Safety of electroconvulsive therapy in patients with asthma.

BACKGROUND: Patients with depression and other psychiatric disorders being considered for electroconvulsive therapy (ECT) may also have asthma. Since ECT requires the administration of general anaesthesia, it is assumed that extra care should be taken with asthmatic patients before and during ECT. We sought to investigate the safety of ECT in asthmatic patients. METHODS: A retrospective review was conducted of the medical records of all of the patients with currently active and managed asthma who underwent ECT for severe depressive syndromes at Mayo Clinic, Rochester, Minnesota, between 1 January 1998, and 30 June 2006. RESULTS: Thirty-four patients with asthma who also underwent ECT were identified. Of these, 27 (79%) were women. The median age was 45 years (range 23-84 years). All 34 patients were using asthma medications daily at the time of ECT. The 34 patients underwent a total of 459 ECT sessions. Four (12%) patients experienced exacerbation of their asthma on a total of five occasions. Each exacerbation was successfully treated with standard asthma medications, and all four patients completed their courses of ECT. CONCLUSION: ECT in patients with asthma appears to be safe. Although exacerbation of asthma after ECT was rare in our series, a prospective study would be needed to determine the precise risk of pulmonary complications of ECT in asthmatic patients.

Neuropeptide Y phase advances the in vitro hamster circadian clock during the subjective day with no effect on phase during the subjective night.

The mammalian daily (circadian) clock is located in the suprachiasmatic nuclei of the hypothalamus. Clock function can be detected by the measurement of the circadian change in spontaneous firing rate of suprachiasmatic nuclei cells in a brain slice preparation in vitro. We investigated the effects of neuropeptide Y on this rhythm of firing rate in hamster suprachiasmatic nuclei neurons. Slices were prepared using standard techniques. On the 1st day in vitro, neuropeptide Y (200 ng/200 nL; 47 pmol) was applied as a microdrop to the suprachiasmatic nuclei region at various times. Spontaneous single-unit firing was measured for 6-12 h on the 2nd day in vitro. Peak firing rate in treated slices was compared with that of untreated control slices to measure phase shifts induced by the peptide. Neuropeptide Y induced phase advances of circa-3h when applied during the subjective day (ZT 2-10) but did not significantly alter phase when applied during the subjective night. The phase shifts to neuropeptide Y in the hamster tissue in vitro are similar in phase dependency and magnitude to shifts measured in vivo.

Protein kinase C inhibition and activation phase advances the hamster circadian clock.

The mammalian circadian clock is located in the suprachiasmatic nuclei (SCN). Clock function can be detected by the measurement of the circadian change in cellular firing rate of SCN cells in vitro. We investigated the effects of protein kinase C (PKC) inhibition and activation on this rhythm of firing rate in hamster SCN neurons. PKC inhibition by chelerythrine chloride application phase advances the in vitro circadian rhythm during the late subjective night and early subjective morning, Zeitgeber time (ZT) 20-24 and ZT 0-4. No effect of PKC inhibition on clock phase was seen during ZT 6-18. Activation of PKC via phorbol 12-myristate 13-acetate (PMA) phase advanced the clock at all phases tested. Thus, at some circadian phases both inhibition and activation of PKC can advance circadian rhythms.

Inhibition of protein kinase A phase delays the mammalian circadian clock.

The suprachiasmatic nuclei (SCN) contain the mammalian circadian clock whose rhythm of firing rate can be recorded in vitro for several days. Application of a protein kinase A (PKA) inhibitor onto the SCN at Zeitgeber time (ZT) 10 on the first day in vitro phase delayed the rhythm of firing rate expressed by SCN neurons on the subsequent day in vitro. Application of the inhibitor (Rp-cAMPS) at other circadian phases did not phase shift the rhythm. These results suggest that during approximately 1 h in the late subjective day the presence and activity of PKA plays a role in setting the phase of the mammalian circadian clock.

Circadian phase shifts to neuropeptide Y In vitro: cellular communication and signal transduction.

Mammalian circadian rhythms originate in the hypothalamic suprachiasmatic nuclei (SCN), from which rhythmic neural activity can be recorded in vitro. Application of neurochemicals can reset this rhythm. Here we determine cellular correlates of the phase-shifting properties of neuropeptide Y (NPY) on the hamster circadian clock in vitro. Drug or control treatments were applied to hypothalamic slices containing the SCN on the first day in vitro. The firing rates of individual cells were sampled on the second day in vitro. Control slices exhibited a peak in firing rate in the middle of the day. Microdrop application of NPY to the SCN phase advanced the time of peak firing rate. This phase-shifting effect of NPY was not altered by block of sodium channels with tetrodotoxin or block of calcium channels with cadmium and nickel, consistent with a direct postsynaptic site of action. Pretreatment with the glutamate receptor antagonists (DL-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione disodium) also did not alter phase shifts to NPY. Blocking GABAA receptors with bicuculline (Bic) had effects only at very high (millimolar) doses of Bic, whereas blocking GABAB receptors did not alter effects of NPY. Phase shifts to NPY were blocked by pretreatment with inhibitors of protein kinase C (PKC), suggesting that PKC activation may be necessary for these effects. Bathing the slice in low Ca2+/high Mg2+ can block phase shifts to NPY, possibly via a depolarizing action. A depolarizing high K+ bath can also block NPY phase shifts. The results are consistent with direct action of NPY on pacemaker neurons, mediated through a signal transduction pathway that depends on activation of PKC.