Time-course effects of aerobic exercise training on cardiovascular and renal parameters in 2K1C renovascular hypertensive rats

Exercise training (Ex) has been recommended for its beneficial effects in hypertensive states. The present study evaluated the time-course effects of Ex without workload on mean arterial pressure (MAP), reflex bradycardia, cardiac and renal histology, and oxidative stress in two-kidney, one-clip (2K1C) hypertensive rats. Male Fischer rats (10 weeks old; 150–180 g) underwent surgery (2K1C or SHAM) and were subsequently divided into a sedentary (SED) group and Ex group (swimming 1 h/day, 5 days/week for 2, 4, 6, 8, or 10 weeks). Until week 4, Ex decreased MAP, increased reflex bradycardia, prevented concentric hypertrophy, reduced collagen deposition in the myocardium and kidneys, decreased the level of thiobarbituric acid-reactive substances (TBARS) in the left ventricle, and increased the catalase (CAT) activity in the left ventricle and both kidneys. From week 6 to week 10, however, MAP and reflex bradycardia in 2K1C Ex rats became similar to those in 2K1C SED rats. Ex effectively reduced heart rate and prevented collagen deposition in the heart and both kidneys up to week 10, and restored the level of TBARS in the left ventricle and clipped kidney and the CAT activity in both kidneys until week 8. Ex without workload for 10 weeks in 2K1C rats provided distinct beneficial effects. The early effects of Ex on cardiovascular function included reversing MAP and reflex bradycardia. The later effects of Ex included preventing structural alterations in the heart and kidney by decreasing oxidative stress and reducing injuries in these organs during hypertension.

The role of DcR3 in systemic lupus erythematosus and islet β-Cell viability and function

Le récepteur DcR3 (Decoy receptor 3) est un membre de la famille des récepteurs aux facteurs de nécrose tumorale (TNF). Il est fortement exprimé dans les tissus humains normaux ainsi que les tumeurs malignes. DcR3 est un récepteur pour trois ligands de la famille du TNF tels que FasL, LIGHT et TL1A. Étant une protéine soluble donc dépourvue de la portion transmembranaire et intracytoplasmique, le récepteur DcR3 est incapable d’effectuer une transduction de signal intracellulaire à la suite de son interaction avec ses ligands. De ce fait, DcR3 joue un rôle de compétiteur pour ces derniers, afin d’inhiber la signalisation via leurs récepteurs fonctionnels tels que Fas, HVEM/LTbetaR et DR3. Lors de nos précédentes études, nous avons pu démontrer, que DcR3 pouvaist moduler la fonction des cellules immunitaires, et aussi protéger la viabilité des îlots de Langerhans. À la suite de ces résultats, nous avons généré des souris DcR3 transgéniques (Tg) en utilisant le promoteur du gène β-actine humaine afin d’étudier plus amplement la fonction de ce récepteur. Les souris Tg DcR3 ont finalement développé le syndrome lupus-like (SLE) seulement après l’âge de 6 mois. Ces souris présentent une variété d'auto-anticorps comprenant des anticorps anti-noyaux et anti-ADN. Elles ont également manifesté des lésions rénales, cutanées, hépatiques et hématopoïétiques. Contrairement aux modèles de lupus murin lpr et gld, les souris DcR3 sont plus proche du SLE humain en terme de réponse immunitaire de type Th2 et de production d'anticorps d'anti-Sm. En péus, nous avons constaté que les cellules hématopoïétiques produisant DcR3 sont suffisantes pour causer ces pathologies. DcR3 peut agir en perturbant l’homéostasie des cellules T pour interférer avec la tolérance périphérique, et ainsi induire l'autoimmunité. Chez l'humain, nous avons détecté dans le sérum de patients SLE des niveaux élevés de la protéine DcR3. Chez certains patients, comme chez la souris, ces niveaux sont liés directement aux titres élevés d’IgE. Par conséquent, DcR3 peut représenter un facteur pathogénique important du SLE humain. L’étude des souris Tg DcR3, nous a permis aussi d’élucider le mécanisme de protection des îlots de Langerhans. Le blocage de la signalisation des ligands LIGHT et TL1A par DcR3 est impliqué dans une telle protection. D'ailleurs, nous avons identifié par ARN microarray quelques molécules en aval de cette interaction, qui peuvent jouer un rôle dans le mécanisme d’action. Nous avons par la suite confirmé que Adcyap1 et Bank1 joue un rôle critique dans la protection des îlots de Langerhans médiée par DcR3. Notre étude a ainsi élucidé le lien qui existe entre la signalisation apoptotique médiée par Fas/FasL et la pathogénèse du SLE humain. Donc, malgré l’absence de mutations génétiques sur Fas et FasL dans le cas de cette pathologie, DcR3 est capable de beoquer cette signalisation et provoquer le SLE chez l’humain. Ainsi, DcR3 peut simultanément interférer avec la signalisation des ligands LIGHT et TL1A et causer un phénotype plus complexe que les phénotypes résultant de la mutation de Fas ou de FasL chez certains patients. DcR3 peut également être utilisé comme paramètre diagnostique potentiel pour le SLE. Les découvertes du mécanisme de protection des îlots de Langerhans par DcR3 ouvrent la porte vers de nouveaux horizons afin d'explorer de nouvelles cibles thérapeutiques pour protéger la greffe d'îlots.

