IDENTIFICACIÓN DE HELMINTOS EN ZARIGÜEYAS (Didelphis Marsupialis) EN EL SUROCCIDENTE COLOMBIANO / IDENTIFICATION OF HELMINTHES IN OPOSSUMS (Didelphys marsupialis) IN THE COLOMBIAN SOUTHWEST REGION

El presente estudio tiene como objetivo describir e identificar los helmintos presentes en zarigüeyas (D. marsupialis). El estudio se realizó en la vertiente oriental de la cordillera occidental, a las márgenes del río Cali, municipio de Santiago de Cali, departamento de Valle del Cauca, Colombia. Los resultados parasitológicos revelan que las zarigüeyas encontradas presentan un alto porcentaje de parasitismo por helmintos.

The present study aims to describe and identify helminthes in possums (D. marsupialis). The study was conducted on the eastern slope of the Western Cordillera on the bamks of Cali River, in the municipality of Santiago de Cali, Department of Valle del Cauca, Colombia. The parasitological results reveal that opossums found show a high percentage of parasitism by helminthes.

Assessment of right ventricular afterload by pressure waveform analysis in acute pulmonary hypertension.

AIM: To characterize hydraulic right ventricle (RV) afterload by pulmonary arterial pressure waveform analysis in an acute pulmonary hypertension (PH) model. METHODS: Pulmonary artery (PA) flow and pressure were recorded in six anesthetized sheep. Acute isobaric PH was induced by phenylephrine (active) and PA mechanical constriction (passive). We estimated the amplitude of the forward and reflected pressure waves according to the inflection point. In most cases the inflection pressure was smooth, thus the inflection point was defined as the time at which the first derivative of pulmonary arterial pressure reached its first minimum. We calculated the input and characteristic (Z(C), time-domain Li method) impedances, the capacitance index (stroke volume/pulse pressure), the augmentation index (AI) (reflected pressure/pulse pressure), the fractional pulse pressure (pulse pressure/mean pressure) and the wasted energy generated by the RV due to wave reflection during ejection (E(W)). RESULTS: Pulse pressure, fractional pulse pressure, AI and Z(C) increased and capacitance index decreased during passive PH with respect to control (P < 0.05). In contrast, Z(C) and the capacitance index did not change and E(W) and the AI decreased during active PH. Pulse pressure correlated with E(W) and Z(C) and the AI was correlated with E(W) (r > 0.6, P < 0.05). CONCLUSION: PA pressure waveform analysis allows the quantification of the dynamic RV afterload. Prospective clinical studies will be necessary to validate this time-domain approach to evaluate the dynamic RV afterload in chronic PH.

El laboratorio clínico en hematología de aves exóticas / The clinic laboratory in hematology of exotic birds

El empleo de las técnicas de laboratorio en la práctica veterinaria, es una herramienta indispensable que aporta información valiosa en el momento de confirmar un diagnóstico. El hemograma es uno de los estudios de rutina con mayor importancia. Los parámetros normales en el hemograma, pueden ser un indicador del buen estado de salud del animal. Sin embargo, un hemograma normal, no excluye la posibilidad de que el ave sea un portador asintomático de entidades como la psitacosis, enfermedades víricas, o infecciones localizadas. La presente revisión analiza la información relacionada con el papel del laboratorio clínico en la hematología aviar.

The use of laboratory techniques in veterinary practice is an indispensable tool which renders valuable information for the confirmation of a diagnosis. The blood analysis is one of most important routine analysis, since normal parameters can be a good indicator of good animal health. However, a normal blood analysis does not exclude the possibility that a bird is carrying entities such as psittacosis, virus diseases, or localized infections. The present review analyses the information related to the role of the clinical laboratory in bird hematology.

