Cerebrovascular changes in the rat brain in two models of ischemia

Olalekan Michael Ogundele; Duyilemi Chris Ajonijebu; Philip Adeyemi Adeniyi; Olusoji Ibukunoluwa Alade; Wasiu Gbolahan Balogun; Ansa Emmanuel Cobham; Azeez Olakunle Ishola; Amin Abdulbasit

doi:10.1016/j.pathophys.2014.08.002

Cerebrovascular changes in the rat brain in two models of ischemia

Pathophysiology. 2014 Sep;21(3):199-209. doi: 10.1016/j.pathophys.2014.08.002. Epub 2014 Aug 10.

Authors

Olalekan Michael Ogundele¹, Duyilemi Chris Ajonijebu², Philip Adeyemi Adeniyi³, Olusoji Ibukunoluwa Alade⁴, Wasiu Gbolahan Balogun⁴, Ansa Emmanuel Cobham⁴, Azeez Olakunle Ishola⁴, Amin Abdulbasit⁵

Affiliations

¹ Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria. Electronic address: ola.ogundele@abuad.edu.ng.
² Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria.
³ Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria.
⁴ Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, Kwara State, Nigeria.
⁵ Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Kwara State, Nigeria.

PMID: 25156812
DOI: 10.1016/j.pathophys.2014.08.002

Abstract

Background: Vascular occlusion and cyanide neurotoxicity induces oxidative stress and degeneration in the brain. This oxidant induced stress changes the vascular dynamics of cerebral blood vessels, and participates in homeostatic response mechanisms which balance oxygen supply to hypoxic stress-sensitive neurons. The associated changes in vascular morphology include remodeling of the microvasculature and endothelial changes, alterations in regional circulation and variations in the blood brain barrier (BBB). This study compares alterations in physiology of the cerebral artery after a short-term oxidative stress induced by cyanide toxicity and vascular occlusion.

Method: Adult Wistar rats (N=30) were divided into three groups; vascular occlusion (VO) (n=12), potassium cyanide administration (CN) (n=12) and Control-CO (n=6). The CN rates were treated with 30mg/kg of orally administered KCN while the VO was subjected to global vascular occlusion, both for a duration of 10 days, described as the treatment phase. Control animals were fed on normal rat chow and water for 10 days. At the end of the treatment phase, n=6 animals in each of the VO, CN and VO groups were anesthetized with sodium pentobarbital (50IP) and the CCA exposed, after which pin electrodes were implanted to record the spikes form the tunica media of the CCA. After day 10, treatment was discontinued for these animals, each remaining in the VO and CN groups (VO-I and CN-I) until day 20 (withdrawal phase) following which the spikes were recorded using the procedure described above.

Results/discussion: Vascular occlusion and cyanide toxicity increased vascular resistance in the MCA (reduced lumen thickness ratio) and increased the diameter of the CCA after the treatment phase of 10 days. After 10 days of withdrawal, the VO group showed a reduction in resistance and an increase in the lumen width/wall thickness ratio (LWR) while the CN group showed increased resistance and a reduction in LWR.

Conclusion: Cyanide toxicity increased vascular resistance by inducing degenerative changes in the wall of the artery while vascular occlusion increased resistance through mechanical stress and increased thickness of arterial wall. After the withdrawal phase, vascular resistance diminished in the VO to a significantly greater extent than the CN.

Keywords: Cyanide; Ischemia; Lumen/wall thickness ratio (LWR); Oxidative stress; Perfusion; Stroke.