This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Tanaka, K. Articles by Muramatsu, K. Search for Related Content PubMed PubMed Citation Articles by Tanaka, K. Articles by Muramatsu, K.

Stroke, Vol 20, 668-673, Copyright © 1989 by American Heart Association

ARTICLES

Effects of a selective inhibitor of cyclic AMP phosphodiesterase on the pial microcirculation in feline cerebral ischemia

K Tanaka, F Gotoh, Y Fukuuchi, T Amano, D Uematsu, J Kawamura, T Yamawaki, N Itoh, K Obara and K Muramatsu
Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.

We evaluated the effects of cilostazol, a selective inhibitor of cyclic adenosine monophosphate phosphodiesterase, on the pial vessels of adult cats subjected to endothelial damage followed by middle cerebral artery occlusion. Six cats were treated with cilostazol and four with 30% N,N- dimethylformamide in 70% saline (solvent). The brain surface was irradiated with ultraviolet rays through a cranial window for 3 minutes to selectively damage the endothelium of the pial vessels in both groups. Beginning 32 minutes after termination of the irradiation, the middle cerebral artery was occluded for 30 minutes. Thirty minutes before occlusion, intravenous infusion of 30 micrograms/kg/min cilostazol or 0.1 ml/kg/min solvent was begun and continued until the end of the study. Before occlusion, the infusion of cilostazol induced a significant (p less than 0.05) dilatation while the infusion of solvent produced no significant changes in the diameter of the pial arteries. The pial veins of solvent-treated cats showed significant (p less than 0.05) constriction during occlusion, whereas cilostazol- treated cats exhibited only mild constriction of the pial veins. The formation of platelet thrombi after occlusion was significantly (p less than 0.05) inhibited in the pial veins of cilostazol-treated compared with solvent-treated cats. Similarly, the microcirculation of the pial veins was effectively restored after reopening of the middle cerebral artery in cilostazol-treated compared with solvent-treated cats. Our data suggest that cilostazol is an effective antithrombotic agent as well as a potent vasodilator acting on vascular smooth muscle.

This article has been cited by other articles:

				M. Fukasawa, H. Nishida, T. Sato, M. Miyazaki, and H. Nakaya 6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (Cilostazol), a Phosphodiesterase Type 3 Inhibitor, Reduces Infarct Size via Activation of Mitochondrial Ca2+-Activated K+ Channels in Rabbit Hearts J. Pharmacol. Exp. Ther., July 1, 2008; 326(1): 100 - 104. [Abstract] [Full Text] [PDF]

				S. Y. Park, J. H. Lee, C. D. Kim, W. S. Lee, W. S. Park, J. Han, Y.-G. Kwak, K. Y. Kim, and K. W. Hong Cilostazol Suppresses Superoxide Production and Expression of Adhesion Molecules in Human Endothelial Cells via Mediation of cAMP-Dependent Protein Kinase-Mediated Maxi-K Channel Activation J. Pharmacol. Exp. Ther., June 1, 2006; 317(3): 1238 - 1245. [Abstract] [Full Text] [PDF]

				F. Honda, H. Imai, M. Ishikawa, C. Kubota, T. Shimizu, M. Fukunaga, and N. Saito Cilostazol Attenuates Gray and White Matter Damage in a Rodent Model of Focal Cerebral Ischemia Stroke, January 1, 2006; 37(1): 223 - 228. [Abstract] [Full Text] [PDF]

				M.-J. Kim, K.-G. Park, K.-M. Lee, H.-S. Kim, S.-Y. Kim, C.-S. Kim, S.-L. Lee, Y.-C. Chang, J.-Y. Park, K.-U. Lee, et al. Cilostazol Inhibits Vascular Smooth Muscle Cell Growth by Downregulation of the Transcription Factor E2F Hypertension, April 1, 2005; 45(4): 552 - 556. [Abstract] [Full Text] [PDF]

				S. Y. Park, J. H. Lee, Y. K. Kim, C. D. Kim, B. Y. Rhim, W. S. Lee, and K. W. Hong Cilostazol Prevents Remnant Lipoprotein Particle-Induced Monocyte Adhesion to Endothelial Cells by Suppression of Adhesion Molecules and Monocyte Chemoattractant Protein-1 Expression via Lectin-Like Receptor for Oxidized Low-Density Lipoprotein Receptor Activation J. Pharmacol. Exp. Ther., March 1, 2005; 312(3): 1241 - 1248. [Abstract] [Full Text] [PDF]

				J. M. Choi, H. K. Shin, K. Y. Kim, J. H. Lee, and K. W. Hong Neuroprotective Effect of Cilostazol against Focal Cerebral Ischemia via Antiapoptotic Action in Rats J. Pharmacol. Exp. Ther., March 1, 2002; 300(3): 787 - 793. [Abstract] [Full Text] [PDF]

				S.-i. Hayashi, R. Morishita, H. Matsushita, H. Nakagami, Y. Taniyama, T. Nakamura, M. Aoki, K. Yamamoto, J. Higaki, and T. Ogihara Cyclic AMP Inhibited Proliferation of Human Aortic Vascular Smooth Muscle Cells, Accompanied by Induction of p53 and p21 Hypertension, January 1, 2000; 35(1): 237 - 243. [Abstract] [Full Text] [PDF]

				D. L. Dawson, B. S. Cutler, M. H. Meissner, and D. E. Strandness Jr Cilostazol Has Beneficial Effects in Treatment of Intermittent Claudication : Results From a Multicenter, Randomized, Prospective, Double-blind Trial Circulation, August 18, 1998; 98(7): 678 - 686. [Abstract] [Full Text] [PDF]