Occlusion Of Left Common Carotid Artery Research Articles

Amentoflavone attenuates oxidative stress and neuroinflammation induced by cerebral ischemia/reperfusion in rats by targeting HMGB1-mediated TLR4/NF-κB signaling pathway

Surveys indicated that stroke classified among the leading cause of death as well as combined death and disability worldwide resulting in a great loss for the global economy. The present study aims to evaluate the neuroprotective potential of the biflavonoid amentoflavone (AMNT) in alleviating cerebral ischemia/reperfusion (IR) injury in rats, and to elucidate the possible underlying mechanism of an experimental condition with similar circumstances to stroke. Cerebral ischemia was achieved through left common carotid artery occlusion for 60 min, followed by blood flow restoration. Sham-operated control rats subjected to the same surgical process except for brain IR. Rats were orally administered AMNT/ or vehicle for three days’ prior surgical operation, and for another three days after left brain IR. Rats of all groups were assessed for neurological deficits 24 h following brain IR. Each group was divided into two subgroups one for the rotarod testing and biochemical assessment while the other subgroup to perform the activity cage testing, histopathological study, immunohistochemistry, and gene expression analysis. AMNT enhanced brain levels of GSH and CAT activities, suppressed neuroinflammation via reducing the inflammatory cytokines in the serum, and enhanced brain contents of TBK1 and IFNβ. AMNT downregulated TLR4-/NF-κB signaling pathway as a result of the HMGB1 suppression. Moreover, AMNT blocked apoptotic cell death by suppressing the NF-κB signaling pathway and reducing the activation of caspase-3. These findings revealed that AMNT attenuates I/R–induced cerebral injury possibly by regulating the HMGB1-mediated TLR4/NF-kB pathway. Thus, AMNT could provide potential preventive and therapeutic option for cerebral stroke.

Quercetin Exerts a Protective Effect on Ischemic Stroke-induced Memory Deficits in Mice

Objectives Brain injury resulting from an ischemic stroke affects cognitive performance by disrupting the hippocampus. Several processes are involved in brain injury progression, including inflammation, glutamate excitotoxicity, and modulated brain peptide systems such as the melanocortin system. Reports show that quercetin exerts neuroprotective activity. This study investigates quercetin’s role in the cognitive function of ischemic stroke-induced mice and the possible mechanisms involved. Materials and Methods ICR mice were used. The left unilateral common carotid artery occlusion was conducted for 4 h to induce an ischemic stroke in the mice. Quercetin 50, 100, and 200 mg/kg were administered to separate groups intraperitoneally for 7 days. Cognitive function was examined using the T-maze test. The hippocampal mRNA expressions of NR2A, NR2B, melanocortin 4 receptor (MC4R), pro-opiomelanocortin precursors (POMC), and nuclear factor 2 (Nrf2) were examined using reverse transcription-polymerase chain reaction. Results It was found that stroke disrupted cognitive function. Quercetin administration ameliorated cognitive impairment. Quercetin attenuated the stroke-induced decrease in MC4R mRNA expression. Moreover, quercetin suppressed the stroke-induced increase in the hippocampal mRNA expression of NR2A. Conclusion Quercetin ameliorates cognitive deficits and normalizes impaired hippocampal melanocortin and glutamatergic signaling in ischemic stroke-induced mice.

Ischemic Stroke due to Intracerebral Steal from Calvarial Metastasis: a Case Report (P2-5.001)

