The Effects of Clonidine and Prazosin on Heart Rate and Blood Pressure inereased by Ketamine.
10.4097/kjae.1987.20.6.721
- Author:
Man Sik RHEE
1
;
Woong Mo IM
;
Sung Su CHUNG
Author Information
1. Department of Anesthesiology, Chonnam National University Medical School, Kwang-ju, Korea.
- Publication Type:Original Article
- MeSH:
Blood Pressure*;
Brain;
Clonidine*;
Heart Rate*;
Heart*;
Humans;
Ketamine*;
Prazosin*
- From:Korean Journal of Anesthesiology
1987;20(6):721-727
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Ketamine, a dissociative anesthetic, produces an increase in heart rate and blood pressure, but the precise mechanism of the cardiovascular stimulating affects of ketamine is not understood clearly. Clonidine, an antihypertensive agent, is an alpha-2 agonist that appears to act primarily on the CNS, where it apparently produces a decrease in the sympathetic outflow from the brain. Prazosin is antihypertensive agent that appears to evert its vasodilator action through the blockade of postsynaptic alpha-1 receptors. In order to investigate the effects of clonidine and prazosin on the heart rate and blood pressure increased by ketamine, ketamine was administered intravenously following administration of clonidine or prazosin in conscious patients. The results were as follows : 1) Intravenous ketamine (2 mg/kg) produced significant increases in heart rate and blood pressure by as much as 25%. 2) Intravenous clonidine (1.25 ug/kg) produced a decrease in the heart rate by 5 beats per minute and decreased blood pressure significantly. 3) In the clonidine pretreated group (1.25 ug/kg, lV), intravenous ketamine (2 mg/kg/kg, lV) produced significant increases in the heart rate and blood pressure without attenuation with clonidine 4) In the prasosin pretreated group (2 mg/kg~70 kg, PO), ketamine (2 mg/kg, lV) produced increases the in heart rate and blood pressure without attenuation with prasosin. From the above results, it was inferred that the action site of the cardiovascular stimulating effect of ketamine isn't a postsynaptic alpha-1 receptor and is different from the action site of clonidine.