Niveles séricos de tetrayodotironina libre (T4L), mediante el método de electroquimioluminiscencia en caninos / Free tetraiodothyronine (FT4) serum levels by electrochemiluminescence method in canines

El presente estudio establece valores de referencia para niveles séricos de tetrayodotironina libre (T4L) en caninos mediante el método de electroquimioluminiscencia. Se utilizaron 180 caninos que fueron divididos en grupos según la edad y el sexo. Se encontraron diferencias altamente significativas (P<0,0001) relacionadas con la edad, sin encontrarse diferencias significativas con respecto al sexo para dicha hormona. Los resultados de este estudio sugieren que las concentraciones séricas de tetrayodotironina libre (ng/L) en caninos menores de 1año, de 1 a 7 años y mayores de 7 años, oscilan entre 9,90-11,74 ng/L, 8,51-11,74 ng/L y 7,48-8,64 ng/L, respectivamente. La determinación de T4L mediante electroquimioluminiscencia, puede considerarse útil como ayuda diagnóstica de posibles alteraciones tiroideas.

The present study establishes references values for free Tetraiodotironine (FT4) in canines using eletrochemiluminescence method. Blood samples from 180 canines divided in six groups of age (males and females), 30 animals for each group were used. Significant differences (P<0.0001) was found between age groups but not between sex groups. The canine average values for FT4 using this technique were as follow: younger than 1 year of age , 9.9 - 11.7 ng/L; from 1 to 7 years of age, 8.1 - 11.7 ng/L; older than 7 years of age 7.4- 8.6 ng/L. The electrochemiluminiscence method for measuring FT4 is valuable diagnostic tool in canine medicine.

Papel del factor de crecimiento semejante a la insulina (IGF-1) en la regulación de la función ovárica / Role of the insulin-like growth factor (IGF-1) in the ovaric function regulation

Ha sido reportado que numerosos factores de crecimiento y citoquinas suprimen la producción del estradiol por las células de la granulosa in vitro, pero la asociación de la expresión de tales factores in vivo representado en los folículos sanos y su significado fisiológico no son claros. La propuesta de esta revisión es mostrar estudios que soportan la importancia in vivo e in vitro del factor de crecimiento semejante a insulina (IGF-1), un factor de naturaleza peptídica que se origina en las células de la teca y que por diversos mecanismos interviene en las funciones de crecimiento, desarrollo y maduración folicular, así como sus productos en interacción directa con otros factores tipo gonadotropinas, esteroides gonadales y aromatasa en rumiantes, equinos, cerdos y humanos. El IGF-1 juega un importante papel en la foliculogénesis inducida por las gonadotrofinas, en la esteroidogénesis ovárica y en la función del cuerpo lúteo (CL), así como también modula la función pituitaria e hipotalámica. La revisión tambén explora los efectos del status nutricional en las concentraciones circulantes del IGF-1 y el papel endocrino del IGF-1 en el eje reproductivo.

Improved right ventricular-vascular coupling during active pulmonary hypertension.

Right ventricular adaptation to pulmonary hypertension (PH) is an important prognostic factor. Pulmonary artery (PA) smooth muscle activation attenuates arterial dysfunction during acute PH. We investigated the role of the pulmonary artery vascular smooth muscle activation on the right ventricular-vascular coupling during acute PH. PA flow, pressure, and diameter, right ventricular and aortic pressures were recorded in six anesthetized sheep. Acute PH was induced by phenylephrine (APH) and PA mechanical constriction (PPH). We calculated the PA buffering function, the incremental elastic modulus and pulmonary vascular compliance. Pulmonary vascular impedance and right ventricular hydraulic power were calculated through Fourier approach. We also quantified the magnitude and timing of the reflected wave. Right ventricular-vascular coupling was assessed by the energy transmission ratio. Pulmonary buffering function and vascular compliance increased (P<0.05) and arterial wall stiffness decreased (P<0.05) during APH with respect to PPH. Although total input resistance increased and reflected wave came back earlier during PH states (P<0.05), only PPH produced a rightward shift of the pulmonary impedance and a more prominent reflected wave. Accordingly, APH determined a minor increase of total hydraulic power with a smaller pulsatile to total power ratio and energy transmission ratio (P<0.05). In conclusion, isobaric PA vasoconstriction prevents the pulsatile hydraulic load to increase by preserving the PA buffering function and the reflected wave magnitude. Thus, vascular smooth muscle activation of the main PA improves the energy transfer from the right ventricle to the hypertensive pulmonary circulation, and this may play relevant role in the right ventricular adaptation to acute PH.

