Multi-span transmission using phase and amplitude regeneration in PPLN-based PSA.

We demonstrated multi-span transmission using a periodically poled LiNbO(3) (PPLN) based phase sensitive amplifier (PSA). An in-line PSA with a carrier recovery and phase locking system is implemented as a repeater amplifier in a recirculating loop. We achieved a PSA gain as high as + 18 dB and a high external gain of + 12 dB for the in-line PSA as a black box. The impairments caused by phase noise resulting from fiber nonlinearity and intensity noise caused by the amplified spontaneous emission (ASE) of an optical amplifier are largely suppressed using the phase and amplitude regeneration capabilities of the PSA. The ultra long-haul transmission of a 28-Gb/s binary phase shift keying (BPSK) signal over 5400 km was achieved with phase and amplitude regeneration.

Anesthetic management of a patient with laryngeal amyloidosis.

A 73-year-old woman who suffered from progressive hoarseness for 6 years and dysphagia without pain for 1 year presented with a soft tissue deposition on the posterior region of the vocal cords and narrowing in the subglottic area. Biopsy of this soft tissue and histological examination revealed laryngeal amyloidosis. A tracheostomy and partial removal of the amyloid were performed with general anesthesia. The airway was secured with a smaller diameter endotracheal tube, which was inserted atraumatically with Magill's forceps. The larynx is a rare site for amyloidosis. Laryngeal amyloidosis is fragile and hemorrhagic. Therefore, massive bleeding may occur during intubation. Anesthetists should take care in intubating the tracheas of these patients and be aware of other systemic diseases in laryngeal amyloidosis.

Inhibition by vecuronium of carbachol-induced influx of 22Na+, 45Ca2+ and secretion of catecholamines in cultured bovine adrenal medullary cells.

In cultured bovine adrenal medullary cells, vecuronium, pancuronium and D-tubocurarine reduced carbachol-induced 45Ca2+ influx and catecholamine secretion by inhibiting 22Na+ influx via nicotinic receptor-ion channel complex with IC50 values of 0.43, 7.6 and 3.9 mumol/l, respectively. IC50 values of pancuronium and D-tubocurarine observed in adrenal medulla were one order of magnitude higher than the plasma concentrations of these muscle relaxants reported to produce 50% neuromuscular blockade, while IC50 of vecuronium was quite close between adrenal medulla and skeletal muscle.

Inhibition of 22Na influx by tricyclic and tetracyclic antidepressants and binding of [3H]imipramine in bovine adrenal medullary cells.

In bovine adrenal medullary cells we investigated the effects of antidepressants on ionic channels and secretion of catecholamines. Tricyclic (imipramine, amitriptyline and nortriptyline) and tetracyclic (maprotiline and mianserin) antidepressants inhibited carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines (IC50, 14-96 microM). Influx of 22Na, 45Ca and secretion of catecholamines due to veratridine also were inhibited by these drugs (IC50, 10-17 microM). However, antidepressants did not suppress high concentration of K-induced 45Ca influx and catecholamine secretion, suggesting that antidepressants do not inhibit voltage-dependent Ca channels. [3H]Imipramine bound specifically to adrenal medullary cells. Binding was saturable, reversible and with two different equilibrium dissociation constants (13.3 and 165.0 microM). Tricyclic and tetracyclic antidepressants competed for the specific binding of [3H]imipramine at the same concentrations as they inhibited 22Na influx caused by carbachol or veratridine. Carbachol, d-tubocurarine, hexamethonium, tetrodotoxin, veratridine and scorpion venom did not inhibit the specific binding of [3H]imipramine. These results suggest that tricyclic and tetracyclic antidepressants bind to two populations of binding sites which are functionally associated with nicotinic receptor-associated ionic channels and with voltage-dependent Na channels, and inhibit Na influx. Inhibition of Na influx leads to the reduction of Ca influx and catecholamine secretion caused by carbachol or veratridine.

Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells.

The effects of ketamine, an intravenous anesthetic, on 22Na influx, 45Ca influx and catecholamine secretion were investigated in cultured bovine adrenal medullary cells. Ketamine inhibited carbachol-induced 45Ca influx and catecholamine secretion in a concentration-dependent manner with a similar potency (IC50 40 microM). Ketamine also reduced veratridine-induced 45Ca influx and catecholamine secretion (IC50 260 microM) but did not affect high K-induced 45Ca influx and catecholamine secretion. The influx of 22Na caused by carbachol or by veratridine was suppressed by ketamine with a concentration-inhibition curve similar to that of 45Ca influx and catecholamine secretion. Inhibition by ketamine of the carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines was not reversed by the increased concentrations of carbachol. These observations indicate that ketamine, at clinical concentrations, can inhibit nicotinic receptor-associated ionic channels and that the inhibition of Na influx via the receptor-associated ionic channels is responsible for the inhibition of carbachol-induced Ca influx and catecholamine secretion. At higher concentrations, the anesthetic also inhibits voltage-dependent Na channels but has no effect on voltage-dependent Ca channels.