Evaluation of mitochondrial function in a model of developmental programming of hypertension associated with transient neonatal oxygen exposure

UNE EXPOSITION NÉONATALE À L’OXYGÈNE MÈNE À DES MODIFICATIONS DE LA FONCTION MITOCHONDRIALE CHEZ LE RAT ADULTE Introduction: L’exposition à l’oxygène (O2) des ratons nouveau-nés a des conséquences à l’âge adulte dont une hypertension artérielle (HTA), une dysfonction vasculaire, une néphropénie et des indices de stress oxydant. En considérant que les reins sont encore en développement actif lors des premiers jours après la naissance chez les rats, jouent un rôle clé dans le développement de l’hypertension et qu’une dysfonction mitochondriale est associé à une augmentation du stress oxydant, nous postulons que les conditions délétères néonatales peuvent avoir un impact significatif au niveau rénal sur la modulation de l’expression de protéines clés du fonctionnement mitochondrial et une production mitochondriale excessive d’espèces réactives de l’ O2. Méthodes: Des ratons Sprague-Dawley sont exposés à 80% d’O2 (H) ou 21% O2 (Ctrl) du 3e au 10e jr de vie. En considérant que plusieurs organes des rats sont encore en développement actif à la naissance, ces rongeurs sont un modèle reconnu pour étudier les complications d’une hyperoxie néonatale, comme celles liées à une naissance prématurée chez l’homme. À 4 et à 16 semaines, les reins sont prélevés et les mitochondries sont extraites suivant une méthode d’extraction standard, avec un tampon contenant du sucrose 0.32 M et différentes centrifugations. L’expression des protéines mitochondriales a été mesurée par Western blot, tandis que la production d’ H202 et les activités des enzymes clés du cycle de Krebs ont été évaluées par spectrophotométrie. Les résultats sont exprimés par la moyenne ± SD. Résultats: Les rats mâles H de 16 semaines (n=6) présentent une activité de citrate synthase (considéré standard interne de l’expression protéique et de l’abondance mitochondriales) augmentée (12.4 ± 8.4 vs 4.1 ± 0.5 μmole/mL/min), une diminution de l’activité d’aconitase (enzyme sensible au redox mitochondrial) (0.11 ± 0.05 vs 0.20 ± 0.04 μmoles/min/mg mitochondrie), ainsi qu’une augmentation dans la production de H202 (7.0 ± 1.3 vs 5.4 ± 0.8 ρmoles/mg protéines mitochondriales) comparativement au groupe Ctrl (n=6 mâles et 4 femelles). Le groupe H (vs Ctrl) présente également une diminution dans l’expression de peroxiredoxin-3 (Prx3) (H 0.61±0.06 vs. Ctrl 0.78±0.02 unité relative, -23%; p<0.05), une protéine impliquée dans l’élimination d’ H202, de l’expression du cytochrome C oxidase (Complexe IV) (H 1.02±0.04 vs. Ctrl 1.20±0.02 unité relative, -15%; p<0.05), une protéine de la chaine de respiration mitochondriale, tandis que l’expression de la protéine de découplage (uncoupling protein)-2 (UCP2), impliquée dans la dispersion du gradient proton, est significativement augmentée (H 1.05±0.02 vs. Ctrl 0.90±0.03 unité relative, +17%; p<0.05). Les femelles H (n=6) (vs Ctrl, n=6) de 16 semaines démontrent une augmentation significative de l’activité de l’aconitase (0.33±0.03 vs 0.17±0.02 μmoles/min/mg mitochondrie), de l’expression de l’ATP synthase sous unité β (H 0.73±0.02 vs. Ctrl 0.59±0.02 unité relative, +25%; p<0.05) et de l’expression de MnSOD (H 0.89±0.02 vs. Ctrl 0.74±0.03 unité relative, +20%; p<0.05) (superoxide dismutase mitochondriale, important antioxidant), tandis que l’expression de Prx3 est significativement réduite (H 1.1±0.07 vs. Ctrl 0.85±0.01 unité relative, -24%; p<0.05). À 4 semaines, les mâles H (vs Ctrl) présentent une augmentation significative de l’expression de Prx3 (H 0.72±0.03 vs. Ctrl 0.56±0.04 unité relative, +31%; p<0.05) et les femelles présentent une augmentation significative de l’expression d’UCP2 (H 1.22±0.05 vs. Ctrl 1.03±0.04 unité relative, +18%; p<0.05) et de l’expression de MnSOD (H 1.36±0.01 vs. 1.19±0.06 unité relative, +14%; p<0.05). Conclusions: Une exposition néonatale à l’O2 chez le rat adulte mène à des indices de dysfonction mitochondriale dans les reins adultes, associée à une augmentation dans la production d’espèces réactives de l’oxygène, suggérant que ces modifications mitochondriales pourraient jouer un rôle dans l’hypertension artérielle et d’un stress oxydant, et par conséquent, être un facteur possible dans la progression vers des maladies cardiovasculaires. Mots-clés: Mitochondries, Reins, Hypertension, Oxygène, Stress Oxydant, Programmation

