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La enfermedad de Chagas constituye un problema de salud pública en Venezuela, cuya principal consecuencia es el desarrollo de una Miocardiopatía Chagásica Crónica (MCHC). Las causas no son bien conocidas y en la actualidad no existe tratamiento específico, ni modelos animales que sustentes investigaciones para comprender su patogenia. Este trabajo plantea un modelo animal basado en el uso de Ciclofosfamida (CF). Para este fin se utilizaron 41 ratas Spargue Dawley de tres semanas de edad divididas en 4 grupos: Control (CC; n=12), Control Ciclofosfamida (CCF n=9), Control T. cruzi (TC; n=6) y Experimental Ciclofosfamida-T. cruzi (CFTC n=14). Los grupos TC y CFTC fueron inoculados con 100 parásitos/gr. de tripomastigotos de la cepa YBM. CF y CFTC fueron tratados con FC a razón de 29 mg/kg, 2 veces por semans 5 veces. La parasitemia fue valorada cada semana utilizando un hemocitometro. Posteriormente se realizaron estudios electrocardiogr ficos (EKG), bajo anestesia con Pentobarbital 40 mg/kg de peso con el fin de valorar la funcionalidad card¡aca y la respuesta vagal a la Felinefrina (1 mg/kg). Los resultados reflejaron qye: la CF en combinación con T. cruzi produce una parasitemia significativamente mayor y más prolongada, aumenta el número de trastornos electyrocardiogr ficos tales como: extrasístoles, bajo Voltaje del complejo QRS y RR variable, falta de onda "S", y PR y QT prolongados. La CF por si sola produce una respuesta bradicardizante inducida por FE más prolongada. En conclusión, la CF induce una MChC en rtas infectadas con T.cruzi.

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Una alimentación balanceada, donde se contemple un consumo adecuado de grasas y 4 o más raciones de frutas y vegetales son una forma de proveer al organismo de Vitaminas, entre ellas Vitaminas: E, A y C: Estas son consideradas Vitaminas Antioxidantes y se les atribuye un papel importante en la prevención de patologías en las cuales están involucrados los radicales libres tales como infecciones, enfermedades cardiocirculatorias y degenerativas crónicas, cáncer, proceso de envejecimiento, etc. En este sentido la OMS ha establecido que un estado optimo de antioxidantes esenciales es un prerrequisito de salud y debería reducir el riesgo de sufrir enfermedades crónicas. En función de esto, una información adecuada acerca de sus fuentes diabéticas, requerimientos, farmacocinética y su toxicidad son necesarias para el uso racional de estas vitaminas

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Few studies have evaluated the relationship between drugs of abuse consumption and plasma levels of vitamin C. Because of the importance of vitamin C due to its role in prevention of acute and chronic diseases, this study was carried out with the purpose of testing the influence of consumption of drugs of abuse on the plasmatic levels of vitamin C (ascorbic acid) of 56 male chronic users of drugs of abuse with an age range of 16 to 40 years. The following was performed: 1) A survey of consumption to determine the kind, frequency and quantity of drug(s) used and 2) The plasmatic levels of vitamin C in fasting condition, using the Rue and Kuether method. The results obtained showed that 89% of the population under study used drugs for the first time before the age of 18, and 78.4% started with marijuana; 60.7% of them were mixed drug users. The average level of plasmatic ascorbic acid was 0.89 +/- 0.06 mg/dL, nevertheless, according to nutritional category, 76% have values greater than 0.4 mg/dL and 23.2% were at moderated risk (0.35 +/- 0.01 mg/dL) of vitamin C deficiency. Likewise, classifying them in the antioxidant category (according to the suggested values of Gey, 1993) it was obtained that 55.4% had suboptimal or inadequate concentrations to carry out its antioxidant protective function. The length of time of drug's consumption influenced on the ascorbic acid level too. It can be concluded that chronic consumption of drugs of abuse can negatively influence the plasmatic levels of ascorbic acid, leading these patients to a latent condition of vitamin C deficiency. Finally it is necessary to deepen the study of vitamin C levels of users of drugs of abuse.

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It's well known that physical growth and intellectual activity is influenced by nutritional status. With the purpose of evaluate the fasting effects on the cognitive functions, anthropometric state and cognitive functions (logic and school work performance), under fasting and post-breakfast condition were assessed in a group of 68 school children age 9 and 10 years, who studied in a private school (1998-1999). Logic reasoning was measured with Raven test and attention, precision, velocity and fatigue with the Lepez test. The main of the children (80%) were well-nourished and 20% had showed overweight. At breakfast condition all subjects were over 50 percentil for Raven test. Consumption of breakfast influence on logic reasoning (p < 0.001) and school work performance (p < 0.01). It is concluded that in these well nourished children, breakfast consumption improved cognitive performance.

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Some individuals with functional limitations or in some clinical or field areas have troubles to get stature and body weight measurement done. It does exist the alternative of estimating these variables from measurements of body segments like knee height (KH) and mid arm circumference (MAC). Of a sample of 113 healthy Venezuelan children, both sexes, 9 to 14 years of age, equations suggested by Ross Laboratories for estimating stature and body weight were applied. It was concluded that the need for an adjustment was evident which done using multiple regression analysis. This allowed us to generate estimated stature an weight by KH and MAC tables, for Venezuelan children.

