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Objetivou-se a partir deste relato, apresentar e discutir um caso de Carcinoma lobular pleomórfico incipiente em fêmea canina, 12 anos, Poodle, atendida no Hospital de Medicina Veterinária da Universidade Federal da Bahia (UFBA). Para tal, foram ressaltados os dados referentes aos achados clínicos, anatomo-histopatológicos, imuno-histoquí- micos e terapêuticos. O diagnóstico definitivo foi firmado pelo exame histopatológico que revelou células dispostas individualmente, com padrão linear, dispostos em “fila indiana”, ou dispersos no estroma, com células por vezes bizarras e multinucleadas, além de intenso pleomorfismo nuclear e alto índice mitótico. Foi realizada a avaliação imuno-histoquí- mica para melhor caracterização do tumor e auxílio na conduta terapêutica. O tratamento indicado foi a quimioterapia com carboplatina, no entanto houve evolução do quadro clínico e o animal veio a óbito 54 dias após o procedimento cirúrgico. O presente relato descreve pela primeira vez o CLP em cadela no seu estádio inicial, contribuindo para o entendimento do caráter biológico desta neoplasia.

O artigo inicia com uma reflexão acerca da articulação que os relatos de viagens - reais ou imaginárias - podem cumprir junto ao discurso moderno sobre as diversidades e as alteridades. Considera, ainda, os relatos como exercício de poder, na medida em que, segundo Foucault, a força do poder reside na produção de efeitos positivos no nível do desejo e do saber. Para tanto, lembra os cronistas responsáveis pelas primeiras descrições do Novo Mundo, cujos livros de viagens adquiriram autoridade sobre as regiões estrangeiras ao desvelar seus mistérios, como a descrição de costumes, hábitos alimentícios, vestimenta e relações familiares, entre outros, e orientando, assim, os novos viajantes. As narrativas de viagens feitas por mulheres são então introduzidas a partir da especificidade de suas abordagens. Afinal, ao irromper o espaço público, elas necessitam estabelecer uma relação entre o espaço, o conhecimento e a autoridade, e, para validar seus discursos, servem-se da história e da referência às fontes consultadas. Marquesa Calderón de la Barca, Isabel Pesado de Mier, as irmãs Larraínzar, Condessa de Merlín e Nísia Floresta são algumas das escritoras aqui trabalhadas.This article begins with a reflection about the influences of the travel reports - real or imaginary ones - on the modern discourse, diversity, and alterities. It also considers the reports as a power instrument, since, according to Foucault, the force of power resides in the production of positive effects in both knowledge and desire levels. Thus, the chroniclers responsible for the first descriptions of the New World are visited. Their books were very useful to the new travelers by revealing the mystery of the foreign lands, as well as their customs, alimentary habits, dressing ways, and familiar relationships, among others. The narratives written by women are then introduced considering the specificity of their approach. After all, when appearing to the public, they need to establish a relationship between space, knowledge and authority, and, in order to validate their discourse, they make use of history and references to the consulted sources. Marquesa Calderón de la Barca (Life in Mexico during a residence of two years in that country, de 1843); Condessa de Merlín (La Havane, de 1844); and Nísia Floresta (Itinerário de uma viagem à Alemanha, de 1857) are some of the writers analyzed here.

Neste ensaio pretende-se fazer uma aproximação à identidade cultura no Caribe, conceito de difícil definição devido à unidade diversa das culturas que conformam o espaço caribenho. Para esse propósito serão estudados textos narrativos de língua hispânica no contexto de outras narrativas caribenhas para comprovar como o fenômeno da identidade encontra um lugar na representação literária. Palavras-chaves: Identidade. História. Narrativa Caribenha Resumen En este ensayo se pretende una aproximación a la identidad cultural en el Caribe, concepto de difícil definición, debido a la unidad diversa de las culturas que conforman el espacio Caribe. Para ese propósito se estudian textos narrativos de habla hispana, en el contexto de otras narrativas caribeñas, para comprobar cómo el fenómeno de la identidad encuentra un lugar en la representación literaria. Palabras claves: Identidad. Historia,. Narrativa Caribeña Abstract Caribbean cultural identity is a difficult concept to define, due to the diverse unity of the cultures grown in the Caribbean world. This paper tries to explore such a definition through different narrative texts, mainly in Spanish, but also those in other languages spoken in the area, to reach the conclusion that identity finds a way of expressing itself in literary representation. Keywords: Identity. History. Caribbean Narrative