<h3>Objective:</h3> NA <h3>Background:</h3> Malignancy is an important risk factor for ischemic stroke. Various mechanisms may explain the association between cancer and ischemic stroke, including hypercoagulation, accelerated atherosclerosis, and toxic effects of chemotherapy and radiation. Here, we report a rare case in which a patient with known occlusive radiation vasculopathy (ORV) presented with ischemic strokes caused by an “intracerebral steal” phenomenon from new metastatic calvarial lesions. <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 64-year-old woman with remote history of left neck squamous cell carcinoma and prior left frontal stroke from left common carotid artery (CCA) occlusion secondary to ORV presented to the emergency department with acute-onset right hemiparesis. Brain magnetic resonance imaging revealed scattered infarcts in the convexity of the left hemisphere as well as adjacent calvarial destruction. On functional and structural MRI, the calvarial lesion demonstrated increased vascularity and diffusion restriction. CT angiography redemonstrated complete occlusion of the left CCA and strong right-to-left collateral circulation across the anterior communicating artery. The remainder of the stroke workup, including echocardiogram, laboratory analyses, venous dopplers, and carotid ultrasound was unrevealing. CT scans of the chest, abdomen and pelvis revealed only lytic lesions in the T11 vertebra, left ilium and right sacrum, and biopsy of the latter revealed adenocarcinoma. <h3>Conclusions:</h3> In this patient, neck radiation therapy had resulted in a chronic occlusion of the left CCA. Years later, a hypervascular skull metastasis drew from this limited blood supply, causing ischemic strokes in the parenchyma adjacent to the hypermetabolic calvarial metastasis. This case of an “intracerebral steal” phenomenon demonstrates how hypervascular extradural lesions may also lead to ischemia, particularly in cases of ipsilateral poor hemodynamic reserve. <b>Disclosure:</b> Miss Murthy has nothing to disclose. Dr. Kumar has nothing to disclose. Dr. Testai has received personal compensation in the range of $5,000-$9,999 for serving as an Expert Witness for Swanson Martin &amp; Bell, LLP. Dr. Testai has received publishing royalties from a publication relating to health care. Edward Michals has stock in Off Color Brewing. Edward Michals has received personal compensation in the range of $100,000-$499,999 for serving as a Staff Physician with University of Illinois.

Effect of Mucuna pruriens on brain NMDA receptor and tau protein gene expression in cerebral ischemic rats.

Present study aimed to assess effect of pre-treatment with Mucuna pruriens seed extract and its bioactive molecule(s) on NMDAR and Tau protein gene expression in cerebral ischemic rodent model. Methanol extract of M. pruriens seeds was characterized by HPLC, and β-sitosterol was isolated by flash chromatography. In vivo studies to observe the effect of pre-treatment (28 days) with methanol extract of M. pruriens seed and β-sitosterol on the unilateral cerebral ischemic rat model. Cerebral ischemia induced by left common carotid artery occlusion (LCCAO) for 75min (on day 29) followed by reperfusion for 12h. Rats (n = 48) divided into four groups. GroupI (control,Untreated + LCCAO)-No pre-treatment + cerebral ischemia; GroupII(β-sitosterol + Sham)-pre-treatment with β-sitosterol, 10mg/kg/day + sham-operated; GroupIII(β-sitosterol + LCCAO)-pre-treatment with β-sitosterol, 10mg/kg/day + cerebral ischemia; GroupIV(methanol extract + LCCAO)-pre-treatment with methanol extract of M. pruriens seeds, 50mg/kg/day + cerebral ischemia. Neurological deficit score was assessed just before sacrifice. Experimental animals were sacrificed after 12h reperfusion. Brain histopathology was performed. Gene expression of NMDAR and Tau protein of left cerebral hemisphere (occluded side) was performed by RT-PCR. Results revealed that the neurological deficit score was lower in groups III and IV compared to group I. NMDAR and tau protein mRNA expression in left cerebral hemisphere were upregulated in Group I, downregulated in groups III and IV. Histopathology of left cerebral hemisphere (occluded side) in Group I showed features of ischemic brain damage. Groups III and IV, left cerebral hemisphere showed less ischemic damage compared GroupI. Right cerebral hemisphere showed no areas of ischemia-induced brain changes. Pre-treatment with β-sitosterol and methanol extract of M. pruriens seeds may reduce ischemic brain injury following unilateral common carotid artery occlusion in rats.

Propofol ameliorates ischemic brain injury by blocking TLR4 pathway in mice.

Ischemic brain injury is one of the most serious perioperative complications. However, effective preventative methods have not yet been established. This study aimed to investigate whether propofol has neuroprotective effects against ischemic brain injury, with a specific focus on Toll-like receptor 4 (TLR4). Focal brain ischemia was induced via a combination of left common carotid artery occlusion and distal left middle cerebral artery coagulation in mice. Either propofol (10 mg/kg) or vehicle was intravenously injected 10 min prior to the induction of brain ischemia in wild-type and TLR4 knockout mice. Infarct volume, pro-inflammatory cytokine expression, inflammatory cell infiltration, and neurobehavioral function were assessed. Propofol administration significantly reduced infarct volume in wild-type mice (26.9 ± 2.7 vs 15.7 ± 2.0 mm3 at day 7), but not in TLR4 knockout mice. Compared with the control mice, the propofol-treated wild-type mice exhibited lower levels of IL-6 (0.57 ± 0.23 vs 1.00 ± 0.39 at 24 h), and smaller numbers of TLR4-expressing microglia in the penumbra (11.7 ± 3.1 vs 25.1 ± 4.7 cells/0.1 mm2). In conclusion, propofol administration prior to ischemic brain insult attenuated brain injury by blocking the TLR4-dependent pathway and suppressing pro-inflammatory cytokine production.

N-Nitro-L-Arginine-Methyl ester Exerts Neuroprotection byInhibiting Inflammation in Cerebral Injury Induced by Transient Ischemia/Reperfusion in Rats

Cerebral ischemia-reperfusion injury is a pivotal cause of deaths due to cerebrovascular accidents. Further research efforts are needed to reveal the mechanism underlying its aggravation or alleviation. We previously reported the antioxidant effect of N-Nitro-L-Arginine- Methyl Ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, on rats subjected to transient focal cerebral ischemia-reperfusion (I/R). The aim of this work was to explore further neuroprotective anti-inflammatory effects of L-NAME. This study involved 30 adult male Wistar rats divided into three groups with ten rats in each: sham-operated (control), I/R group of rats subjected to 30 minutes of left common carotid artery (CCA) occlusion followed by 24-hour of reperfusion and test group infused with L-NAME intraperitoneally 15 minutes before the same I/R period. Neurological assessments were evaluated, Western blotting used to estimate Nuclear factor-kappa B (NF-?B), ELISA used to detect Tumor necrosis factor- α (TNF-α), and Nitric oxide metabolites were measured colorimetrically, as well as H&amp;E staining to assess brain damage. Compared with the I/R group, the neurological score, infarction area, and the inflammatory biomarkers NF-?B, TNF-α, and NO were significantly decreased in L-NAME treated rats (P =0.001). As a conclusion from the current study, L-NAME showed potential neuroprotection through it is an anti-inflammatory effect on a rat’s model of transient focal cerebral ischemia-reperfusion.

Single-stage repair for ascending aortic aneurysm, artery stenosis and occlusion of neck vessels caused by Takayasu arteritis

Takayasu arteritis results in a variety of vascular symptoms, and there are some cases in which progressive vascular lesions require surgical intervention. We present a case with ascending aortic aneurysm, right common carotid artery stenosis, left common carotid artery occlusion and left subclavian artery stenosis caused by Takayasu arteritis that was successfully treated with total arch replacement and ascending aorta to right internal carotid artery bypass.

Takayasu arteritis with congestive heart failure in 26-year-old male: a case report

BackgroundTakayasu arteritis (TA) is included in large vessel vasculitis with unknown aetiopathogenesis. TA is one of the rare diseases with a predilection for young women. The diagnosis of TA is difficult due to variation in clinical presentations and non-specific initial symptoms. This case demonstrates rare TA in a young male with congestive heart failure as the predominant manifestation.Case presentationWe report a 26-year-old male presented with severe dyspnea, palpitation, orthopnea, paroxysmal nocturnal dyspnea, and claudication in the left arm. Four limbs blood pressure discrepancy was present. Chest X-ray showed cardiomegaly with calcification aortic arch and pulmonary edema. Echocardiography revealed that left ventricular ejection fraction decreased with severe aortic and mitral valve regurgitation. Computed tomography angiography showed stenosis of the left common carotid artery and total occlusion of the left subclavian artery with collateral artery. There was vascular thickness and calcification from the peri-aortic valve, ascending aorta, aortic arch, and thoracic descending aorta until abdominal aorta with high-grade stenosis on the inferior side of the renal artery branching accompanied by a post-stenotic dilatation.ConclusionsThis patient’s heart failure was precipitated by secondary hypertension and aortic regurgitation caused by vasculitis of TA. In general, there is no difference in the management of congestive heart failure in patients with TA. Optimized pharmacology therapy with combination steroid and methotrexate successfully inducing remission of TA after 3-months follow-up.

Ruptured anterior communicating artery aneurysms associated with left common carotid artery occlusion due to Takayasu arteritis: an autopsy case report

Ruptured anterior communicating artery aneurysms associated with left common carotid artery occlusion due to Takayasu arteritis: an autopsy case report

A case of blunt left common carotid artery occlusion with right high rib fractures and transverse process fracture of the cervical spine

A case of blunt left common carotid artery occlusion with right high rib fractures and transverse process fracture of the cervical spine

Thyroid Necklace: Communicating Branches Between External Carotid Arteries Through the Superior Thyroid Arteries

A 79 year old female with headache, syncope, mild aphasia, and dysarthria was diagnosed with a left common carotid artery occlusion. Computed tomography angiography showed a necklace (A, white arrow) of extracranial communications between external carotid arteries through the superior thyroid arteries. This symptomatic patient underwent a hybrid procedure including distal common carotid endarterectomy, retrograde recanalisation of the occlusion, and covered stent implantation (7 x 50 mm and 8 x 100 mm Viabahn, W.L. Gore Associates, Inc, Flagstaff, AZ, USA). The post-operative course was uneventful, with symptom relief and patency of the common and internal carotid arteries (B).Image 1

Takayasu's Arteritis with Symptomatic Brachiocephalic Artery Stenosis and Left Common Carotid Artery Occlusion Undergoing Partial Arch Replacement after Coronary Artery Bypass Grafting

Takayasu's Arteritis with Symptomatic Brachiocephalic Artery Stenosis and Left Common Carotid Artery Occlusion Undergoing Partial Arch Replacement after Coronary Artery Bypass Grafting

Carotid Ulceration in a Young Woman with SAPHO Syndrome

A 25 year old woman was recently diagnosed with SAPHO (synovitis-acne-pustulosis-hyperostosis-osteitis) syndrome. On magnetic resonance imaging, performed for chronic left sternoclavicular pain, incidental left common carotid artery (CCA) occlusion was diagnosed. During further diagnostic work up, duplex ultrasound also revealed newly appeared but asymptomatic intima-media ulceration of the contralateral CCA, (A, arrow), confirmed by computed tomography (B, right CCA ulceration, arrow; left CCA occlusion, asterisk). Characteristic arterial involvement associated with recurrent oral ulceration and skin lesions indicated Behçet's disease. Treatment included steroids, methotrexate, and infliximab. Duplex ultrasound after two weeks revealed healing of the ulcerated right CCA, with intimal regeneration clearly noted.Image 1

Neuroprotective effect of astrocyte-derived IL-33 in neonatal hypoxic-ischemic brain injury

BackgroundInterleukin-33 (IL-33) is a well-recognized pleiotropic cytokine which plays crucial roles in immune regulation and inflammatory responses. Recent studies suggest that IL-33 and its receptor ST2 are involved in the pathogenesis of neurological diseases. Here, we explore the effect of IL-33/ST2 signaling in neonatal hypoxic-ischemic (HI) brain injury and elucidate the underlying mechanisms of action.MethodsThe brain HI model was established in neonatal C57BL/6 mice by left common carotid artery occlusion with 90 min hypoxia and treated with IL-33 at a dose of 0.2 μg/day i.p. for 3 days. TTC staining and neurobehavioral observation were used to evaluate the HI brain injury. Immunofluorescence and flow cytometry were applied to determine the expression of IL-33 and its receptor ST2 on brain CNS cells and cell proliferation and apoptosis. OGD experiment was used to assay the viability of astrocytes and neurons. RT-qPCR was used to measure the expression of neurotrophic factor-associated genes.ResultsThe expression level of IL-33 was markedly enhanced in astrocytes 24 h after cerebral HI in neonatal mice. Exogenous delivery of IL-33 significantly alleviated brain injury 7 days after HI, whereas ST2 deficiency exacerbated brain infarction and neurological deficits post HI. Flow cytometry analyses demonstrated high levels of ST2 expression on astrocytes, and the expression of ST2 was further elevated after HI. Intriguingly, IL-33 treatment apparently improved astrocyte response and attenuated HI-induced astrocyte apoptosis through ST2 signaling pathways. Further in vitro studies revealed that IL-33-activated astrocytes released a series of neurotrophic factors, which are critical for raising neuronal survival against oxygen glucose deprivation.ConclusionsThe activation of IL-33/ST2 signaling in the ischemic brain improves astrocyte response, which in turn affords protection to ischemic neurons in a glial-derived neurotrophic factor-dependent manner.

Intra-arterial in-situ bevacizumab injection effect on angiogenesis. Results on a swine angiogenesis model

Background and purposeIn this study we tested the effect of antiangiogenics on a swine angiogenesis model that shares some brain AVM histological characteristics. The objective was to determine bevacizumab effects on retia volumes and on vessels’ wall. Materials and methodsFifteen pigs were divided into 3 groups: Five animals served as controls (group A), 5 animals underwent endovascular left external and common carotid artery occlusion (group B) and 5 animals underwent the same procedure and had an intra-arterial in-situ injection of bevacizumab (groupC) 2 months after the occlusion. A DSA associated with 3D-rotational angiography was performed at day 0 and at 3 months in all groups in order to measure rete mirabile volumes. The animals were sacrificed at 3 months and the retia were harvested for pathological and immunohistochemistry examinations. ResultsAll VEGF-A receptors were blocked at the site of injection and there was a local enhanced endothelial proliferation and apoptosis. The volume of the retia remained unchanged after the bevacizumab injection. Retia vessels presented comparable media thickness, higher endothelial proliferation and apoptosis after the anti-VEGF injection. ConclusionA single in-situ injection of bevacizumab in this swine angiogenesis model showed no change in retia volume and an extensive blockage of VEGF receptors at the site of injection one month later. Rete mirabile vessels presented comparable media thickness, higher endothelial proliferation and apoptosis after the anti-VEGF injection, suggesting that bevacizumab antiangiogenic effect does not fragilize vessel wall. More studies are needed to confirm these preliminary insights of in-situ antiangiogenic effect on vascular malformations.

Neuroprotective effects of neurotropin in a mouse model of hypoxic-ischemic brain injury.

Ischemic-hypoxic insult leads to detrimental effects on multiple organs. The brain is especially vulnerable, and it is hard to regenerate once damaged. Currently, therapeutic options are very limited. Previous studies have reported neuroprotective effects of neurotropin, a non-protein extract derived from the inflamed skin of rabbits inoculated with vaccinia virus, using a murine model of peripheral nerve injury and cultured cell lines. However, whether neurotropin might have protective effects against brain injuries remains unclear. We, therefore, investigated the neuroprotective effect of neurotropin and possible underlying mechanisms, using a mouse model of hypoxic-ischemic brain injury. Hypoxic-ischemic brain injury was induced via a combination of the left common carotid artery occlusion and exposure to hypoxic environment (8% oxygen) in adult male C57BL/6 mice. Immediately following induction of hypoxia-ischemia, mice received either saline or 2.4 units of neurotropin. The survival rate, neurological function, infarct volume, and expression of inflammatory cytokines were evaluated. Compared to the control group, the neurotropin group exhibited a significantly higher survival rate (100% vs. 62.5%, p < 0.05) and lower neurological deficit scores (1; 0-2 vs. 3; 0-5, median; range, p < 0.05) after the hypoxic-ischemic insult. The administration of neurotropin also reduced infarct volume (18.3 ± 5.1% vs. 38.3 ± 7.2%, p < 0.05) and mRNA expression of pro-inflammatory cytokines. The post-treatment with neurotropin improved survival and neurological outcomes after hypoxic-ischemic insult. Our results indicate that neurotropin has neuroprotective effects against hypoxic-ischemic brain injury by suppressing pro-inflammatory cytokines.

