ABSTRACT
Objective To investigate the effects of insulin on vascular diameter of the peri -infarct region and infarct volume after cerebral infarction in mice. Methods Forty male C57/BL6j mice w ere randomly divided into a control group ( n = 5), a cerebral infarction group ( n = 15), a cerebral insulin resistance group (n = 5), and a cerebral insulin resistance infarction group ( n = 15). A model of cerebral infarction w as induced by the photochemical method. A model of cerebral insulin resistance w as induced by intracerebroventricular injection of streptozocin. Tw o -photon confocal microscope w as used to in vivo evaluate the changes of vascular diameter in the peri-infarct region at 20 min after insulin injection into the cerebelomedulary cistern. After modeling of cerebral infarction, artificial cerebrospinal fluid or insulin (10 ng/ml) w as immediately injected into the cerebelomedulary cistern, and the effect of insulin on cerebral infarct volume w as evaluated at 24 h after infarction. Results Insulin did not have significant effect on various types of cerebral vascular diameters in the normal control group, but it significantly contracted cerebral arteries ( -23.16% ±6.86% and -23.32% ±6.40%, respectively; al P <0.001) and penetrating arteries ( -15.20% ±5.51% and -16.40% ±4.27%, respectively; al P < 0.001) in the cerebral insulin resistance group and the cerebral insulin resistance infarction group, but it did not have any effect on the diameters of the cerebral veins. There w ere no significant differences in the vasoactive effects of insulin betw een the cerebral infarction group and the normal control group, as w el as betw een the cerebral insulin resistance group and the cerebral insulin resistance infarction group. Insulin significantly reduced the volume of cerebral infarction in the cerebral infarction group (9.0 ±1.0 mm3 vs.6.0 ±1.2 mm3; t = 4.294,P =0.002), and it did not have significant effect on the volume of cerebral infarction in the cerebral insulin resistance infarction group ( 12.6 ±2.3 mm3 vs.11.6 ±1.7 mm3; t = 0.782, P = 0.456). Conclusions Insulin can reduce ischemic brain injury in normal mice and can not affect the cerebrovascular diameter of the peri-infarct region. The neuroprotective effect of insulin is not significant in cerebral insulin resistance in mice, and it may be associated w ith the vasoconstrictor effects of insulin in the peri -infarct region.
ABSTRACT
Objective To examine cerebrovascular reactivity to CO2 inhalation in mice. Methods In vivo Two-Pho?ton imaging technique was used to record the reaction of cerebral cortical vessels including penetrating artery, surface vein and capillary in 5 male C57 mice after CO2 inhalation under a thinned-skull cranial window. Nitric oxide syntheses inhibitor L-NAME and Prostaglandin syntheses inhibitor Indomethacin were used to block different vasodilator pathways, respectively. Results Different mouse cortical vessels displayed different degrees of dilation to 1-minute 5%CO2 inhala?tion. The penetrating artery exhibited the most obvious dilation (45.01%±4.45%). L-NAME intervention significantly di?minished cerebravascular CO2 reactivity(P<0.05). Indomethacin significantly attenuated the dilation of artery but not capillary comparing with L-NAME intervention(P<0.05). Conclusions Different vessels react differently to CO2 inhala?tion in which postaglandins and NO signal pathways are involved.