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J Ortiz

Publications and source records attributed to J Ortiz.

At least 127 records · Page 7Linked to original sources
PubMed1985

[Sensitivity of the motor endplate to carbachol in the presence of sulfhydryl reagents].

The effect that bath application of sulphydryl reagents (SR) exerts on frog sartorius motor endplate sensitivity to iontophoretically applied carbachol (CCh) has been studied. Sensitivity to CCh is expressed as the ratio of the CCh potential (mV) to the nanocoulombs delivered by the iontophoretic pulse and has been determined before and after addition of SR to the bath. Two groups of SR have been tested: oxidizing reagents, o-iodosobenzoate and reducing agents, dithiothreitol (DTT). CCh was applied iontophoretically by means of a microelectrophoretic programmer with constant current source. Exposure of the muscle to 1 mM DTT in a bath pH range of 7-8 for 2 to 85 min showed no significant differences in endplate sensitivity to CCh before and after addition of the reducing agent. o-Iodosobenzoate at a 1 mM bath concentration (pH 7) for 2 to 19 min strongly decreases endplate sensitivity to CCh. The statistical methods used were Wilcoxon rank tests and linear regression. Since previous studies have shown that oxidizing and reducing SR evoke depolarizations when applied iontophoretically at the endplate region, these results suggest that activation of the receptor is achieved only when SR are delivered iontophoretically, and that discrepancies observed can be attributed mainly to the different techniques of drug application.

Animals↗
PubMed1984

Cross-sectional echocardiographic features of "absent" pulmonary valve. Report of two cases.

"Absence" of the pulmonary valve was recognized by cross-sectional echocardiography in two infants having relatively atypical clinical manifestations for this cardiac malformation. Both had associated lesions: tetralogy of Fallot and ventricular septal defect, respectively, which were also detected by this non-invasive technique. The findings which strongly suggested the diagnosis were the presence of a ridge of rudimentary pulmonary valvular tissue at the level of the pulmonary annulus and the aneurysmal dilation of the pulmonary arteries. The short axis view at the level of the great arteries was the best approach for visualization of these anatomical abnormalities. The parasternal long axis and sub-costal four-chamber views were also helpful in detecting the associated lesions. In both cases the diagnoses were confirmed at autopsy.

Echocardiography↗
PubMed1983

Metabolism of cadaverine and pipecolic acid in brain and other organs of the mouse.

Cadaverine and pipecolic acid metabolism was investigated in vitro in several organs of the mouse by measuring 14CO2 formation from labeled precursors. The liver showed the highest formation of 14CO2 from [1,5-14C]-cadaverine, whereas brain demonstrated a much lower formation. Anaerobiosis or inhibition of monoamineoxidase (MAO) activity significantly reduced 14CO2 formation in every organ, but inhibition of diamine oxidase (DAO) activity had no effect in brain and kidney. Piperidine was formed from cadaverine in vitro only in the large intestine and its content. This formation is probably of bacterial origin. Under a variety of experimental conditions we were unable to demonstrate any formation of piperidine in brain from cadaverine. Biosynthesis in vitro of [3H]-piperidine from D,L-[3H]-pipecolic acid was very low in brain and kidney. With the exception of brain and kidney, no other organs showed any formation of [3H]-piperidine. Neither MAO nor DAO inhibition influenced [3H]-piperidine formation in the large intestine with its content. Following 1 hr incubation at 37 degrees C under aerobic conditions, the levels of [14C]-pipecolic acid and [3H]-piperidine recovered from mouse brain homogenate did not indicate any significant degradation of these two substances. Our results suggest that under in vitro conditions, cadaverine is not a precursor of piperidine in brain, liver, heart, and kidney and that only very low levels of piperidine can be formed from pipecolic acid in brain. Outside the brain, formation of piperidine from pipecolic acid is detectable only in kidney and in the content of the large intestine. The latter is probably of bacterial origin. Our results do not support previous findings from other authors on an endogenous origin of piperidine in brain from cadaverine and pipecolic acid, and they suggest that a) cadaverine is not a precursor of piperidine in brain, b) the conversion of pipecolic acid into piperidine in the brain does not constitute a major metabolic pathway, and c) the main source of piperidine in the CNS may be of nonneural origin.

Animals↗
PubMed1983

Accumulation and metabolism of pipecolic acid in the developing brain of the mouse.

In newborn mice, following i.p. injections of D,L-[3H]PA (pipecolic acid, 28 micrograms/kg), accumulation of radioactivity continues to increase up to 24 h. In adults, radioactivity peaks at 5 min and remains approximately constant up to 5 h, and then declines slowly to 24 h. Fifteen-day-old mice follow the newborn pattern, while 30-day-old mice show the same trend as the adult. Radioactivity in plasma shows essentially the same pattern of accumulation in adult and newborn animals with some quantitative differences. Secretion of radioactivity in the urine is significantly higher in the adult than in the newborn during the interval between 10 min and 5 h. Accumulation of radioactivity at 24 h in the newborn brain shows a preferential localization to the olfactory bulb, the anterior telencephalon and the diencephalon. Two hours after the i.p. injection, approximately 70% of the radioactivity recovered in brain is due to PA. This percentage increases to 75% and 87% at 5 and 24 h respectively. Alpha-aminoadipic acid (alpha-Aaa) a major metabolite of PA was identified in brain extracts at 5 h. The maximal formation of alpha-Aaa in relation to PA occurs approximately at 5 h. No other brain metabolites of PA could be identified with this chromatographic system. The present results show that access of PA to the brain is easier in the newborn mouse than in the adult. In addition, our results demonstrate, for the first time, the presence of PA metabolism in the newborn mouse.

2-Aminoadipic Acid↗
PubMed1982

Accumulation, elimination, release and metabolism of pipecolic acid in the mouse brain following intraventricular injection.

Following i.c.v. (intracerebral ventricular) injections of D,L-[3H]pipecolic acid (PA), it is reabsorbed from the ventricles and redistributed to various brain regions. The highest accumulation is found in three brain regions ipsilateral to the injection site, hippocampus, neocortex, striatum, and in the diencephalon. Following preloading in vivo, the radioactivity is released from hippocampus slices in the perfusion medium after depolarization induced by high K+. During perfusion with a Ca++ free medium containing EGTA, a significant reduction of release is observed. The radioactivity of D,L-[3H]PA in the brain shows a more rapid phase of decrease from 0 to 2 hours and a slower phase from 2 to 5 hours. At 5 hours, only 28% radioactivity, represented mainly by PA, is left in the brain. Kidney secretion represents the major route of elimination of the injected PA. The presence of alpha-aminoadipic acid both in brain and urine was observed. Probenecid (200 mg/kg) significantly increases the accumulation of i.c.v. injected D,L-[3H]PA in brain and kidney. The presence of a regional accumulation of PA in certain brain regions, its metabolism in brain, its enhanced retention following probenecid administration and its Ca++ dependent release following high K+ stimulation, all constitute indirect evidence for a neuronal localization of this brain endogenous aminoacid.

Animals↗