[Stability of prostaglandin E1 when fractioned into polypropylene syringes]. / Estabilidad de prostaglandina E1 fraccionada en jeringas de polipropileno.

UNLABELLED: Prostaglandin E1 is indicated for the temporary maintenance of patent ductus arteriosus in newborns with ductus-dependent congenital heart defects. Since the standard daily dose is smaller (0.2-0.4 ml) than one ampoule (1 ml), we performed a chemical stability study of prostaglandin E1 when it is fractioned into polypropylene syringes. Three concentrations were studied: 500 mg/ml (original), and 1:2 and 1:4 dilutions in sodium chloride 0.9%. Syringes were kept at 4 degrees C for 30 days. Prostaglandin E1 levels were determined by using high-pressure chromatography. In all three formulations, the concentrations underwent no statistically significant changes over time (p>0.05). CONCLUSION: PGE1 is chemically stable at 4 degrees C for 30 days when fractioned into polypropylene syringes, both in the original and the 1:2 and 1:4 diluted formulations.

Estabilidad de prostaglandina E1 fraccionada en jeringas de polipropileno / Stability of prostaglandin E1 when fractioned into polypoprylene syringes

La prostaglandina E1 está indicada para mantener de forma temporal la persistencia del ductus arterioso en recién nacidos con alteraciones cardiacas congénitas ductus-dependiente. Dado que la dosis diaria usual es menor (0,2-0,4 ml) que el contenido de una ampolla (1 ml), realizamos un estudio de estabilidad química de la prostaglandina E1 fraccionada en jeringas de polipropileno. Se estudiaron tres concentraciones: 500 µg/ml (original ) y diluciones 1:2 y 1:4 en solución fisiológica. Las jeringas se conservaron a 4 °C, por 30 días. Los niveles de prostaglandina E1 fueron determinados por cromatografía de alta presión. Las concentraciones, en las tres formulaciones, no se modificaron en función del tiempo de manera estadísticamente significativa (p > 0,05). Conclusión: la PGE1 fraccionada en jeringas de polipropileno es químicamente estable a 4 °C, por treinta días, tanto para la formulación original como para las diluciones 1:2 y 1:4, en solución fisiológica (AU)

Localization of GABA- and glutamate-like immunoreactivity in the cardiac ganglion of the lobster Panulirus argus.

Wholemount immunohistochemical methods were used to examine the localization of gamma-aminobutyric acid (GABA) and glutamate within the cardiac system of the Caribbean spiny lobster Panulirus argus. All of the GABA-like immunoreactivity (GABAi) in the cardiac ganglion originated from a single bilateral pair of fibers that entered the heart via the two dorsal nerves. Each GABAi axon bifurcated upon entering the ganglion and gave rise to varicose fibers that surrounded the somata and initial segments of the five large motor neurons. The four small posterior cells did not appear to receive somatic contacts. Double-labeling experiments in which individual motor neurons were injected with Neurobiotin showed that their dendritic processes, which project to muscle bundles adjacent to the ganglion and are thought to respond to stretch, were also accompanied by branches of the GABAi fibers. Glutamate-like immunoreactivity (GLUi) was present in each of the motor neuron cell bodies. In some preparations, GLUi was also detected in large caliber fibers in the major ganglionic nerves. These fibers gave rise to more slender branches that innervated the cardiac muscle bundles. GLUi was also found in the small cell bodies and in fibers surrounding motor neuron somata. Taken together, these findings support previous electrophysiological, pharmacological and anatomical studies indicating that GABA mediates extrinsic inhibition and that glutamate acts as a neuromuscular and intraganglionic transmitter in this system. While axosomatic contacts may play a major role in both transmitter systems, the GABAergic inhibition also appears to involve substantial axodendritic synaptic signaling.

Ranitidine plus bromazepam in the treatment of duodenal ulcer: effect on gastric acid secretion.

The effect of adding bromazepam to treatment of duodenal ulcer with ranitidine was investigated in 30 out-patients. Under double-blind conditions one group of 15 patients received, for 14 days, 300 mg ranitidine and 6 mg bromazepam in the evening as a single dose. The other group received the same dose of ranitidine together with placebo, also for 14 days. In addition to measurements of gastric acid secretion after fasting and following histamine provocation, psychological ratings (Hamilton Anxiety Rating Scale and Zung Self-Assessment Scale for Anxiety) were carried out. Basal acid secretion was the same in both groups. During treatment, maximal acid output was significantly lower in the group of patients taking bromazepam than in those taking placebo. Similarly, significant differences were seen in favour of bromazepam in the psychological tests. It is concluded that these results confirm that bromazepam exerts a significant influence on acidity, over and above the effect of ranitidine. This effect, in all probability, is modulated by the emotional environment of individuals.