Hamilton S. Davis

The effect of halothane (fluothane) on the thalamus and midbrain reticular formation.

Emerging as an important anzsthetic agent in the past few years, halothane (fluothane) has undergone many clinical and laboratory investigations. These studies have been directed primarily toward its circulatory and respiratory effects. There have been a few studies of its central nervous system effects with regard to the electroencephalographic changes associated with varying depths of anzsthesial 2 . The work of French, Verzeano and Magoun3 has more recently focused attention on the actions of anzsthetics at subcortical levels, particularly on the ‘reticular activating system’ of the midbrain core. To our knowledge, the effects of halothane on this region have not yet been reported. The present study describes in the cat the effects of halothane on evoked responses in the postero-ventrolateral (PV L) nucleus of the thalamus representing a relay point in the classical lateral afferent systems and in the reticular formation (RF) of the midbrain at the level of the superior colliculus, representing a point in the indirect central afferent system. Results obtained point to a response similar qualitatively, but different quantitatively, to that obtained by previous studies i n this laboratory with other commonly used volatile anzsthetic agen ts4.

Vagomimetic effects of morphine and innovar in man.

EVERAL animal studies have shown the S effects of narcotics, especially morphine, on heart rate (HR), suggesting vagal stimulation.1-5 According to these studies, morphine produces a slowing in HR as a result of both vagal stimulation and sympathetic depression. The present study was undertaken to determine whether morphine or Innovar,@ a widely used mixture which includes the synthetic narcotic fentanyl, has a vagal-stimulant effect in man. If narcotics have this effect, it is reasonable to expect that more atropine would be required to achieve a desired rise in HR. One might also assume that, since atropine in small doses is reported to produce vagal stimulation,6 such small doses in patients given narcotics would further reduce the HR. Larger doses of atropine, however, would be expected to block the cardiac vagal endings and overcome any vagomimetic influence of the narcotics.