Abstract
In order to approach an understanding of the mechanism underlying the appearance of the reversal of vasomotor reflexes produced by increase in either strength or frequency of the sciatic nerve stimulation, an attempt has been made to observe vasomotor changes in both nonanesthetized and anesthetized cats. The animals were either prebulbarly decerebrated, or were immobilized with Flaxedil. The vagal nerves were bilaterally severed.
1) In nonanesthetized cats, depression of blood pressure was not elicited by the stimulation of the sciatic nerve. The responses always were elevation of blood pressure at each frequency of 2, 5, 50 and 100/sec. The elevation was obtained even with brief pulse duration of 0.01 msec.
2) After intravenous administration of Nembutal in the dose of 3-5 mg/kg, depression of blood pressure was obtained with weak stimulation at the frequencies of 2 and 5/sec. After intravenous administration of 6-9 mg/kg Nembutal, the depression was elicited with weak stimulation at the frequencies of 50 and 100/sec. Therefore, the reversal of vasomotor reflexes from a depressor to a pressor, was produced by increase in either strength or frequency of stimulation.
3) In nonanesthetized cats, depression of blood pressure was not elicited by the stimulation of the depressor area of Wang and Ranson (1939)8) or of Alexander (1946)1) in the bulbar reticular formation. However, the depression was obtained by the stimulation of this area after intravenous adnmistration of 6-9 mg/kg Nembutal.
From these results, it was suggested that anesthetic suppression of the pressor center in the bulbar reticular formation plays an important role in producing the reversal of vasomotor reflexes.
The present study has been supported by grants from the Rockefeller Foundation and from the Japanese Ministry of Education.
