@article {Haws24, author = {C W Haws and J K Gourley and D D Heistad}, title = {Effects of nimodipine on cerebral blood flow.}, volume = {225}, number = {1}, pages = {24--28}, year = {1983}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {The purposes of this study were to compare the effects of the calcium entry blocker nimodipine (Bay e 9736) on blood flow with brain and other organs and to examine effects on regional cerebral blood flow. Cerebral blood flow was measured by the microsphere method. Determinations were made during intracarotid and i.v. nimodipine infusions in anesthetized and unanesthetized rabbits. In unanesthetized rabbits, i.v. infusion of 0.1 micrograms/kg x min nimodipine produced a 2-fold increase in cerebral blood flow and a 1.5-fold increase in myocardial flow without an increase in blood flow to other organs and with a small decrease in arterial pressure. A dose of 1.0 micrograms/kg x min produced further increases in flow to brain, myocardium and muscle despite reducing arterial pressure. Blood flow increased significantly in both cerebral gray and white matter and increased similarly in cerebrum, cerebellum and brainstem. In anesthetized rabbits, intracarotid infusion of nimodipine produced dose-dependent increases in cerebral blood flow; i.v. nimodipine produced an increase in cerebral blood flow with no change in cerebral O2 consumption. Thus, at low doses that have little effect on aortic pressure, nimodipine causes a selective increase in cerebral and myocardial blood flow. Nimodipine increases blood flow in all regions of the brain. The increase in blood flow is the result of a direct vasodilator effect and is not secondary to increased cerebral metabolism.}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/225/1/24}, eprint = {https://jpet.aspetjournals.org/content/225/1/24.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }