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William I. Rosenblum, MD

Arch Neurol. 1970;23(3):266-270.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

CONSTRICTION of cerebral arterioles has recently been observed over areas of experimental infarction.^1,2 The mechanism of this constriction is not understood, but it has been stated that the segmental constriction illustrated in these reports² does not resemble passive collapse due to reduced perfusion pressure.¹ Instead, it has been suggested that some chemical agent is released from the ischemic tissue, and that this hypothetical substance produces the constriction observed.¹ Since perfusion pressure is reduced in the area of infarction, it occurred to us that at least one other factor might account for the vasoconstriction beside the regional release of a vasoconstrictor. This factor would be an increased sensitivity of the vessels to a constricting influence. Although many publications have been written about the effect of altered pressure on vascular diameter^3,4 and about the effects of chronic hypertension on cerebrovascular reactivity,⁴ we could find no . . . [Full Text PDF of this Article]

Author Affiliations
Richmond, Va

From the Division of Neuropathology, Medical College of Virginia, Health Science Division, Virginia Commonwealth University, Richmond, Va.

Footnotes
Accepted for publication March 18, 1969.

Reprint requests to Division of Neuropathology, Box 17, Medical College of Virginia, Richmond, Va 23219 (Dr. Rosenblum).

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