Resumen

This article begins with a reflection about the influences of the travel reports – real or imaginary ones – on the modern discourse, diversity, and alterities. It also considers the reports as a power instrument, since, according to Foucault, the force of power resides in the production of positive effects in both knowledge and desire levels. Thus, the chroniclers responsible for the first descriptions of the New World are visited. Their books were very useful to the new travelers by revealing the mystery of the foreign lands, as well as their customs, alimentary habits, dressing ways, and familiar relationships, among others. The narratives written by women are then introduced considering the specificity of their approach. After all, when appearing to the public, they need to establish a relationship between space, knowledge and authority, and, in order to validate their discourse, they make use of history and references to the consulted sources. Marquesa Calderón de la Barca (Life in Mexico during a residence of two years in that country, de 1843); Condessa de Merlín (La Havane, de 1844); and Nísia Floresta (Itinerário de uma viagem à Alemanha, de 1857) are some of the writers analyzed here.

Se reseñó el libro: House/garden/nation. Space, gender, and etnicity in postcolonial Latin American literatures by women.

Study Objective: To evaluate the effects of angiotensin-converting enzyme (ACE) inhibition on continuous pulse oximetry recordings of arterial oxygen saturation (SpO2)., Design: Open-label study., Setting: Cardiology clinics at two large teaching hospitals., Patients: Eight patients with New York Heart Association Functional Class (NYHA FC) II-III heart failure., Interventions: Patients were studied after an ACE inhibitor washout (baseline, B), and after 3 months following resumption of therapy (ACE)., Measurements and Main Results: Monitoring times for B and ACEI were approximately 22 hours. Reduction trends were observed for number (190 +/- 170 vs 125 +/- 67 B vs ACEI), magnitude (8.2 +/- 1.4% vs 7.5 +/- 1.8%), and duration (2.45 +/- 2.8 vs 1.35 +/- 0.8 min) of desaturations/monitoring period, and for nadir SpO2/desaturation (88.1 +/- 1.5% vs 89.9 +/- 3.3%). The B desaturation index [(cumulative desaturation time/monitoring period time) x 100, a measure of hypoxic stress or burden] decreased from 19.4 +/- 8.1% to 11.9 +/- 8.1% at ACEI (p = 0.024)., Conclusion: Long-term ACE inhibitor therapy improves the profile of SpO2 values over time in patients with NYHA FC II-III heart failure.

