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Conference Paper: Brain injury and neurogenesis after intracerebral haemorrhage in hypertensive rats

TitleBrain injury and neurogenesis after intracerebral haemorrhage in hypertensive rats
Authors
KeywordsMedical sciences
Issue Date2010
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk
Citation
The 15th Medical Research Conference; Department of Medicine, The University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 suppl. 1, p. 53, abstract no. 89 How to Cite?
AbstractINTRODUCTION: Effective treatments for intracerebral haemorrhage (ICH) are awaited to reduce its morbidity and mortality. Hypertension is the most important risk factor for ICH. Neurogenesis following ICH in nomotensive rats has been confirmed. In this study, we used a rat renovascular hypertension (RVHT) model, and investigated the effects of hypertension on the pathophysiological and histological changes, and neural stem cell proliferation after induction of ICH. METHODS: RVHT was achieved by applying a silver clip onto the left renal artery. At 6 weeks after renal artery constriction, the mRNA levels of angiogensin II type 1 (AT1) and type 2 (AT2) receptors in the brain were determined by reverse transcription–polymerase chain reaction. ICH was induced by an intrastriatal injection of bacterial collagenase IV in the left brain in both normotensive and hypertensive rats. Left femoral artery was cannulated for continuous monitoring of blood pressure for 4 hours after the induction of ICH. Haematoma volume was quantified at 24 hours after ICH induction. 5’-Bromo-2’-deoxyuridine (BrdU) was used to label cell proliferation from the 6th day to the 9th day after ICH. Rats were killed at 10 days after ICH. BrdU+ and CD31 (an endothelial cell marker) immunoreactive cells were detected using immunofluorescence. Behavioural tests were performed at 1, 3, 7, 10, and 21 days after ICH. RESULTS: RVHT rats showed up-regulation of AT1 receptor in the brain. Following induction of ICH, both the normotensive and RVHT rats demonstrated an acute hypertensive response. As compared to normotensive rats, RVHT rats demonstrated a larger haematoma volume, and greater deficits at all time-points. However, at 10 days after ICH, more BrdU+ cells were detected over the perihaematoma area of RVHT rats than normotensive rats. Moreover, many BrdU+ cells within the ipsilateral basal ganglia of RVHT rats also co-expressed CD31. CONCLUSION: Renovascular hypertension aggravates histological and functional injury partly via up-regulation of AT1 receptor in the brain. Increased brain injury in hypertensive rats induces increased neural stem cell proliferation and angiogenesis after ICH. Experimental ICH in hypertensive rats is a suitable model for evaluation of pathophysiology and treatment of patients with hypertensive ICH.
Persistent Identifierhttp://hdl.handle.net/10722/126380
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorSang, Yen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2010-10-31T12:25:20Z-
dc.date.available2010-10-31T12:25:20Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 15th Medical Research Conference; Department of Medicine, The University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 suppl. 1, p. 53, abstract no. 89en_HK
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/126380-
dc.description.abstractINTRODUCTION: Effective treatments for intracerebral haemorrhage (ICH) are awaited to reduce its morbidity and mortality. Hypertension is the most important risk factor for ICH. Neurogenesis following ICH in nomotensive rats has been confirmed. In this study, we used a rat renovascular hypertension (RVHT) model, and investigated the effects of hypertension on the pathophysiological and histological changes, and neural stem cell proliferation after induction of ICH. METHODS: RVHT was achieved by applying a silver clip onto the left renal artery. At 6 weeks after renal artery constriction, the mRNA levels of angiogensin II type 1 (AT1) and type 2 (AT2) receptors in the brain were determined by reverse transcription–polymerase chain reaction. ICH was induced by an intrastriatal injection of bacterial collagenase IV in the left brain in both normotensive and hypertensive rats. Left femoral artery was cannulated for continuous monitoring of blood pressure for 4 hours after the induction of ICH. Haematoma volume was quantified at 24 hours after ICH induction. 5’-Bromo-2’-deoxyuridine (BrdU) was used to label cell proliferation from the 6th day to the 9th day after ICH. Rats were killed at 10 days after ICH. BrdU+ and CD31 (an endothelial cell marker) immunoreactive cells were detected using immunofluorescence. Behavioural tests were performed at 1, 3, 7, 10, and 21 days after ICH. RESULTS: RVHT rats showed up-regulation of AT1 receptor in the brain. Following induction of ICH, both the normotensive and RVHT rats demonstrated an acute hypertensive response. As compared to normotensive rats, RVHT rats demonstrated a larger haematoma volume, and greater deficits at all time-points. However, at 10 days after ICH, more BrdU+ cells were detected over the perihaematoma area of RVHT rats than normotensive rats. Moreover, many BrdU+ cells within the ipsilateral basal ganglia of RVHT rats also co-expressed CD31. CONCLUSION: Renovascular hypertension aggravates histological and functional injury partly via up-regulation of AT1 receptor in the brain. Increased brain injury in hypertensive rats induces increased neural stem cell proliferation and angiogenesis after ICH. Experimental ICH in hypertensive rats is a suitable model for evaluation of pathophysiology and treatment of patients with hypertensive ICH.-
dc.languageengen_HK
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk-
dc.relation.ispartofHong Kong Medical Journalen_HK
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectMedical sciences-
dc.titleBrain injury and neurogenesis after intracerebral haemorrhage in hypertensive ratsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, RTF: rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros174977en_HK
dc.identifier.volume16en_HK
dc.identifier.issuesuppl. 1en_HK
dc.identifier.spage53en_HK
dc.identifier.epage53-
dc.publisher.placeHong Kong-
dc.description.otherThe 15th Medical Research Conference; Department of Medicine, The University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 suppl. 1, p. 53, abstract no. 89-

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