PubMed · 7140315
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Barton, C R Lake, T G Rainey, B Chernow. 1982. Is catecholamine release pH mediated?. https://doi.org/10.1097/00003246-198211000-00010
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In order to gain some insight into the fate of fumarate synthesised in the cytosol in the purine nucleotide cycle and in amino acid catabolism, the capability of both rat kidney mitochondria and acidotic rat kidney mitochondria to take up either externally synthesised, via adenylsuccinate lyase, or added fumarate in exchange with intramitochondrial malate or aspartate was tested by means of both spectrophotometric and isotopic techniques. The appearance of either malate or aspartate caused by the presence of fumarate was revealed outside normal and acidotic mitochondria by using specific substrate detecting systems. Consistently, externally added fumarate was found to cause efflux of either [14C]-malate or [14C]-aspartate from loaded mitochondria. The occurrence in rat kidney mitochondria of two separate translocators, i.e., fumarate/malate and fumarate/aspartate carriers, is shown in the light of saturation kinetics and the different inhibitor sensitivity. The fumarate/aspartate antiporters found in normal and acidotic mitochondria appear to differ from each other.
BACKGROUND: Severe hyperphosphatemia resulting from the use of laxatives and enemas with high levels of phosphate has been the subject of many case reports. These have generally focused on the hypernatremia and hypocalcemia that develop and become life-threatening. Less attention has been paid to the metabolic acidosis of phosphate intoxication. METHODS: In-depth analysis of a case of severe hyperphosphatemia and review of the literature for cases with sufficient data to permit correlation between the phosphate concentration, acidosis, and anion gap. RESULTS: Marked metabolic acidosis with a large increase in the anion gap was present in our patient. The correlation between these parameters and the plasma phosphate concentration was highly significant. Despite a paucity of data in most case reports, we did uncover other cases of anion gap-positive metabolic acidosis in patients with hyperphosphatemia. CONCLUSIONS: Among high-risk patients, including the elderly and debilitated, the presence of metabolic acidosis, hypernatremia, an increased anion gap, and low plasma calcium levels or a prolonged QT interval on the electrocardiogram should raise suspicion of phosphate intoxication.
A 71-year-old man presented with incoherent, slurred speech, auditory hallucinations, and tachypnea. According to the neighbor who called for emergency medical service, the man had appeared to be in good health the day before. On admission, his blood pressure was normal.