Continuous, 24-hour, ambulatory pulse oximetry was used in 10 subjects with New York Heart Association functional class II to III heart failure and in 5 age-matched controls to test the prevailing view that arterial oxygen saturation is preserved during wakefulness in chronic mild to moderate heart failure. Subjects with heart failure were stabilized on digitalis and diuretics at the time of the study. All subjects maintained time-activity logs, with an emphasis on self-reported sleep and wakefulness. A desaturation event was defined as a decrease in arterial oxygen saturation > or = 4% from baseline lasting > 5 seconds. Variables assessed included total desaturation events, decrease in arterial oxygen saturation duration/event, nadir of arterial oxygen saturation/event, and desaturation index ([cumulative desaturation time/total monitoring time] x 100). The ratio of self-reported wakefulness:sleep desaturation time was 47:53% for subjects with heart failure versus 64:36% for controls (p = NS). Mean (+/- SEM) time of arterial oxygen saturation < 90% was 123 +/- 67 minutes for subjects with heart failure versus 22 +/- 25 minutes for controls (p < 0.01). Total desaturations were 220 +/- 63 and 76 +/- 35 (p = NS) for the heart failure and control groups, respectively. The heart failure group had a statistically, significantly greater decrease in arterial oxygen saturation, and a longer duration and deeper nadir of the desaturation event than did the age-matched control group. The desaturation index was 21 +/- 3% and 4 +/- 1% for the heart failure and control groups, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-three patients with severe systemic hypertension defined as a diastolic blood pressure (DBP) > or = 120 mm Hg were randomized in a single-blind fashion to be treated with either intravenous fenoldopam mesylate (FNP) or sodium nitroprusside (NTP). Fenoldopam mesylate and NTP infusion rates began at 0.1 microgram/kg/minute and 0.5 microgram/kg/minute, respectively and were titrated to achieve a goal DBP of between 95 and 110 mm Hg; or a reduction of at least 40 mm Hg if the baseline DBP was > 150 mm Hg. Fenoldopam mesylate (n = 15) reduced blood pressure from 217/145 +/- 6/5 to 187/112 +/- 6/3 mm Hg (P < .001) at an average infusion rate of 0.5 +/- 0.1 microgram/kg/minute. The average time to achieve goal DBP with FNP was 1.5 +/- 1.4 hours. Nitroprusside (n = 18) reduced blood pressure from 210/136 +/- 5/2 to 172/103 +/- 6/2 mm Hg (P < .001) at an average infusion rate of 1.2 +/- .24 micrograms/kg/minute. Nitroprusside response time averaged 2 +/- 2.5 hours. There was no significant difference between the magnitude of effect seen with either FNP or NTP; nor was there any difference observed in the adverse effect rates of the two agents. Fenoldopam mesylate and NTP demonstrate similar overall efficacy in the treatment of severe systemic hypertension.

Study Objective: To determine the acute hemodynamic response of single-dose coadministration of ibopamine plus nifedipine or diltiazem in patients with New York Heart Association functional class (NYHA FC) II-III congestive heart failure., Design: A single-blind, placebo-controlled, two-paired, crossover study., Setting: Cardiology clinics at two large teaching hospitals., Patients: Eight patients with NYHA FC II-III congestive heart failure who met the inclusion criteria were selected randomly., Interventions: All patients underwent right heart catheterization. Day 1 consisted of concomitant calcium channel blocker plus placebo, with cardiac and peripheral hemodynamic recordings from 30 minutes-24 hours. The design was equivalent on day 2, with single-dose administration of ibopamine plus calcium channel blocker., Measurements and Main Results: Single-dose nifedipine-diltiazem augmented cardiac output and stroke volume secondary to decreasing systemic vascular resistance. The nifedipine-ibopamine and diltiazem-ibopamine subgroups demonstrated relatively equal hemodynamics, augmenting cardiac index (nifedipine 43%, p < 0.05; diltiazem 40%, p < 0.05 vs baseline) while decreasing systemic vascular resistance (nifedipine 41%, p < 0.05; diltiazem 28%, p NS vs baseline) 30 minutes after the dose. In contrast to single-dose diltiazem, the diltiazem-ibopamine subgroup exhibited an increased left ventricular filling pressure (122%, p < 0.05 vs baseline) and mean pulmonary artery pressure (43%, p < 0.05 vs baseline) at 30 minutes after the dose. One patient experienced a transient episode of chest pain associated with increased heart rate and blood pressure with diltiazem-ibopamine., Conclusion: Diltiazem and ibopamine should be coadministered with caution in patients with coronary artery disease and left ventricular dysfunction.

Quinapril, a nonsulfhydryl ACE inhibitor, was evaluated in ten New York Heart Association (NYHA) functional class (FC) II-III CHF patients to determine its effects on regional blood flow [effective renal plasma flow (ERPF), renal blood flow (RBF), renal vascular resistance (RVR), hepatic blood flow (HBF), hepatic vascular resistance (HVR), segmental limb pressure (SLP), creatinine clearance (CRCL)] and cardiac function [left ventricular ejection fraction (LVEF)]. Previous vasodilator therapy was withdrawn 2 weeks before baseline measurements. Stable regimens of digoxin and diuretics were continued throughout the study. ERPF was assessed using p-aminohippurate (PAH), HBF by indocyanine green (ICG) clearance, and LVEF by radionuclide scintography. Segmental limb pressures were measured by Doppler flow detection. Measurements were performed at baseline (B) and after 4 weeks of quinapril therapy (10 mg BID). Quinapril increased renal (P less than 0.05) and hepatic blood flow (P = 0.06) and significantly reduced renal and hepatic vascular resistance. Glomerular filtration rate and left ventricular ejection fraction were unchanged. Mean arterial pressure and brachial segmental pressures decreased without change in heart rate. Noninvasive cardiovascular assessments indicate that quinapril improves regional blood flow while exhibiting no change in left ventricular ejection fraction, in patients with NYHA FC II-III CHF.

