The effects of K+ depolarization and of stimulation by veratridine on apparent cytosolic free Ca2+ (Ca2+cyt) and net Ca2+ accumulation were measured in isolated rat brain presynaptic nerve terminals ...(synaptosomes). Ca2+cyt was determined with fura-2, and Ca2+ accumulation was measured with tracer 45Ca. Ca2+cyt was approximately 325 nM in synaptosomes incubated in the normal physiological salt solution under resting conditions. When K+o was increased from the normal 5 mM to 30 or 50 mM, 45Ca uptake and Ca2+cyt both increased within 1 s. Both increases were directly related to Ca2+o for Ca2+o = 0.02-1.2 mM; however, the increase in 45Ca uptake greatly exceeded the increase in Ca2+cyt. With small Ca2+ loads (< or = 100 mumol/L of cell water, equivalent to the Ca2+ entry during a train of < or = 60 impulses), the 45Ca uptake exceeded the increase in Ca2+cyt by a factor of nearly 1,000. This indicates that approximately 99.9% of the entering Ca2+ was buffered and/or sequestered within approximately 1 s. With larger Ca2+ loads, a larger fraction of the entering Ca2+ was buffered; approximately 99.97% of the load was buffered with loads of 250-425 mumol/L of cell water. The ratio between the total Ca2+ entry and the increase in Ca2+cyt, the "calcium buffer ratio," beta, was therefore approximately 3,500:1. This ratio was somewhat lower than the ratio of total intraterminal calcium: Ca2+cyt, which ranged between approximately 7,300:1 and 12,800:1. When the synaptosomes were activated with 10 microM veratridine (Ca2+o = 0.2-0.6 mM), 45Ca influx and Ca2+cyt increased progressively for approximately 10 s (beta = 2,700:1-3,050:1) and then leveled off.
A rare case of exocrine pancreatic damage in a patient with Wegener's granulomatosis is reported. The pancreatic amino acid consumption test, a new tubeless technique, revealed exocrine pancreatic ...insufficiency before and after immunosuppressive therapy. The presence of exocrine pancreatic insufficiency in this patient raises the possibility of pancreatic involvement in Wegener's granulomatosis.
A study was conducted to investigate poststimulatory depression in respiratory activities induced by superior laryngeal nerve (SLN) stimulation in cats. Results from the use of the opiate agonist ...naloxone suggest a role of endogenous opioids in the genesis or modulation of poststimulatory respiratory depression.
Anesthesia in Apert syndrome Ciceri, G; Arosio, G; Brunatti, M ...
Minerva anestesiologica
63, Številka:
5
Journal Article
The anaesthetic technique chosen for a laparohysterectomy in a woman affected by Apert's acrocephalosyndactilia is described. Difficulties in performing tracheal intubation were overcome by mean of ...loco-regional anesthesia (LRA). In order to minimize the anaesthetic risk, a standardised preoperative evaluation and assessment integrating the usual investigations and the possibility of employing intubation techniques as alternative to direct laryngoscopy are suggested.
The effects of gamma-aminobutyric acid (GABA) on the spontaneous efflux of 3Hnorepinephrine (3HNE) were studied in synaptosomes prepared from rat hippocampus and prelabelled with 3HNE. It had been ...observed previously that, when synaptosomes were exposed in superfusion to GABA, the basal release of the tritiated catecholamine was enhanced, apparently with no involvement of the known GABA receptors. The mechanisms underlying this effect have now been investigated. The potency of GABA as a releaser of 3HNE was decreased by lowering the Na+ content of the superfusion medium, and its effect disappeared at 23 mM Na+. The GABA-induced 3HNE release was counteracted by the GABA uptake inhibitor N-(4,4-diphenyl-3-butenyl)nipecotic acid (SKF 89976A), but it was unaffected by the NE uptake blockers desmethylimipramine and nisoxetine. The GABA-induced release of 3HNE was Ca2+-dependent and tetrodotoxin-sensitive. The data support the hypothesis that GABA provoked 3HNE release by a novel mechanism which involves penetration into the noradrenergic nerve terminals through a GABA carrier located on the NE terminals themselves. This uptake process might be electrogenic and provoke depolarization of the nerve terminals, causing an exocytotic release of 3HNE.
We report the case of a young man suffering from epilepsy who developed chronic calcified pancreatitis after ten years of therapy with the anticonvulsant drugs carbamazepine and phenytoin. Long-term ...anticonvulsant drug therapy may have a contributory role in the development of chronic pancreatitis by chronic stimulation of cytochromes P-450.
