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NEUROSURGICAL ANESTHESIOLOGY

The Effects of Transient Cerebral Ischemia on Vasopressin-Induced Vasoconstriction in Rabbit Cerebral Vessels

Masahiko Kumazawa, MD^*, Hiroki Iida, MD^*, Masayoshi Uchida, MD, Mami Iida, MD, Motoyasu Takenaka, MD^*, Naokazu Fukuoka, MD^*, Tomohiro Michino, MD^*, and Shuji Dohi, MD^*

From the *Department of Anesthesiology and Pain Medicine, Gifu University Graduate School of Medicine, Gifu City, Gifu, Japan; Department of Anesthesiology and Critical Medicine, Oregon Health and Science University, Portland, Oregon; and Department of Cardiology, Gifu University Graduate School of Medicine; Gifu City, Gifu, Japan.

Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology and Pain Medicine, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu City, Gifu 501-1194, Japan. Address e-mail to iida{at}gifu-u.ac.jp.

Abstract

BACKGROUND: Vasopressin is a drug of choice for use during cardiopulmonary resuscitation because several experimental studies have shown that it is better than epinephrine at increasing systemic perfusion pressure and improving cerebral perfusion pressure without increasing myocardial oxygen consumption. We used a pial window preparation to determine the effects of vasopressin when applied topically to pial vessels and whether any effects were altered after cerebral ischemia in rabbits (n = 27).

METHODS: We first examined the effects of topical application of arginine-vasopressin (AVP) (10^–11 M, 10^–9 M, 10^–7 M, and 10^–5 M, sequentially). We then examined the effects of topical application of AVP (10^–9 M and 10^–7 M, sequentially) before and after a 5-min intervention consisting of cerebral ischemia produced by inflation of a neck tourniquet plus systemic hypotension or systemic hypotension alone.

RESULTS: Pial arteriolar diameters were (a) dilated by 10^–11 M AVP [7% ± 11% (P = 0.014 versus baseline)], but constricted by 10^–9 M, 10^–7 M, and 10^–5 M AVP [7% ± 14%, 20% ± 14%, and 16% ± 16% (each P < 0.05), respectively], and (b) constricted before hypotension (7% ± 10% at 10^–9 M, 20% ± 15% at 10^–7 M) or ischemia (7% ± 11% at 10^–9 M, 21% ± 15% at 10^–7 M). However, after the 5-min of ischemia, the decrease in diameter induced by 10^–7 M AVP was significantly reduced but not by hypotension alone [hypotension control group: 7% ± 10% at 10^–9 M, 19% ± 14% at 10^–7 M; ischemia group: 5% ± 11% at 10^–9 M, 10% ± 13% at 10^–7 M (P = 0.35 versus hypotension control)].

CONCLUSIONS: Topical application of AVP (except at the lowest concentration used here) induced concentration-dependent vasoconstriction of pial arterioles in anesthetized rabbits. The vasoconstrictor effect of 10^–7 M AVP was reduced after transient (5-min) cerebral ischemia.