. Hemodynamic signs of heart failure were revealed as indicated by increase of HR, RR, CVP, PAP, and PCWP as well as a decrease of CO, stroke volume, and MAP 3 months after the first CME. Multiple sequential intracoronary microembolization can effectively induce myocardial dysfunction with clinical and hemodynamic signs of chronic ischemic cardiomyopathy. The present model may be suitable in experimental work on heart failure and left ventricular assist devices, for example, for studying the impact of mechanical unloading, mechanisms of recovery, and reverse remodeling. [source] Central Bromocriptine-Induced Tachycardia is Reversed to Bradycardia in Conscious, Deoxycorticosterone Acetate-Salt Hypertensive RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2001Saad Lahlou The present study investigated the effect of bromocriptine on heart rate and the principal site of action of this agonist in conscious, deoxycorticosterone acetate-salt hypertensive rats, in which altered central dopaminergic activity has been previously reported. Intravenous administration of bromocriptine (150 ,g/kg) increased heart rate (49±5 beats/min.) in uninephrectomized control rats, while it induced a significant bradycardia (50±6 beats/min.) in deoxycorticosterone acetate-salt hypertensive rats. In the latter animals, intravenous (500 ,g/kg) or intrathecal (40 ,g/rat at T9,T10) pretreatment with domperidone, a selective dopamine D2 receptor antagonist that does not cross the blood-brain barrier, reduced partially, but significantly, the bradycardiac responses to bromocriptine (reduction of about 44% and 48% of the maximal effect, respectively). In contrast, the bromocriptine-induced bradycardia was fully abolished by intravenous pretreatment with metoclopramide (300 ,g/kg), a dopamine D2 receptor antagonist that crosses the blood-brain barrier, or by combined pretreatment with intravenous and intrathecal domperidone. These results indicate that, in deoxycorticosterone acetate-salt hypertensive rats, bromocriptine decreases rather than increases heart rate, an effect that is mediated partly through a peripheral D2 dopaminergic mechanism and partly through stimulation of spinal dopamine D2 receptors. They further support the concept that, in normotensive, conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at both peripheral and spinal dopamine D2 receptors. [source] | ||||||||||