Prevalencia de enfermedad de Fabry en pacientes en lista de trasplante y posttrasplante renal en fundación cardioinfantil Bogotá

Introducción: La Enfermedad de Fabry (EF), es una enfermedad multisistémica de almacenamiento lisosomal ligada al cromosoma X que afecta principalmente a hombres, pero también puede causar significativa morbilidad en las mujeres heterocigotas (1–5). La deficiencia de la enzyma α-galactosidaseA (α-Gal A,) provoca acumulación de glicosfingolipidos que afectan diferentes tipos celulares entre ellos el endotelio vascular en vasos de pequeño calibre, células epiteliales y Músculo liso en el sistema cardiovascular (cardiomiocitos), sistema nervioso y células epiteliales tubulares del riñón (6,7). Complicaciones como la falla renal es la causa de muerte más frecuente en la EF (7,8). La incidencia se ha calculado en 1 de cada 117.000 nacidos vivos. (9). Objetivos: Determinar la prevalencia de la Enfermedad de Fabry en pacientes con Insuficiencia renal terminal que se encuentren en lista de trasplante y Post-trasplante Renal en Fundación Cardioinfantil Bogotá. Materiales y Métodos: Se realizó un estudio observacional en donde se evaluó la prevalencia de la EF en todos los sujetos mayores de 18 años que se encuentren en lista de trasplante y post-trasplante renal. Resultados: La prevalencia de Enfermedad de Fabry en 98 pacientes con enfermedad renal crónica fue de 7.1% para la muestra general y 12.9% para la muestra con etiología idiopática Conclusiones: La Enfermedad de Fabry es una importante casusa de Enfermedad Renal Crónica Terminal principalmente en el grupo de etiología idiopática. Palabras Clave: Enfermedad de Fabry (FA)

Pulsioximetría de pacientes en hemodiálisis, de la unidad de terapia renal – fundación cardioinfantil, análisis para establecer recomendaciones