Physicians have been urged to reduce the use of the pulmonary artery catheter. However, there are no guidelines to help the clinician make the decision to use or withhold invasive monitoring in the individual patient. This study was designed to examine the accuracy of physician estimates of cardiac function in a spectrum of patients with hemodynamic instability to determine whether differences in accuracy among subgroups would suggest subgroups of patients who could be managed without invasive measurements. Physician estimates of cardiac index were found to be sufficiently accurate in patients without acute heart disease that initial management without invasive monitoring may be appropriate in selected cases. However, due to the general inaccuracy of physician estimates, efforts to improve the accuracy of clinical judgments of cardiac function and hemodynamic status should be pursued with vigor in patients both with and without acute cardiac dysfunction.

To determine the maintenance of pharmacodynamic effects of fenoldopam mesylate, a dopamine-1 agonist, the invasive hemodynamic profiles of 33 patients with New York Heart Association functional class III to IV congestive heart failure were examined. Fenoldopam mesylate was initiated at 0.1 micrograms/kg/min and titrated to a cardiac index greater than or equal to 25% above baseline. Upon achievement of optimal hemodynamics, maintenance infusion was begun (mean dose 0.6 micrograms/kg/min). Fenoldopam mesylate (baseline vs maximal effect) decreased systemic vascular resistance by 37% (p less than 0.001), left ventricular filling pressure by 16% (p less than 0.05) and mean arterial pressure by 11% (p less than 0.05), with an associated augmentation in cardiac index and stroke volume index by 27% (p less than 0.001). Attenuation of hemodynamic effect (maximal effect vs time) was noted in cardiac index (14% p less than 0.001), systemic vascular resistance (13% p less than 0.05) and stroke volume index (13% p less than 0.05). None of the parameters exhibited complete attenuation to baseline values. Fenoldopam mesylate improves cardiac output and lowers systemic vascular resistance with relative attenuation of pharmacodynamic effect during a 24-hour intravenous infusion.

Four case reports have been published that document a clinically significant drug interaction between nifedipine and quinidine in patients with left ventricular dysfunction. To define the population at risk and the mechanisms involved in manifestations of this interaction, 12 patients currently treated with quinidine for either ventricular or supraventricular arrhythmias were stratified into two groups based on left ventricular ejection fraction (EF) measurements (group A greater than 35%; group B less than 35%). The interaction was conducted through two phases: oral quinidine (Q) and oral quinidine plus nifedipine (N + Q). Pharmacokinetic modeling of total body clearance (CL) and AUC were assessed for each phase. One patient (group A, 70% EF) exhibited the interaction with a 41% decrease in steady-state serum quinidine concentrations. The patient's AUC and CL were 48.2 micrograms/ml.hr (Q) versus 28.6 micrograms/ml.hr (N + Q) and 94.4 ml/min (Q) versus 159.1 ml/min (N + Q), respectively. There was no difference in AUC or CL between the Q and N + Q phases or between groups A and B for the entire population. The N + Q interaction is not hemodynamically mediated. Clinical consideration of the possibility of this low-frequency interaction should be noted.

The pharmacy and therapeutics committee-based clinical evaluation can be a useful tool in the economic and functional effectiveness of a restrictive formulary system. We utilized this concept to evaluate a generic formulation of procainamide hydrochloride (PA) for admission to our formularies. The study performed was a randomized, single-blind, crossover comparison of the serum-concentration profiles of two preparations (Squibb vs. Ascot) of conventional-release PA. Ten outpatients requiring chronic PA therapy for the control of ventricular dysrhythmias were evaluated. The resultant dose-adjusted data showed no significant difference between mean serum PA concentrations at any sample time, area under the serum concentration-time curves, mean peak serum PA concentrations achieved, or peak-trough fluctuations. Relative bioavailability was calculated to be 0.972 +/- 0.59. The Ascot preparation demonstrated a delay of 15 minutes before the onset of absorption; however, it also showed an earlier tmax in comparison to the Squibb formulation. Generic substitution of Ascot PA in place of Squibb PA may be implemented with significant cost savings.