Comparison of the Tei index with invasive measurements of right ventricular function.

The Doppler-derived Tei index has been reported to be clinically useful in assessing global right ventricular function. It could increase in response to combinations of increased pulmonary artery pressure and/or ventricular dysfunction. We compared the Tei index with invasive measurements of right ventricular function during acute pulmonary hypertension. Right and left ventricular pressures, pulmonary and aortic pressures, pulmonary flow and right ventricular volume by sonomicrometry were measured in six anaesthetized sheep. Graded pulmonary arterial hypertension was induced by a mechanical occlusion maneuver. Pressure-volume loops were generated during preload reduction through caval occlusion. Epicardial echocardiograms were also performed. Invasive indexes including preload recruitable stroke work, ventricular diastolic time constant and stiffness constant, and cardiac output were assessed, as were noninvasive echocardiographic indexes including Tei index and E/A ratio. The right ventricular pressure-volume loop became rectangular, with well-defined isovolumic phases. The slope of preload recruitable stroke work was increased significantly during pulmonary pressure of 30 mm Hg. The ventricular time constant showed a significant increase with no change of chamber stiffness during pulmonary pressure of 35 mm Hg. Concomitantly, the Tei index increased significantly from 0.06+/-0.03 to 0.31+/-0.06, together with the shortening of the ejection time and a decrease of the E/A ratio (P<0.05). Thus, the right ventricular Tei index was noted to be affected by acute graded afterload increase. The alteration in invasive measurements of systolic and diastolic function makes the Tei index a sensitive indicator of right ventricular dysfunction in the settings of acute pulmonary hypertension.

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension.

Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure, and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH: 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH). To evaluate the direct effect of VSM activation, isobaric (PPH vs. APH) and isometric (CTL vs. APPH) analyses were performed. We calculated the local BF from the elastic (EPD) and viscous (etaPD) indexes as etaPD/EPD and the characteristic impedance (ZC) from pressure and flow to evaluate CF as 1/ZC. We also calculated the absolute and normalized cross-sectional pulsatility (PCS and NPCS, respectively), the dynamic compliance (CDYN), the cross-sectional distensibility (DCS), and the pressure-strain elastic modulus (EP). The isobaric analysis showed increase of CF, BF, and etaPD (P < 0.01) and decrease of EPD (P < 0.05) during APH in respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P < 0.01). The isometric analysis showed increase of E(PD) and etaPD (P < 0.01), nonsignificant difference in BF (even in the presence of a significant mean PA pressure rise, from 14 (SD 6) to 25 (SD 8) mmHg, P < 0.01), and decrease in CF (P < 0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF (P < 0.01) and increased EPD (P < 0.05) with regard to their previous steady states (CTL and APH). Nonsignificant differences were found in EPD between PPH and APPH. VSM activation (APH and APPH) increased etaPD (P < 0.01) respect to their previous passive states (CTL and PPH), but no significant differences were found within similar levels of VSM activation. In conclusion, VSM plays a relevant role in main pulmonary artery function during acute pulmonary hypertension, because isobaric vasoconstriction induced by VSM activation improves both BF and CF, mainly due to the increase in etaPD concomitant with the arterial compliance. CDYN and DCS were the more pertinent clinical indexes of arterial elasticity. Additionally, the etaPD-mediated preservation of the BF could be evaluated by the geometric related indexes (PCS and NPCS), which appear to be qualitative markers of arterial wall viscosity status.

