Effects of ketamine, midazolam, thiopental, and propofol on brain ischemia injury in rat cerebral cortical slices
Abstract
AIM:
To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices.
METHODS:
Cerebral cortical slices were incubated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine, midazolam, thiopental, and propofol were quantitatively evaluated by ELISA reader of absorbance (A) at 490 nm, which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured.
RESULTS:
Progressive prolongation of OGD resulted in decreases of TTC staining. The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P<0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD (P<0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited the decrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 micromol/L) and thiopental (400 micromol/L) partly attenuated this decrease. Propofol at high concentration (100 micromol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P<0.01).
CONCLUSION:
Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.
Keywords:
To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices.
METHODS:
Cerebral cortical slices were incubated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine, midazolam, thiopental, and propofol were quantitatively evaluated by ELISA reader of absorbance (A) at 490 nm, which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured.
RESULTS:
Progressive prolongation of OGD resulted in decreases of TTC staining. The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P<0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD (P<0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited the decrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 micromol/L) and thiopental (400 micromol/L) partly attenuated this decrease. Propofol at high concentration (100 micromol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P<0.01).
CONCLUSION:
Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.