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1 Young rabbits were treated for 30 days or 6 weeks with propranolol or oxprenolol to provide dose-levels similar to those used clinically. 2 Relative to litter matched controls the treated rabbits exhibited a reduced rate of growth. 3 Morphometric studies showed that prolonged beta-adrenoceptor blockade had no effect on the myofibrillar volume as a proportion of cell volume. 4 Prolonged beta-blockade increased the proportion of the extracellular space occupied by vascular tissue.

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Using isolated, Langendorff-perfused, electrically-paced guinea-pig hearts, we have investigated the rise in resting tension that occurs when mammalian heart muscle becomes hypoxic. Substrate-depletion, tachycardia, hyperthyroidism, and inotropic interventions (ouabain, isoprenaline, and beta-receptor antagonists at concentrations which increase inotropic state) enhanced the rate of development of this increase in resting tension. 3.86 mumol.litre-1 propranolol, 0.22 to 2.20 mumol.litre-1 verapamil or removing Ca2+ from the extracellular phase at the start of the hypoxic episode prevented (or delayed) the rise in resting tension. Adding these same agents or removing Ca2+ from the extracellular phase after the hypoxia-induced rise in resting tension had started to develop failed to prevent its progression. These results provide some support for an hypothesis that the hypoxia-induced increase in resting tension is independent of an enhanced Ca2+ influx.

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Experiments were undertaken to determine if drugs (verapamil, propranolol, and methylprednisolone sodium saccinate) that protect the fine ultrastructure of heart muscle against damage caused by hypoxia, protect mitochondrial function. Mitochondrial function was assessed in terms of oxidative phosphorylating and Ca2 +-accumulating activities. Isolated rabbit hearts were used, and hypoxic conditions induced by reducing the perfusate PO2 from 80.8 to 0.80 kPa (600 to 6 mmHg). The drugs were either added at the start of the hypoxic perfusion or (verapamil and propranolol) the rabbits were pretreated with them. Verapamil, propranolol and, to a lesser extent, methylprednisolone sodium succinate, provided protection evidenced by the maintainance of near normal mitochondrial oxidative phosphorylating and Ca2 +-accumulating activities after 60 min hypoxic perfusion. When added directly to mitochondria isolated from hypoxic-perfused muscle, the drugs had no effect.

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Experiments were undertaken to further investigate the protective effect of methylprednisolone sodium succinate on hypoxic heart muscle. Hypoxia was induced in isolated Langendorff perfused rat and rabbit hearts by gassing the perfusate with 95% N2 + 5% CO2. The hypoxia-induced damage was quantitated in terms of an altered ultrastructure and increased resting tension. When added at the start of the hypoxic episode 6 X 10(-5) mol.litre-1 methylprednisolone sodium succinate protected the fine ultrastructure of the heart, and delayed the increase in resting tension. This protective effect could not be accounted for in terms of the sodium succinate moiety.

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The ability of several beta-adrenoceptor antagonists with partial agonist activity (dl-oxprenolol, dl-acebutolol and dl-practolol) to attenuate the release of CPK that occurs during hypoxia (pO2 less than 0.8 kPa [6 MMHg]) has been studied and compared with the protection provided by dl-propranolol. dl-propranolol attenuated the hypoxic-induced release of CPK. The activity resided in the l isomer. dl-oxprenolol, acebutolol, and practolol were either less effective than propranolol in preventing CPK release, or they exacerbated the release. The protective effect of dl-propranolol extended to the hypoxic hyperthyroid heart but not to hearts that were perfused under aerobic (pO2 greater than 80 kPa [600 mmHg]) Ca2+-free conditions.

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The ability of beta-adrenoceptor antagonists, with and without intrinsic sympathomimetic activity, and of verapamil to protect the heart against hypoxia-induced damage was investigated. Damage was quantitated in terms of a raised end-diastolic resting tension and creatine phosphokinase (CPK) release. The results indicate that both the d and the l isomers act differently, the isomers preventing CPK release and the d isomers preventing the increase in resting tension.

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The four-year follow-up study reported herein represents the continuation of a previous cross-sectional study carried out in a rural community (Belen, Venezuela). The earlier study included 1,210 persons out of a total of 1,656 inhabitants, all over five years of age, and demonstrated a high prevalence of Chagas' infection (47.3 per cent) and a high rate of Chagas' disease seropositivity among those with chronic myocardial heart disease (84.8 per cent); heart disease was found in 17.3 per cent of persons studied. It included clinical, electrocardiographic and radiological analyses

The present report describes the results of the four-year follow-up study performed in 812 persons, which permitted to establish the incidence of Chagas' infection (16.3 per cent) and that of chagasic heart disease (2.2 per cent) in four years. The report also included the clinical, electrocardiographic and radiological analyses of cases with previous heart disease as well as new cases. Different evolutive electrocardiographic patterns have been found, including serial electrocardiographic variations ranging from normal to definitely abnormal. The mortality occurred in the sample during the observation period is reported(AU)

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The paper reports on a 4-year follow-up study that represents the continuation of a previous cross-sectional study on Chagas' disease carried out in a rural community (Belén) in Venezuela. The earlier study included 1210 persons all over 5 years of age out of a total of 1656 inhabitants and demonstrated a high prevalence of Chagas' infection (47.3%) and a high rate of Chagas' disease seropositivity among those with chronic myocardial heart disease (84.8%); heart disease was found in 17.3% of persons studied. The follow-up study was based on 812 persons and established that in the sample the frequency of Chagas' infection was 16.3% and that of heart disease 2.2%. Clinical, electrocardiographic and radiological analyses were made on patients with previous heart disease as well as on new patients. Different evolutive electrocardiographic patterns have been found, including variations ranging from normal to definitively abnormal.

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