[The vascular smooth muscle of great arteries: local control site of arterial buffering function?]. / El músculo liso vascular de las grandes arterias: ¿sitio de control local de la función de amortiguamiento arterial?

INTRODUCTION AND OBJECTIVES: To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function. MATERIAL AND METHOD: Aortic and pulmonary artery pressure and diameter were measured in six anesthetized sheep under baseline conditions, and during arterial hypertension induced by mechanical vascular occlusion (passive), and i.v. phenylephrine (active). Arterial wall elasticity and viscosity were calculated, and buffering function was characterized: a) locally as the viscosity/elasticity ratio, and b) globally for each circuit, as the time-constant of ventricular relaxation. RESULTS: Viscoelasticity was higher in the aorta than in the pulmonary artery (p < 0.05), however, parietal buffering function was similar in both. Global buffering function was highest in the systemic circuit (p < 0.05). During passive hypertension, elasticity was significantly increased with no change in viscosity; this led to a significant reduction in local buffering function, and in global buffering function in each circuit. During active hypertension, viscosity increased (p < 0.05), while local and global buffering functions returned to baseline values. CONCLUSIONS: The viscosity/elasticity ratio was higher in the aorta than in the pulmonary artery, and arterial wall buffering function was similar in both vessels. Systemic global buffering function was higher than pulmonary circuit buffering function. Elasticity depends on intravascular pressure, whereas viscosity is a marker of the degree of smooth muscle activation. Smooth muscle activation may benefit the cardiovascular system by maintaining local and global buffering functions.

El músculo liso vascular de las grandes arterias: ¿sitio de control local de la función de amortiguamiento arterial? / The vascular smooth muscle of great arteries: local control site of arterial buffering function?

Introducción y objetivos. Determinar la viscosidad y elasticidad de las arterias aorta y pulmonar y el efecto de la activación del músculo liso vascular sobre la capacidad de amortiguamiento arterial. Material y método. En 6 ovejas anestesiadas se midieron la presión y el diámetro aórtico y pulmonar, en condiciones basales y de hipertensión: a) pasiva, mediante la oclusión mecánica vascular, y b) activa, mediante fenilefrina intravenosa. Se calcularon la elasticidad y viscosidad parietal y se caracterizó la capacidad de amortiguamiento: a) la parietal, mediante el cociente viscosidad/elasticidad, y b) la global de cada circuito mediante la constante de tiempo de descenso de la presión arterial diastólica. Resultados. La viscoelasticidad aórtica fue mayor que la pulmonar (p < 0,05), mientras que ambas arterias tuvieron un amortiguamiento parietal similar. El circuito sistémico presentó un mayor amortiguamiento global (p < 0,05). Durante la hipertensión pasiva se produjo un aumento significativo de la elasticidad sin cambios en la viscosidad, lo que determinó una reducción significativa del amortiguamiento parietal, mientras que el amortiguamiento global de cada circuito disminuyó significativamente. En la hipertensión activa aumentó la viscosidad (p < 0,05), mientras que el amortiguamiento parietal y global recuperaron los valores basales. Conclusiones. La aorta presentó mayor viscoelasticidad que la arteria pulmonar, con un amortiguamiento parietal similar. El amortiguamiento global sistémico fue mayor que el pulmonar. Mientras que la elasticidad depende de la presión intravascular, la viscosidad es un marcador de la activación muscular. La activación muscular resultaría beneficiosa para el sistema cardiovascular, al mantener las funciones de amortiguamiento parietal y global (AU)

[Acute pulmonary hypertension: protective role of vascular smooth muscle activation]. / Hipertención pulmonar aguda: función protectora de la activación del músculo liso vascular.