This prospective study evaluated the ability of continuous SvO2 measurements to predict the onset and duration of action of the oral vasodilator, fenoldopam. Eight patients with New York Heart Association functional class 3 CHF received 100 mg fenoldopam in the fasted state. Serial hemodynamic parameters and SvO2 measurements were obtained at baseline and up to eight hours postdose. Although wide interpatient variability was observed, the SvO2-time response curve produced a similar trend as the CI-time response curve. The SvO2 may be a useful drug monitoring parameter in patients with NYHA class 3 CHF. Seriously ill patients may not have a good CI/SvO2 correlation. This is most likely due to an unstable oxygen consumption rate at the tissue level. Therefore, we recommend establishing the relationship between CI and SvO2 prior to its use as a drug monitoring parameter.

This study evaluates the effects of a standardized meal on cardiovascular hemodynamics in 12 patients with New York Heart Association Class III congestive heart failure. This was done as part of a larger study in which an orally active dopaminergic agonist was given on two mornings, once with a standardized breakfast and once fasting, and one morning a placebo was given with the breakfast. The order of days was randomized. Hemodynamic data were obtained over 8 h each day. There were significant changes in several hemodynamic variables after the placebo-food regimen lasting up to 1.5 h: cardiac index rose from 1.8 +/- 0.4 to 2.2 +/- 0.5 L/min.m2 at 30 min (p less than .001) and to 2.0 +/- 0.5 L/min.m2 at one hour (p less than .05); stroke volume index rose from 20 +/- 7 to 24 +/- 7 ml/min at 30 min (p less than .05) and to 23 +/- 7 ml/min at one hour (p less than .05); systemic vascular resistance fell from 1890 +/- 685 to 1534 +/- 497 dyne.sec/cm5 at 30 min (p less than .001) and to 1668 +/- 524 dyne.sec/cm5 at one hour (p less than .05). Mixed venous oxygen saturation was measured continuously in seven patients and rose significantly at one and 1.5 h. We conclude that food ingestion can have a significant effect on cardiovascular hemodynamics and that this effect should be considered when therapeutic effects are to be guided by invasive hemodynamic monitoring in this population.

The hemodynamic effects of increasing oral doses of nifedipine (10 to 30 mg) were studied in 12 patients who had low output heart failure. With each set of hemodynamics, serum concentrations of nifedipine were measured to determine the concentration/response relationships. Eleven of twelve patients responded acutely to nifedipine, defined as a reduction in systemic vascular resistance (SVR), and an augmentation in cardiac index (CI) and stroke volume index (SVI). The differential dose effects (X +/- SD) for SVR and SVI for baseline (N = 11), 10 mg (N = 10), 20 mg (N = 3) and 30 mg (N = 4) were: 1913 +/- 486, 1102 +/- 221, 1128 +/- 166, 803 +/- 176 and 17.9 +/- 4.8, 23.8 +/- 4.5, 31 +/- 0.42, 33 +/- 3.5, respectively. All nifedipine doses reduced SVR and increased CI and SVI compared with baseline (P less than .001). The increase in CI and SVI was significantly correlated to the mg/kg dose of nifedipine (r = 0.79; P less than .001). Nifedipine administration resulted in no significant change in central venous pressure, pulmonary capillary wedge pressure, or pulmonary vascular resistance. No relationship could be demonstrated between serum concentrations of nifedipine and any hemodynamic effect. Conclusions drawn were: (1) the afterload reduction effects of nifedipine are acutely efficacious in a large portion of patients with heart failure and this activity supercedes the negative inotropic effects of the drug at doses between 10 and 30 mg; (2) the magnitude of the hemodynamic effects are dose dependent.(ABSTRACT TRUNCATED AT 250 WORDS)