Effect of feed restriction on intake of Moringa oleifera and Leucaena leucocephala and growth performance of rabbits.

Two experiments were conducted to evaluate the effect of feed restriction on intake of Moringa oleifera (MO) or Leucaena leucocephala (LL) and growth of rabbits. In experiment one, 45 rabbits (male and female) weighing 1.18 ± 0.15 kg were used. They were randomly distributed to three feed restriction treatments (20, 30, and 40%) with 15 rabbits each (9 females and 6 males) and they were offered M. oleifera (MO) ad libitum. In experiment two, 45 growing male rabbits weighing 0.63 ± 0.113 kg were used. They were randomly assigned to 0, 20, and 30% feed restriction diets, and they have free access to L. leucocephala (LL). Intake of MO increased (P < 0.05) conforming feed restriction increased (40.6, 52.9, and 55.2 g/day of MO for 20, 30, and 40%, respectively). Daily liveweight gain and feed conversion did not differ (P > 0.05), and economic efficiency was similar among treatments. Consumption of LL increased (P < 0.05) in rabbits under the 30% restriction treatment in comparison to that of rabbits restricted 20% (46.0 and 44.4 g/day, respectively). Total feed intake (LL + feed) was highest in 20% restricted rabbits (108.0, 100.8, and 93.2 g/day for 20, 30, and 0%, respectively). Daily liveweight gain and feed conversion were not affected by feed restriction (P > 0.05). Economic efficiency improved twice in feed-restricted rabbits (2.0 and 2.3 for 20 and 30%, respectively) in contrast to that of the control 0% group (1.1). The results suggest that rabbits restricted up to 30% and supplemented with either MO or LL did not affect growth performance and reduced feed cost.

[Pulsed Doppler in the diagnosis of obstruction of the superior vena cava. Apropos of a case]. / Doppler pulsado en el diagnóstico de obstrucción de vena cava superior. A propósito de un caso.

We report the case of a patient diagnosed as superior vena cava syndrome 8 years after surgical resection of a breast malignancy and treatment with radiotherapy. The study with pulsed Eco-Doppler detected the presence of obstruction to the systemic venous return, allowing us to establish the diagnosis. Confirmation was achieved by means of venography and venous pressure manometry. Usefulness of the Doppler technique in the assessment of systemic venous return is confirmed.

Arrhythmogenic effects of antiarrhythmic drugs in patients with an old myocardial infarction and asymptomatic ventricular ectopic activity as studied by programmed electrical stimulation.

In 22 patients with a previous myocardial infarction and documented Lown class II to IV asymptomatic ventricular arrhythmias, the arrhythmogenic effect of mexiletine (18 patients) and propafenone (10 patients) has been assessed by programmed electrical stimulation. Ventricular arrhythmias induced during the basal study were: repetitive ventricular responses (RVR) (11/22, 50%), nonsustained ventricular tachycardia (VT) (3/22, 14%), sustained VT (7/22, 32%) and ventricular fibrillation (VF) (1/22, 4%). The induction of sustained VT or VF increased to 50% after mexiletine and to 80% following propafenone. An arrhythmogenic effect was found in 7/11 patients (64%) without VT at the control study (P = 0.004). One patient of this group spontaneously developed sustained VT both after mexiletine and propafenone. Only 1/8 patients (13%) with sustained VT/VF at the basal study had RVR after drug administration. The R-R interval of sustained VT at the basal state tended to be faster than that after the drugs (260 +/- 60 ms vs 293 +/- 56 and 332 +/- 77 ms for mexiletine and propafenone, respectively) (P = 0.052). Statistical significance was only reached in the propafenone group (P = 0.03). Facilitation of VT induction after antiarrhythmic drugs is most likely due to a modest lengthening of refractoriness in contrast with a more evident reduction in conduction velocity within the reentry pathway. Our study illustrates that treating asymptomatic ventricular ectopic activity in patients with an old myocardial infarction may be dangerous and that antiarrhythmic drugs show a significant arrhythmogenic potential at least in the laboratory setting.