Differing effects of vasopressin on regional cerebral blood flow of dogs following intracisternal vs. intra-arterial administration

• Published in: Life sciences (1973) Vol. 54; no. 15; pp. PL241 - PL246
• Main Authors: Tsugane, Shinichiro, Suzuki, Yoshio, Kano, Takahisa, Takayasu, Masakazu, Shibuya, Masato, Sugita, Kenichiro
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 1994; Elsevier
• Subjects: Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Cerebrovascular Circulation - drug effects; Cisterna Magna; Dogs; Female; Fundamental and applied biological sciences. Psychology; Hormones and neuropeptides. Regulation; Hypothalamus. Hypophysis. Epiphysis. Urophysis; Injections; Injections, Intra-Arterial; Male; Nitric Oxide - antagonists & inhibitors; omega-N-Methylarginine; Vasopressins - administration & dosage; Vasopressins - pharmacology; Vertebrates: endocrinology; Fissipedia; Carnivora; Intracisternal administration; Central nervous system; Peripheral hemodynamics; Route of administration; Vasopressin; Vertebrata; Mammalia; Animal; Parietal cortex; Neurohypophyseal hormone; Intraarterial administration; Dog; Comparative study; Brain (vertebrata)
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/0024-3205(94)00424-2

We investigated the differential effect of the intracisternal and intraarterial administration of vasopressin on the regional cerebral blood flow (rCBF) in the parietal cortex of dogs. Regional CBF, velocity and blood volume were assayed by laser flowmetry. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF and velocity, without affecting blood volume. However, the intravertebral arterial injection of 1 nmol vasopressin significantly decreased the rCBF and velocity. This discrepancy can be explained by a difference in the affected vasculature; large blood vessels in the subarachnoid space vs. whole cerebral vascular system. The intracisternal and intraarterial injection of the nitric oxide inhibitor N G-monomethyl-L-arginine reduced the rCBF from the base line, and significantly suppressed the rCBF elevation induced by vasopressin. The effect of vasopressin may be considered as the summation of the increased flow from the dilated large vessels via the release of nitric oxide from the endothelium, and of the decreased flow from the contracted small vessels.