Introducción. En Colombia, el 80% de los pacientes con enfermedad renal crónica en hemodiálisis tienen fístula arteriovenosa periférica (FAV) que asegura el flujo de sangre durante la hemodiálisis (1), la variabilidad en el flujo de sangre en el brazo de la FAV hacia la parte distal, puede afectar la lectura de la oximetría de pulso (SpO2) (2), llevando a la toma de decisiones equivocadas por el personal de salud. El objetivo de este estudio es aclarar si existe diferencia entre la SpO2 del brazo de la FAV y el brazo contralateral. Materiales y métodos. Se realizó un estudio de correlación entre los valores de SpO2 del brazo con FAV contra el brazo sin FAV, de 40 pacientes que asistieron a hemodiálisis. La recolección de los datos se llevó a cabo, con un formato que incluyó el resultado de la pulsioximetria y variables asociadas, antes, durante y después de la hemodiálisis. Se comparó la mediana de los deltas de las diferencias con pruebas estadísticas T Student – Mann Whitney, aceptando un valor significativo de p < 0,05. Resultados. No se encontraron diferencias estadísticamente significativas de la SpO2 entre el brazo con FAV y el brazo sin FAV, antes, durante y después de la diálisis, sin embargo si se apreció una correlación positiva estadísticamente significativa. Conclusiones. Se encontró correlación positiva estadísticamente significativa, donde no hubo diferencias en el resultado la pulsioximetría entre el brazo con FAV y brazo sin FAV, por lo tanto es válido tomar la pulsioximetría en cualquiera de los brazos.

Functional analysis of a novel missense NBC1 mutation and of other mutations causing proximal renal tubular acidosis

Mutations in the Na+-HCO3- cotransporter NBC1 cause severe proximal tubular acidosis (pRTA) associated with ocular abnormalities. Recent studies have suggested that at least some NBC1 mutants show abnormal trafficking in the polarized cells. This study identified a new homozygous NBC1 mutation (G486R) in a patient with severe pRTA. Functional analysis in Xenopus oocytes failed to detect the G486R activity due to poor surface expression. In ECV304 cells, however, G486R showed the efficient membrane expression, and its transport activity corresponded to approximately 50% of wild-type (WT) activity. In Madin-Darby canine kidney (MDCK) cells, G486R was predominantly expressed in the basolateral membrane domain as observed for WT. Among the previously identified NBC1 mutants that showed poor surface expression in oocytes, T485S showed the predominant basolateral expression in MDCK cells. On the other hand, L522P was exclusively retained in the cytoplasm in ECV304 and MDCK cells, and functional analysis in ECV304 cells failed to detect its transport activity. These results indicate that G486R, like T485S, is a partial loss of function mutation without major trafficking abnormalities, while L522P causes the clinical phenotypes mainly through its inability to reach the plasma membranes. Multiple experimental approaches would be required to elucidate potential disease mechanism by NBC1 mutations.

Dipeptidyl peptidase IV inhibition downregulates Na(+)-H(+) exchanger NHE3 in rat renal proximal tubule

In the microvillar microdomain of the kidney brush border, sodium hydrogen exchanger type 3 (NHE3) exists in physical complexes with the serine protease dipeptidyl peptidase IV (DPPIV). The purpose of this study was to explore the functional relationship between NHE3 and DPPIV in the intact proximal tubule in vivo. To this end, male Wistar rats were treated with an injection of the reversible DPPIV inhibitor Lys [Z(NO(2))]-pyrrolidide (I40; 60 mg center dot kg(-1)center dot day(-1) ip) for 7 days. Rats injected with equal amounts of the noninhibitory compound Lys[ Z(NO(2))]-OH served as controls. Na(+) -H(+) exchange activity in isolated microvillar membrane vesicles was 45 +/- 5% decreased in rats treated with I40. Membrane fractionation studies using isopycnic centrifugation revealed that I40 provoked redistribution of NHE3 along with a small fraction of DPPIV from the apical enriched microvillar membranes to the intermicrovillar microdomain of the brush border. I40 significantly increased urine output ( 67 +/- 9%; P < 0.01), fractional sodium excretion ( 63 +/- 7%; P < 0.01), as well as lithium clearance ( 81 +/- 9%; P < 0.01), an index of end-proximal tubule delivery. Although not significant, a tendency toward decreased blood pressure and plasma pH/HCO(3)(-) was noted in I40-treated rats. These findings indicate that inhibition of DPPIV catalytic activity is associated with inhibition of NHE3-mediated NaHCO(3) reabsorption in rat renal proximal tubule. Inhibition of apical Na(+) -H(+) exchange is due to reduced abundance of NHE3 protein in the microvillar microdomain of the kidney brush border. Moreover, this study demonstrates a physiologically significant interaction between NHE3 and DPPIV in the intact proximal tubule in vivo.

