massive-pontine-hemorrhage-by-dual-injection-of-autologous-blood

Massive Pontine Hemorrhage by Dual Injection of Autologous Blood

We provide a protocol to establish a massive pontine hemorrhage model in a rat. Rats weighing about 250 grams were used in this study. One hundred ...

the second affiliated hospital of Guangzhou medical university

Intraluminal suture middle cerebral artery occlusion (MCAO) model is the most frequently used model for ischemic stroke. However, the success rate of this model is variable among different research studies. This study aimed to investigate the effect of postischemic temperature on the success rate. A total of 100 C57BL/6 mice were randomized into two groups: control group (n=50), body temperature was allowed to self-regulate after MCAO; temperature-controlled group (n=50), mice were kept warm in an incubator for 12 h after MCAO. The body temperature of animals was measured before, during, and for 12 h after MCAO. Neurological deficits and infarct volumes were measured at 24 h after MCAO. There was significant difference (P<0.05) of the body temperature between the two groups from 0.5 h to 3.5 h post ischemia. Moreover, there was obvious difference between the success rates of the two groups (control group: 52%, temperature-controlled group: 84%, P<0.05). In the successful models, infarct volume was significantly (P<0.05) higher in temperature-controlled group (53.44%±9.83%, n=42) than control group (45.63%±10.24%, n=26). There was significant difference of the modified neurological severity scores (P<0.05), left adhesive tests (P<0.05) between the two groups. Our data demonstrated that postischemic warming contributed to the success of mouse MCAO model.

Keep warm and get success: the role of postischemic temperature in the mouse middle cerebral artery occlusion model.

Astrocytes, the most numerous cells in the human brain, play a central role in the metabolic homeostasis following hypoxic injury. Caveolin-1 (Cav-1), a transmembrane scaffolding protein, has been shown to converge pro-survival signaling in the central nerve system. The present study aimed to investigate the role of Cav-1 in the hypoxia-induced astrocyte injury. We also examined how Cav-1 alleviates apoptotic astrocyte death. To this end, primary astrocytes were exposed to oxygen-glucose deprivation (OGD) for 6 h and a subsequent 24 h reoxygenation to mimic hypoxic injury. OGD significantly reduced Cav-1 expression. Downregulation of Cav-1 using Cav-1 siRNA dramatically worsened astrocyte cell damage and impaired cellular glutamate uptake after OGD, whereas overexpression of Cav-1 with caveolin-1 scaffolding domain peptide attenuated OGD-induced cell apoptosis. Mechanistically, the expressions of Ras-GTP, p-Raf and p-ERK were sequestered in Cav-1 siRNA-treated astrocytes, yet were stimulated after supplementation with caveolin peptide. MEK/ERK inhibitor U0126 remarkably blocked the Cav-1-induced counteraction against apoptosis following hypoxia, indicating Ras/Raf/ERK pathway is required for the Cav-1's pro-survival role. Together, these findings support Cav-1 as a checkpoint for the in hypoxia-induced astrocyte apoptosis and warrant further studies targeting Cav-1 to treat hypoxic-ischemic brain injury.

Caveolin-1 is a checkpoint regulator in hypoxia-induced astrocyte apoptosis via Ras/Raf/ERK pathway.

Vascular endothelial growth factor (VEGF) has been recognized to be a potential pharmaceutical target for treating ischemic stroke, but its severe side effects hinder its widely application. Here, the present study was designed to investigate the effects of VEGF on blood-brain-barrier (BBB) disruption and the underlying mechanisms.

Vascular endothelial growth factor aggravates cerebral ischemia and reperfusion-induced blood-brain-barrier disruption through regulating LOC102640519/HOXC13/ZO-1 signaling.

Researches involving arterial pressure measurements in mice have primarily relied on carotid arterial catheterization. However, in some circumstances, measuring arterial pressure through the carotid arterial impairs accuracy. This study was aimed to evaluate whether femoral artery could displace carotid artery for the blood pressure (BP) measurements in mice. Fifty-six  mice ( = 14 in each group) were randomized into four groups: control, left femoral artery, right femoral artery, and union group, in which BP was measured through left carotid, left femoral, right femoral artery, and simultaneously from right femoral artery and left carotid artery, respectively. Arterial pressure was recorded for 5 min after catheterization. There was no significant difference of the success rate and mortality rate among four groups (> 0.05), and no obvious difference (> 0.05) of catheterization time among the first three groups. For intergroup comparison of arterial pressure, there was no significant difference (> 0.05) of the systolic blood pressure (SBP), diastolic BP, mean arterial pressure, and pulse pressure among the first three groups. For intragroup comparison, SBP, diastolic blood pressure (DBP), mean arterial pressure (MAP) monitored from right femoral artery were similar (> 0.05) with those from left carotid artery, with significantly positive correlation. The mean values of difference of SBP, DBP, and MAP were -1.3, 1.2, and 0.5 mmHg, respectively. Our results indicated that femoral artery catheterization could be a safe, feasible, reliable, and accuracy alternative for the direct measurement of arterial pressure in anesthesia mice.

Li Wu

the second affiliated hospital of Guangzhou medical university

Massive Pontine Hemorrhage by Dual Injection of Autologous Blood