The Effect Of Hypertension On Brain Injury After Intracerebral Hemorrhage In Rats

Spontaneous intracerebral hemorrhage (ICH) is a common and often fatal stroke subtype. Community based studies have indicated a mortality of more than 40%, and many survivors are left with significant neurological deficits. Hypertension and ICH are frequently associated. High blood pressure (BP) is found in 90% of patients with ICH and persists for a few days. About 27% of ICH patients have a systolic blood pressure (SBP) of 160 mmHg or greater were found in emergency department. Transient or sustained high BP was thought to increase the risk of continuous bleeding, subsequent rebleeding, or both within the first 24 h after the initial bleeding. The mechanisms that lead to ICH in hypertension people, the consequence of hypertension to hematomal enlargement (HE), and the pathological change after ICH due to hypertension, however, are still not well understood. The optimal management of acute hypertension in the patients with ICH is still to be discussed. Many clinical trails of aggressive blood pressure lowering in acute ICH are still under investigating.Spontaneously hypertensive rats (SHR), derived from Wistar Kyoto rats (WKY), are the typical models of chronic hypertension, that have been used to learn the effects of chronic arterial hypertension on ischemic stroke. In the present study, we investigated the different outcomes, such as hematoma volume, brain edema formation, neuronal death, iron accumulation and neurological deficits after ICH in SHR and WKY rats using both collagenase and blood injection models.Objective:To investigate the effect of hypertension on hematoma volume after ICH in rats. Method:SHR and WKY rats received collagenase infusion into the right basal ganglia to induce ICH. One day after infusion, the rats were killed to determine the hemoglobin content in the brain. Results:All the rats showed severe symptom of ICH 4 hours after collagenase infusion. And 24 hours after infusion, there were no difference of hemoglobin content in brain between the two strains of rats.Objective:To investigate the effect of hypertension on brain edema and hemotoma developing after ICH, as well as the neurological deficits between the SHR and WKY rats. Method:SHR and WKY rats received 100μL autologous whole blood infusion into the right basal ganglia. On day 1 and 3, each group,6 rats were killed to determine the brain water content. Other 6 rats in each group underwent brain MRI 1,3,14 days after ICH. And also, the neurological deficits were tested 1,7,14 days after ICH. Results:1 and 3 days after ICH, the brain water content was slighter in SHR rats, but showed no difference between SHR and WKY rats. The MRI examination showed slighter brain swelling and smaller T2* lesion in SHR rats compared with those in WKY rats 1,3, and 14 days after ICH, while the SHR rats showed more severe neurological deficits and delay neurological recovering 1,7, and 14 days after ICH.Objective:To investigate the brain injury and the protein expression related with the iron metabolism after ICH influenced by hypertension. Method:SHR and WKY rats received 100μL autologous whole blood infusion into the right basal ganglia. On day 1 and 3, Fluoro-Jade C staining was used to detect degenerating neuronal cells, and Western Blot analysis was used to detect HO-1, DNP, Tf, TfR, and Cathepsin D.Results:It showed higher HO-1, Tf, TfR, DNP expression 3 days and higher Cathepsin D levels in the ipsilateral basal ganglia of WKY rats 1 and 3 days after blood injection. But there were more Fluoro-Jade C positive cells detected in the ipsilateral basal ganglia of SHR rats 1 and 3 days after ICH. Two rat ICH models were used in the present study to compare SHR with WKY rats. It indicated:1. Moderate hypertension (systolic BP≤180mmHg) did not enlarge hemotomal volume induced by collagenase infusion in experimental ICH in rats, neither did the brain water content. But it did attenuate the brain swelling and hemotomal lesion detected by imagining.2. Chronic hypertension led more neuronal degenerating and neurological deficits after ICH in rats, and delay neurological recovery.3. Moderate hypertension decreased protein expression related to iron metabolism and intracellular oxidative stress in rat brain after ICH. Also it lessened the neuronal autophagic reaction.In summary, for the patients with a long history of hypertension, it is useful for the neurological rehabilitation to get proper antihypertensive medication. But it also called us to pay more attention to aggressive antihypertensive treatment in acute phase after ICH.