AIM: To characterize the buffering function of the pulmonary artery in vivo and to determine the role of vascular smooth muscle (VSM) activation in vessel wall elasticity. MATERIAL AND METHOD: Pulmonary artery pressure and diameter were measured in 9 anesthetized sheep. Pulmonary artery hypertension was induced by mechanical occlusion of the pulmonary artery and by phenylephrine infusion (5 microg/kg/min) (PHE). Once the pressure-diameter loop was obtained, hysteresis was reduced to a minimum by increasing the modulus of viscosity. Elasticity was calculated as the first derivative of mean diastolic pressure assuming a purely elastic relation. Pulse wave velocity (PWV) and time constant (tau) were also obtained. RESULTS: Systolic, diastolic, mean and pulse pressures were similar during pulmonary artery hypertension and PHE infusion, but significantly higher in comparison to baseline conditions. Elasticity and diameter of the pulmonary artery increased significantly. In contrast, during VSM activation elasticity remained unchanged and diastolic diameter was reduced. PWV increased during both pulmonary artery hypertension and PHE infusion (p < 0.05); however, the increase during PHE infusion was smaller (15%) than during induced hypertension (33%). tau was significantly reduced during hypertension, but did not change during VSM activation. CONCLUSIONS: VSM activation may offset the deleterious effect of pulmonary artery hypertension on arterial wall stiffness by reducing elasticity and PWV. The VSM may modulate the Windkessel function in the pulmonary artery, preserving elasticity indexes during pulmonary artery hypertension.

Hipertensión pulmonar aguda: función protectora de la activación del músculo liso vascular / Acute pulmonary hypertension: protective role of vascular smooth muscle activation

Objetivo. Caracterizar in vivo la función de amortiguamiento de la arteria pulmonar y determinar la función de la activación del músculo liso vascular (MLV) sobre la elasticidad parietal de la misma. Material y método. Se midieron la presión y el diámetro de la arteria pulmonar en 9 ovejas anestesiadas. La hipertensión pulmonar se indujo mediante la oclusión mecánica de la arteria pulmonar (AP) y la infusión de fenilefrina (5 µg/kg/min) (FEN). A partir del bucle presión-diámetro se minimizó el área de histéresis y aumentaron los valores del módulo viscoso. Se calcularon la elasticidad como la primera derivada de la presión arterial diastólica media de la relación elástica pura, así como la velocidad de la onda del pulso (VOP) y la constante de tiempo (tau). Resultados. Las presiones arteriales sistólica, diastólica, media y de pulso fueron similares durante la oclusión mecánica de la AP y la infusión de FEN, pero significativamente mayores que las basales. En la AP, la elasticidad y el diámetro arterial aumentaron significativamente. Sin embargo, durante la activación del músculo liso vascular, la elasticidad se mantuvo y el diámetro diastólico disminuyó. La VOP aumentó tanto con la oclusión de la AP como con la infusión de FEN (p < 0,05); sin embargo, el aumento con la infusión de FEN fue menor (15 por ciento) que con la oclusión de la AP (33 por ciento). La tau se redujo significativamente en la oclusión de la AP, mientras que no se modificó durante la activación del músculo liso vascular. Conclusiones. La activación del músculo liso vascular neutralizó el efecto deletéreo de la hipertensión pulmonar sobre la rigidez de la pared arterial, reduciendo la elasticidad y la VOP. El músculo liso vascular podría modular la función Windkessel de la arteria pulmonar, preservando los índices de elasticidad durante la hipertensión pulmonar (AU)

Improved pulmonary artery buffering function during phenylephrine-induced pulmonary hypertension.

