Cerebralcare Granule, a Chinese herb compound preparation, improves cerebral microcirculatory disorder and hippocampal CA1 neuron injury in gerbils after ischemia-reperfusion.

AIM OF THE STUDY: Cerebralcare Granule (CG) is a Chinese herb compound preparation that has been used for treatment of cerebrovascular related diseases. However, the effect of post-treatment with CG on ischemia and reperfusion (I/R) induced cerebral injury is so far unclear. MATERIALS AND METHODS: In present study, cerebral global I/R was induced in Mongolian gerbils by clamping bilateral carotid arteries for 30 min followed by reperfusion for 5 days, and CG (0.4 g/kg or 0.8 g/kg) was administrated 3h after the initiation of reperfusion. RESULTS: Post-treatment with CG for 5 days attenuated the I/R-induced production of hydrogen peroxide in, leukocyte adhesion to, and albumin leakage from cerebral microvessels, and, meanwhile, protected neuron from death, reduced the number of caspase-3- and Bax-positive cells, and increased Bcl-2-positive cells in hippocampal CA1 region. CONCLUSION: The results suggest that CG given after initiation of reperfusion is able to ameliorate cerebral microvascular dysfunction and hippocampal CA1 neuron damage caused by I/R.

Treatments with lead expedite hyperthermia-induced thromboembolism in mouse pial microvessels.

Three trials were carried out to study the influence of acute and chronic treatments with lead on hyperthermia-induced thromboembolic activity in pial microvessels of adult male mice. Each trial consisted of four groups, 10 mice (approximately 33 g) per group. Three groups were injected with lead acetate dissolved in a 5% glucose solution (vehicle) at doses of 0.1, 0.5 and 1.0 mg/kg and the control group received only the vehicle. Acute treatments were by a single injection made 1 h (i.p.) in one trial and 24 h (i.p.) in another, prior to the a hyperthermic exposure at 45 degrees C. In the third trial, a single injection was given daily (s.c.) for 7 days. Mice were anesthetized by urethane (1-2 mg/kg, i.p.), the trachea was intubated, a craniotomy was performed and the mouse was placed on the microscope stage of an intravital microscopy set-up. Core body and brain surface temperatures were raised first to 37 degrees C, the animal was stabilized for 30 min then only the brain surface temperature was raised to 45 degrees C by heating the irrigating artificial cerebrospinal fluid. The hyperthermic exposure lasted for 45 min. In all trials, lead at the three doses given (low, medium and high) significantly reduced (p < 0.001) the time of initial thromboembolic activity seen. Lead exerted its influence as quickly as in 1 h, even with the low dose administered. Neither the acute nor chronic treatments affected the degree of arteriolar constriction observed or caused venular diameter change. Arteriolar patency rate at the end of experiment was higher for control than for all lead-treated groups. Data evidenced the rapidity of the adverse influence of lead on the susceptibility to thrombosis, in vivo. The enhanced initiation of thrombotic activity may be attributed to facilitated damage to the microvascular endothelium caused by lead, when challenged by hyperthermia.

[The effect of 3-hydroxypyridine derivatives on postischemic disorders in the autoregulatory reactions of the cerebral vessels]. / Vliianie proizvodnykh 3-oksipiridina na postishemicheskie narusheniia autoreguliatornykh reaktsii mozgovykh sosudov.

Acute experiments on nembutal anesthetized rats showed improvement of cerebral blood flow autoregulation in the postischemic period under the effect of mexidol and the new 3-hydroxypyridine (3-HOP) derivatives LBK-10 and LBK-38 administered for prophylactic and therapeutic, purposes. The role of dopaminergic activity, solubility in lipids, and other factors in the mechanism of the activity of 3-HOP derivatives is analysed.

Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone.

The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilatation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alpha-chloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4 x 10(-8) M to 4 x 10(-3) M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5 h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4 x 10(-3) M.(ABSTRACT TRUNCATED AT 250 WORDS)