Effect of sildenafil in renal ischemia/reperfusion injury in rats

To evaluate the effect of sildenafil, administered prior to renal ischemia/reperfusion (I/R), by scintigraphy and histopathological evaluation in rats. Methods: Twenty-four rats were divided randomly into two groups. They received 0.1 ml of 99mTechnetium-etilenodicisteine intravenous, and a baseline (initial) renal scintigraphy was performed. The rats underwent 60 minutes of ischemia by left renal artery clamping. The right kidney was not manipulated. The sildenafil group (n=12) received orally 1 mg/kg of sildenafil suspension 60 minutes before ischemia. Treatment with saline 0.9% in the control group (n=12). Half of the rats was assessed after 24 hours and half after seven days I/R, with new renal scintigraphy to study differential function. After euthanasia, kidneys were removed and subjected to histopathological examination. For statistical evaluation, Student t and Mann-Whitney tests were used. Results: In the control group rats, the left kidneys had significant functional deficit, seven days after I/R, whose scintigraphic pattern was consistent with acute tubular necrosis, compared with the initial scintigraphy (p<0.05). Sildenafil treatment resulted in better differential function of the left kidneys 24h after reperfusion, compared with controls. Histopathologically, the left kidney of control rats (24 hours after I/R) showed a higher degree of cellular necrosis when compared with the sildenafil treated rats (p<0.05). Conclusion: Sildenafil had a protective effect in rat kidneys subjected to normothermic I/R, demonstrated by scintigraphy and histomorphometry

Repair of lamellar scleral lesions in dogs with preserved equine renal capsule: short report

OBJETIVO: Avaliar o uso da cápsula renal de eqüino preservada em glicerina 98% no reparo de lesões lamelares esclerais em cães. MÉTODOS: Foram utilizados 12 cães, machos e fêmeas, com peso médio de 12kg. Foram realizadas avaliações clínica e morfológica aos 1, 3, 7, 15, 30 e 60 dias de pós-operatório. Após anestesia geral e procedimentos padrões de preparo do campo operatório, foi realizada cantotomia temporal, seguida de incisão conjutival e escleral com área de 0,5x0,5 cm na posição de 1hora, próxima ao limbo. em seguida, um fragmento de mesma dimensão de cápsula renal de eqüino preservada em glicerina, previamente hidratado em solução salina, foi aplicado ao defeito escleral criado sendo fixado com pontos simples isolados com vicryl 7-0®. RESULTADOS: A avaliação clínica revelou blefaroespasmo/fotofobia até o sétimo dia de pós-operatório. Foi observado edema conjuntival até o quinto dia, acompanhado de secreção ocular mucóide, que persistiu até o décimo dia de pós-operatório. Não foram observados sinais clínicos de rejeição do enxerto em todos os animais, em todos os períodos avaliados. Os segmentos anterior e posterior do bulbo ocular não apresentaram sinais de inflamação. A análise morfológica revelou exsudação inflamatória aguda nos períodos precoces e intermediários da avaliação e inflamação crônica nos períodos tardios da observação. Houve incorporação do enxerto ao leito receptor. CONCLUSÃO: Os resultados sugerem que a cápsula renal de eqüino preservada pode ser mais uma alternativa de membrana biológica para o reparo de lesões esclerais lamelares em cães e no homem.

Iatrogenic keratoconjunctivitis sicca in a dog

Anormalidades quali-quantitativas em componentes primários da lágrima podem alterar a dinâmica do filme lacrimal, comprometendo sua função. O filme lacrimal é composto por lipídios, uma fração aquosa e por mucoproteínas. A ceratoconjuntivite seca (CCS) é uma enfermidade freqüentemente diagnosticada em cães, caracterizada pela deficiência da fração aquosa do filme lacrimal, resultando em dessecação e inflamação da conjuntiva e córnea, dor, doença corneana progressiva e redução da visão. Devido à contribuição significativa da glândula da terceira pálpebra na produção da porção aquosa do filme lacrimal, a remoção desta glândula, quando prolapsada, constitui-se em importante causa de CCS iatrogênica. Este trabalho relata um caso clínico de ceratoconjuntivite seca iatrogênica, em um cão da raça Boston Terrier de 10 meses de idade, causada pela remoção cirúrgica da glândula lacrimal da terceira pálpebra, quando esta encontrava-se prolapsada.

