This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by INGENITO, A. J. Articles by PROCITA, L. Search for Related Content PubMed PubMed Citation Articles by INGENITO, A. J. Articles by PROCITA, L.

(Stroke. 1971;2:67.)
© 1971 American Heart Association, Inc.

---

An Analysis of the Effects of Nicotine on the Cerebral Circulation of an Isolated, Perfused, in situ Cat Brain Preparation

ALPHONSE J. INGENITO PH.D.¹; JAMES P. BARRETT PH.D., M.D.²; LEONARD PROCITA PH.D.¹

¹ Department of Pharmacology, Albany Medical College, Albany, New York, 12208
² Department of Pharmacology, Albany Medical College, Albany, New York, 12208; Department of Medicine, Germantown Hospital, Philadelphia, Pennsylvania

Department of Pharmacology, Albany Medical College, Albany, New York, 12208

To determine the effects of nicotine HCl on the cerebral circulation of the cat, without the complicating actions of the drug at other sites in the body, the drug was perfused at concentrations of 1, 10 and 100 µg/ml through a vascularly isolated, perfused in situ cat brain preparation. Cats having selective section of cranial nerves 9, 10, 11 and 12 and the cervical sympathetic trunks comprised various experimental groups. Nicotine was also perfused through an isolated, denervated hindlimb of the same cat for comparative purposes. Nicotine caused only a mild and transient vasoconstriction of the cerebral circulation, mediated primarily by stimulation of the superior cervical ganglia, and a small direct cerebral vasoconstrictor component. An acute tolerance to the cerebral vasoconstrictor effects of repeated increments of nicotine was also observed. The cerebral vasoconstrictor effect of nicotine was diminished in the presence of intact vagi, suggesting a cerebral vasodilator role for these nerves. In contrast, the effect of nicotine on the denervated hindlimb vasculature was a weak but sustained vasodilation. The mechanism of action of nicotine on the cerebral circulation is discussed along with the relevance of these findings to the potential health hazards of tobacco smoking in individuals with cerebrovascular insufficiency.

Note:
Present address: Department of Medicine, Germantown Hospital, Philadelphia, Pennsylvania.

Key Words: cerebral vasoconstriction • innervation of cerebral circulation • vagal cerebral vasodilation • smoking and cerebral ischemia • nicotine and hindlimb circulation • nicotine tolerance