Membrane potential (Vm) and resistance (Rm) of ventral respiratory group (VRG) neurons were measured in the isolated brainstem–spinal cord from newborn rats during bath application of the opioid receptor agonists fentanyl or [D‐Ala2, D‐Leu5]‐enkephalin (Ala‐Leu‐Enk) and of the prostaglandin Et (PGE1). PGE1 (0.1–3 μm) and fentanyl or Ala‐Leu‐Enk (1–50 μm) produced depression and, at higher doses, block of inspiratory nerve activity and respiration‐related postsynaptic potentials. This apnoea was associated with hyperpolarization and Rm fall in 25% of thirty‐two VRG neurons tested, whereas resting Vm and Rm were not changed in the other cells. The selective μ‐ and δ‐receptor blockers naloxonazine (10–20 μm) and naltrindole (50–100 μM) antagonized the effects of 5 μm fentanyl and 50 μM Ala‐Leu‐Enk, respectively. Opioid‐ and PGE1‐evoked respiratory depression was reversed upon elevation of endogenous cAMP levels by stimulating adenylyl cyclase with 100 μM forskolin, activating dopamine D1 receptors with 50–100 μm 6‐chloro‐7,8‐dihydroxy‐3‐allyl‐1‐phenyl‐2,3,4,5‐tetrahydro‐1H‐3‐benzazepine (6‐chloro‐APB) or preventing cAMP breakdown with 50–100 μm isobutylmethylxanthine. The results indicate that opioid‐ or prostaglandin‐induced respiratory depression is due to a fall in cAMP levels in cells responsible for generation of rhythm or providing a tonic drive to the respiratory network. We suggest that elevation of cAMP levels is an effective antidote in neonates against such forms of respiratory depression.

We treated 16 patients with moderately severe to severe generalized myasthenia gravis (MG) by immunoadsorption (perfusion through a resin that adsorbs proteins) of 2,500 ml plasma on each of four alternate days. Fourteen patients who completed treatment all had significant improvement in strength (6 excellent, 6 good, and 2 fair), which began a mean of 42 hours after the first immunoadsorption, reached a maximum 4 days after the fourth immunoadsorption (mean, 250% of baseline strength), and returned to baseline over a mean of 2 months. Thirty-seven grams of plasma proteins were removed during each immunoadsorption, which required no replacement, compared with 175 grams during plasma exchange, which requires replacement with albumin. Serum or plasma concentration of all proteins fell, more so for most of the larger proteins than for the smaller ones: acetylcholine receptor antibody (AChR Ab) fell to a mean of 23% of original level, fibrinogen to 26%, C4 to 29%, IgM to 33%, IgG to 35%, CH50 to 41%, C3 to 42%, IgA to 54%, and albumin to 76%. All proteins, including AChR Ab, returned to their original levels within 1 to 3 weeks after the last immunoadsorption, while improvement in strength lasted a mean of 6 weeks longer. One seronegative patient had excellent improvement lasting more than a month. Activated complement C5a and white blood cell count rose during each immunoadsorption, while activated complement C3a fell, and each returned to its original level within hours. Eight patients had transient symptomatic hypotension attributable to withdrawal of blood more rapidly than it was returned; this hypotension was prevented or ameliorated by intravenous saline.(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the prevalence and clinical assessment of sighs in neonates, we observed three different patterns of sighs: (A) sighs in the absence of apneic pause; (B) sighs with instantly following apneic pause >2 s, and (C) sighs with apneic pause >2 s following 1–3 normal breaths. We investigated preterm and term infants with 12 h nocturnal polygraphic recording. Sighs were more frequent in preterm than in term infants and more so during REM sleep than non-REM sleep. The part of sighs B of total number of sighs increased with gestational age. During REM sleep sighs without apnea were predominant, whereas apnea-associated sighs were mainly found during non-REM sleep.

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