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation. Pulmonary pressure (Konigsberg P7) and diameter (sonomicrometry) were measured in nine anesthetized sheep. Transit pulmonary arterial hypertension was induced by mechanical occlusion of the pulmonary artery (HP) and by phenylephrine infusion (5 microg/kg/min) (PHE). A viscoelastic Kelvin-Voigt model was used. By increasing the values of the viscous modulus, the pressure-diameter hysteresis area was reduced to a minimum in order to obtain the purely elastic pressure-diameter relationship. The elastic index (E) was calculated as the first derivative of the exponential model of the purely elastic pressure-diameter relationship at the mean pressure point. Systolic, diastolic, mean and pulse pressures were similar during HP and PHE, but significantly higher with regard to control steady state. In HP, E and arterial diameter (both its minimum and maximum values) increased significantly. In contrast, when pulmonary hypertension was induced by VSM activation, E was maintained concomitantly with pulmonary artery vasoconstriction. Pulmonary hypertension produced by occlusion of the pulmonary artery increases elasticity. Smooth muscle activation may offset the deleterious effect of pulmonary hypertension on arterial wall elasticity by reducing E and impeding arterial dilatation and collagen recruitment, maintaining BF during pulmonary hypertension.

Sincronización de la contracción del ventrículo derecho frente a un aumento agudo de su poscarga. "Izquierdización" del comportamiento mecánico del ventrículo derecho / Right Ventricular Contraction Synchronization Due to Acute Afterload Increase. Left Ventricle Like Mechanical Properties of the Right Ventricle

Objetivo. El propósito de este trabajo fue demostrar la sincronización de la contracción del ventrículo derecho durante un aumento agudo y moderado de su poscarga. Material y método. En 7 ovejas anestesiadas se registraron simultáneamente las presiones de ambos ventrículos, arteria pulmonar, aorta, flujo pulmonar, y los volúmenes ventriculares por sonomicrometría. Se provocó hipertensión arterial pulmonar mediante la inyección intravenosa de endotoxina de Escherichia coli. Resultados. El aumento agudo de poscarga del ventrículo derecho, medido a través del aumento de la presión media de la arteria pulmonar (11,9 ñ 1,3 a 24 ñ 3,6 mmHg) produjo las siguientes modificaciones sobre el ventrículo derecho sin cambios de precarga ni de contractilidad: a) la elastancia máxima se aproximó al fin de la eyección (127,5 ñ 18,5 ms) y el tiempo de eyección se acortó (57,5 ñ 20,3 ms), de modo que el pico negativo de la primera derivada de la presión ventricular coincidió con el fin de la eyección; b) el bucle presión-volumen adoptó una forma rectangular, apareciendo ambas fases isovolumétricas, y c) la eyección puso de manifiesto una única fase. Conclusiones. La contracción del ventrículo derecho asincrónica o secuencial con poscarga normal adopta un patrón sincrónico similar al del ventrículo izquierdo durante un aumento agudo y moderado de su poscarga. Esta 'izquierdización' del comportamiento mecánico del ventrículo derecho constituye un mecanismo de compensación propio del ventrículo derecho, dado que le permite mantener su función sistólica en situación de poscarga aumentada, independiente de la precarga y de la contractilidad (AU)

Estudio de la fase de relajación del ventrículo derecho / Study of the relaxation phase of the right ventricle

El propósito de este trabajo fue investigar la existencia o no de una fase de relajación isovolumétrica en el ventrículo derecho en animales de experimentación con presión normal en la arteria pulmonar. Fueron registradas simultáneamente las presiones del ventrículo izquierdo, aorta (microtransductores), flujo pulmonar, diámetros ventriculares (sonomicrómetro), en 10 ovejas anesteciadas con pentobarbital intravenoso se obtuvo fuera de línea la primera deriva de las presiones ventriculares, los volúmenes ventriculares y los bucles presión-volumen de ambos ventrículos. El volumen sistólico mínimo ventricular derecho coincidió con el flujo pulmonar O, y ambos con un valor de presión diastólica de 0.5 mmHg en dicho ventrículo. Alcanzado el volumen sistólico mínimo, se inicia un rápido ascenso de la curva de volumen ventricular derecho. El bucle presión-volumen del ventrículo derecho, a diferencia del bucle del ventrículo izquierdo, adoptó una forma no rectangular. La fase eyectiva del ventrículo derecho se extendió hasta el inicio del llenado siguiente. Se concluye que, en el ventrículo derecho, no existe fase de relajación insovulométrica