Inhibition of Na+-pump enhances carbachol-induced influx of 45Ca2+ and secretion of catecholamines by elevation of cellular accumulation of 22Na+ in cultured bovine adrenal medullary cells.

In bovine adrenal medullary cells, we reported that 22Na+ influx via nicotinic receptor-associated Na+ channels is involved in 45Ca2+ influx, a requisite for initiating the secretion of catecholamines (Wada et al. 1984, 1985 b). In the present study, we investigated whether the inhibition of Na+-pump modulates carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured bovine adrenal medullary cells. We also measured 86Rb+ uptake by the cells to estimate the activity of Na+,K+-ATPase. Ouabain and extracellular K+ deprivation remarkably potentiated carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion; this potentiation of carbachol-induced 45Ca2+ influx and catecholamine secretion was not observed in Na+ free medium. Carbachol increased the uptake of 86Rb+; this increase was inhibited by hexamethonium and d-tubocurarine. In Na+ free medium, carbachol failed to increase 86Rb+ uptake. Ouabain inhibited carbachol-induced 86Rb+ uptake in a concentration-dependent manner, as it increased the accumulation of cellular 22Na+. These results suggest that Na+ influx via nicotinic receptor-associated Na+ channels increases the activity of Na+,K+-ATPase and the inhibition of Na+,K+-ATPase augmented carbachol-induced Ca2+ influx and catecholamine secretion by potentiating cellular accumulation of Na+. It seems that nicotinic receptor-associated Na+ channels and Na+,K+-ATPase, both modulate the influx of Ca2+ and secretion of catecholamines by accommodating cellular concentration of Na+.

[Clinical study on hypotensive anesthesia with nitroglycerin].

Deliberate hypotension was induced by using nitroglycerin (NG) during anesthesia in 13 patients with intracranial aneurysm, who underwent clipping surgery. The following results were obtained: Changes in blood pressure were rapid and smooth, before, during and after administration of NG. No patients showed resistance to the drug in this study. Heart rate increased significantly during induced hypotension while a significant reduction was observed in the rate-pressure product (RPP), which correlates with the myocardial oxygen demand. No significant changes were found in pH, PaO2, PaCO2 and base excess (B. E.) while the respiratory index (PaO2/FIO2) as an indicator of pulmonary oxygenation appeared to be significantly reduced.

Influx of 22Na through acetylcholine receptor-associated Na channels: relationship between 22Na influx, 45Ca influx and secretion of catecholamines in cultured bovine adrenal medulla cells.

The effects of carbachol, veratridine and high K on the influx of 22Na were investigated in relation to the influx of 45Ca and the secretion of catecholamines in cultured bovine adrenal medulla cells, in which stimulation of nicotinic but not muscarinic acetylcholine receptor causes the secretory response. (1) Carbachol caused a rapid influx of 22Na, influx of 45Ca and secretion of catecholamines, all of which occurred within 1 min and leveled off thereafter. Influx of 45Ca and secretion of catecholamines caused by carbachol were not inhibited by tetrodotoxin, but were greatly reduced in Na-free medium. Nicotine evoked an influx of 22Na and it was antagonized by hexamethonium and d-tubocurarine but not by tetrodotoxin. Muscarine had no effect on 22Na influx. The concentration-response curve of carbachol for 22Na influx was quite similar to that for 45Ca influx. (2) Veratridine induced a sustained influx of 22Na, influx of 45Ca and secretion of catecholamines, all of which were antagonized by tetrodotoxin. Influx of 45Ca and secretion of catecholamines due to veratridine were not observed in Na-free medium. (3) High K caused an influx of 45Ca and secretion of catecholamines but did not cause an influx of 22Na. High K-induced influx of 45Ca and secretion of catecholamines were not inhibited by tetrodotoxin nor by Na removal. (4) Magnesium, an inhibitor of voltage-dependent Ca channels, inhibited the influx of 45Ca and secretion of catecholamines caused by carbachol, veratridine and high K. These results indicate that cultured bovine adrenal medulla cells have at least three distinct ion channels: (1) nicotinic acetylcholine receptor-associated Na channels which are not inhibited by tetrodotoxin, (2) voltage-dependent Na channels which are kept activated by veratridine and inhibited by tetrodotoxin and (3) voltage-dependent Ca channels. Influx of Ca through voltage-dependent Ca channels is the common ionic event for the secretion of catecholamines caused by either carbachol, veratridine or high K. It seems that the influx of Na through acetylcholine receptor-associated Na channels as well as voltage-dependent Na channels, activates voltage-dependent Ca channels which triggers the secretion of catecholamines.