Reflex effects of aerosolized histamine on phrenic nerve activity.

Studies were conducted in anesthetized, paralyzed dogs on the effect of aerosolized histamine on phrenic nerve activity. The paralyzed dogs were ventilated in phase with their recorded phrenic nerve activity at a constant inspiratory flow-rate, using a cycle-triggered ventilator. Phrenic nerve activity was measured before and during administration of aerosolized histamine while the inspiratory flow-rate and arterial blood gases were kept constant. In addition, before and after histamine, phrenic nerve activity was recorded for single bursts during which the ventilator was switched off. The effects of histamine on respiratory resistance were prevented by prior administration of isoproterenol and atropine. Although no changes occurred in respiratory resistance, histamine increased the instantaneous magnitude of phrenic nerve activity. The effect was evident early in the inspiratory period and was found even when the lungs were not inflated. Inflation of the lungs excited phrenic nerve activity; this effect increased after histamine. All of these actions of histamine were abolished by vagotomy. We conclude that histamine increased phrenic nerve activity during inspiration by a vagal reflex.

Immunoregulatory cell subsets in Goodpasture's syndrome: evidence for selective T suppressor-cell depletion during active autoimmune disease.

In a patient with documented untreated Goodpasture's syndrome, serial determination of T-cell subsets using monoclonal antibodies and flow cytometry revealed a persistent but variable deficiency of T-suppressor cells during the period of active disease. As the percentage of OKT8+ cells (suppressor/cytotoxic T cells) returned to normal levels, anti-basement membrane autoantibody production decreased and finally disappeared. Possible pathogenetic implications of immunoregulatory cell imbalance specifically in reference to Goodpasture's syndrome are discussed.