Doença renal medular cística em uma cadela Yorkshire Terrier: relato de caso

Uma cadela da raça Yorkshire Terrier apresentou hematêmese, distensão abdominal, poliúria e polidipsia. Após o exame clínico do paciente, estabeleceu-se a suspeita clínica de nefropatia. Os resultados dos exames laboratoriais revelaram anemia normocítica normocrômica e concentrações séricas de uréia (306mg/dl) e de creatinina (3,6mg/dl) acima dos valores de referência. Ao ultra-som bidimensional observaram-se áreas císticas hipoecóicas e anecóicas, padrão renal hipercogênico e perda da relação corticomedular. À necropsia, a região medular apresentou grande quantidade de cistos pequenos em meio a tecido conjuntivo fibroso. A lesão tubulointersticial cortical foi a responsável pela insuficiência renal resultante. Firmou-se diagnóstico de nefrite tubulointersticial.

Morphological Features of the Apical Region in the Principal Cells of Mongrel Dog Epididymis

The epithelial principal cells are the predominant cell type of the epididymis. These cells have been shown to be both secretory and endocytic cells. The apical region of the cytoplasm of principal cells in the mongrel dog are located close to the cell apex and tubular lumen, and shown microvilli at the luminal border and present a endocytic apparatus, that consists of coated pits and vesicles, endosomes of varying size, multivesicular bodies, and lysosomes. The endosomes, multivesicular bodies and lysosomes contained the electron-dense patches. These results suggest that principal cells of the epididymis in the dog as possess a highly developed endocytic apparatus play a role in endocytosis. These cells function are similarly to the related in other mammals, in performing endocytosis.

Rat model of depending prostaglandin renal state: Effect of ketoprofen

Introduction .The renal prostaglandins (PGs), vasodilators, preserve kidney function during increased activity of the renin-angiotensin system or renal sympathetic nerves (renal PG-dependent state [RPGD]). Ketoprofen (Ket) inhibits cyclooxygenase and, therefore, the synthesis of PGs. The aim of this study was to determine, in the rat, the action of Ket in the renal histology and function in a RPGD state (stress of anesthesia and hemorrhage). Material and Methods . Twenty male Wistar rats, anesthetized with sodium pentobarbital, were randomly divided into two groups: G1-control ( n = 10) and G2-Ket ( n = 10) submitted to arterial hemorrhage of 30% of volemia (estimated as 6% of body weight) three times (10% each 10 min), 65 min after anesthesia. G2 animals received Ket, 1.5 mg. kg -1 , venously, 5 min after anesthesia and 60 min before the first hemorrhage moment (first moment of the study [M1]). Medium arterial pressure (MAP), rectal temperature (T), and heart rate were monitored. G1 and G2 received para-aminohippurate sodium (PAH) and iothalamate sodium (IOT) solutions during the entire experimental time in order to determine clearance of PAH (effective renal plasma flow [ERPF]) and clearance of IOT (glomerular filtration rate [GFR]) without urine collection (determination of blood concentrations of PAH and IOT through the high-performance liquid chromatography), filtration fraction (FF), and renal vascular resistance (RVR). The animals were sacrificed in M3, 30 min after the third hemorrhage (M2) moment, and the kidneys and blood collected during the hemorrhage periods were utilized for histological study and determinations of hematocrit (Ht), serum creatinine (S Cr ), ERPF, GFR, FF, and RVR, respectively. Results . There were significant reductions of MAP, T, and Ht and a significant increase of S Cr . During the experiment, ERPF and GFR did not change, but ERPF was always higher in G1 than in G2. Ket did not alter FF, which increased in G1 over the duration of experiment. The Ket group had significantly higher RVR than the control group. The histology verified that both G1 and G2 were similar for tubular dilation and necrosis, but they were significantly different for tubular degeneration: G1 > G2. Conclusion . The changes observed in kidney histology probably were determined by hemorrhage and hypotension. Ket inhibited the synthesis of PGs and diminished tubular degeneration.

