Effects of propofol, midazolam and thiopental sodium on outcome and amino acids accumulation in focal cerebral ischemia-reperfusion in rats.
- Author:
Lianhua CHEN
1
;
Qinyan GONG
;
Changsi XIAO
Author Information
- Publication Type:Journal Article
- MeSH: Adenosine Triphosphate; metabolism; Animals; Brain; metabolism; Brain Edema; drug therapy; Brain Ischemia; metabolism; Excitatory Amino Acids; metabolism; Male; Midazolam; pharmacology; Myocardial Infarction; drug therapy; Neuroprotective Agents; pharmacology; Propofol; pharmacology; Rats; Rats, Sprague-Dawley; Reperfusion Injury; prevention & control; Thiopental; pharmacology
- From: Chinese Medical Journal 2003;116(2):292-296
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of propofol, midazolam and thiopental sodium on outcomes and amino acid accumulation in focal cerebral ischemia-reperfusion in rats.
METHODSMale Sprague Dawley (SD) rats were scheduled to undergo 3-hour middle cerebral artery occlusion by intraluminal suture and 24-hour reperfusion. Neurologic outcomes were scored on a 0-5 grading scale. Infarct volume was shown with triphenyltetrazolium chloride staining and measured by an image analysis system. Concentrations of various amino acids (aspartate, glutamate, glycine, taurine, and gama-aminobutyric acid) were measured after 3 hours of reperfusion using high performance liquid chromatography. Propofol, midazolam and thiopental sodium were given intraperitoneally at the beginning of reperfusion.
RESULTSBoth propofol and midazolam attenuated neurological deficits and reduced infarct and edema volumes. Propofol showed better neurological protection than midazolam while thiopental sodium did not exhibit any protective effect. Both propofol and midazolam decreased excitatory amino acids accumulation, while propofol increased gama-aminobutyric acid accumulation in ischemic areas in reperfusion.
CONCLUSIONPropofol and midazolam, but not thiopental sodium, may provide protective effects against reperfusion induced injury in rats subjected to focal cerebral ischemia. This neurological protection may be due to the acceleration of excitatory amino acids elimination in reperfusion.