A study of the effect of hemorrhage on the cardiorespiratory actions of halothane, isoflurane and sevoflurane in the dog

Objective To compare the cardiorespiratory changes induced by equipotent concentrations of halothane (HAL), isoflurane (ISO) and sevollurane (SEVO) before and after hemorrhage.Study design. Prospective, randomized clinical trial.Animals. Twenty-four healthy adult dogs weighing 15.4 +/- 3.4 kg (mean +/- SD).Methods. Animals were randomly allocated to one of three groups (n = 8 per group). In each group, anesthesia was maintained with 1.5 minimum alveolar concentration of HAL (1.3%), ISO (1.9%,) and SEVO (3.5%) in oxygen. Controlled ventilation was performed to maintain eucapnia. Cardiorespiratory variables were evaluated at baseline (between 60 and 90 minutes after induction), immediately after and 30 minutes after the withdrawal of 32 mL kg(-1) of blood (400% of the estimated blood volume) over a 30-minute period.Results. During baseline conditions, ISO and SEVO resulted in higher cardiac index (CI) than HAL. Heart rates were higher with SEVO at baseline. while mean arterial pressure (MAP) and mean pulmonary arterial pressure did not differ between groups. Although heart rate values were higher for ISO and SEVO after hemorrhage, only ISO resulted in a higher CI when compared with HAL. In ISO-anesthetized dogs, MAP was higher immediately after hemorrhage, and this was related to better maintenance of CI and to an increase in systemic vascular resistance index from baseline.Conclusions. Although the hemodynamic responses of ISO and SEVO are similar in normovolaemic dogs, ISO results in better maintenance of circulatory function during the early period following a massive blood loss. Clinical relevance Inhaled anesthetics should be used judiciously in animals presented with blood loss. However, if an inhalational agent is to be used under these circumstances, ISO may provide better hemodynamic stability than SEVO or HAL.

Efeitos do halotano, isoflurano e sevoflurano nas respostas cardiovasculares ao pinçamento aórtico infra-renal: estudo experimental em cães

JUSTIFICATIVA E OBJETIVOS: O pinçamento infra-renal da aorta abdominal pode produzir alterações hemodinâmicas. O objetivo do estudo foi avaliar os efeitos do halotano, isoflurano e sevoflurano sobre a função cardiovascular, em cães submetidos à pinçamento aórtico infra-renal. MÉTODO: O estudo aleatório foi realizado em 30 cães, distribuídos em três grupos, de acordo com o anestésico halogenado utilizado durante a anestesia, em concentrações equipotentes de 0,75 CAM: GH (n=10) - halotano a 0,67%; GI (n=10) - isoflurano a 0,96%; e GS (n=10) - sevoflurano a 1,8%. em todos os animais foi realizada ligadura infra-renal da aorta, por período de 30 min. Os atributos hemodinâmicos foram estudados nos momentos: C (Controle), Ao15 e Ao30, respectivamente após 15 e 30 minutos do pinçamento aórtico, e DAo e DAo15, respectivamente, imediatamente e após 15 min do despinçamento aórtico. RESULTADOS: Durante o pinçamento aórtico houve, em todos os grupos, aumento das pressões arterial média e do átrio direito, e dos índices cardíaco, sistólico e de trabalho sistólico dos ventrículos direito e esquerdo. A pressão da artéria pulmonar aumentou em GI e GS e a pressão pulmonar ocluída em GH e GI. Após o despinçamento aórtico, houve normalização dos atributos que haviam se elevado, com exceção dos índices cardíaco e sistólico, que continuaram elevados, acompanhados de diminuição do índice de resistência vascular sistêmica. Não houve diferença significante entre os grupos em relação aos atributos estudados, com exceção da freqüência cardíaca que foi sempre menor em GH, em relação aos demais grupos, durante o pinçamento e despinçamento aórtico. CONCLUSÕES: No cão, nas condições experimentais empregadas, a inalação do halotano, isoflurano e sevoflurano em concentrações equipotentes (0,75 CAM) não atenua as respostas cardiovasculares ao pinçamento aórtico infra-renal.