Abstract TP573: Nrf2 Activation With Sulforaphane Reduces Post-Stroke Cognitive Impairment in Mice

Introduction: Post-stroke dementia is common in stroke patients and oxidative stress may contributes to its pathogenesis. Nuclear factor erythroid 2 related factor (Nrf2) is a master transcription factor regulating the expression of a series of anti-oxidative enzymes. Sulforaphane (Sfn) is a dietary Nrf2 activator rich in cruciferous vegetables. This study aims to test our hypothesis that Sfn treatment reduces white matter injury and cognitive impairment after ischemic stroke. Methods: Adult male and female wildtype and Nrf2 knockout mice were randomly and blindly assigned into sham, vehicle, and Sfn-treatment groups (n=8-10). Stroke was induced in mice by direct coagulation of the left distal middle cerebral artery and permanent ligation of left common carotid artery occlusion. Sfn in PBS was administered by intraperitoneal injection (20 mg/kg) starting after the surgery and subsequently every other day for 5 weeks. Sensorimotor deficits were assessed using Rota-rod and foot fault tests 3-35 d and cognitive impairment were determined using Morris water maze test 29-34 d after surgery. Brain tissue loss was assessed at 35 d after surgery. In vitro, primary neuronal cultures were treated with vehicle or Sfn (1.5 μM) and chronic hypoxia/ischemia was then induced by incubation with cobalt chloride (250 μM) for 48 h. Neuronal viability was assessed with MTT assay. Results: Wildtype mice exhibited significantly sensorimotor deficits and long-term cognitive impairment after stroke. Sfn treatment alleviated these sensorimotor deficits, long-term cognitive impairment, and brain infarct size in wildtype mice. Nrf2 knockout mice also exhibited significantly sensorimotor deficits and long-term cognitive impairment after stroke; however, Sfn treatment didn’t affect these sensorimotor. In cultures, neuronal survival rate in Sfn group was significantly higher compared with vehicle group. Nrf2 knockdown with Nrf2-shRNA abolished the protective effects of Sfn. Conclusion: Sfn treatment reduces cognitive impairment after stroke in mice in a Nrf2 depended manner. Nrf2 may be a promising target to reduce post-stroke cognitive impairment.

A Case of Upper Limb Arterial Embolization from Aortic Arch Intimal Sarcoma.

We report a case with aortic intimal sarcoma who presented with left upper limb arterial embolization from tumor. A 79-year-old female patient presented with paleness and left upper limb paralysis. A transesophageal echocardiogram revealed a mobile and fragile mass attached in the aortic arch. Contrast-enhanced computed tomography showed a massive irregular tumor in the aortic arch with left common carotid and subclavian artery occlusion. Total arch replacement was performed, and tumor was resected en bloc. Although the postoperative course was uneventful, multiple metastasis to the limbs was observed. The patient died 6 months postoperatively.

Neuroprotective effects of topiramate and memantine in combination with hypothermia in hypoxic-ischemic brain injury in vitro and in vivo

Hypoxic-ischemic encephalopathy (HIE) is a major cause of perinatal mortality and subsequent severe neurological sequelae. Mild hypothermia is a standard therapy for HIE, but is used only in selected Reference Centers and in neonates >1800 g. Since neuronal death following HIE occurs by a cascade of events triggered by activation of glutamate receptors, we used in vitro and in vivo models of HIE to examine whether the AMPA/kainate receptor antagonist topiramate and the NMDA receptor antagonist memantine could exert neuroprotective effects, alone or in combination with hypothermia. For the in vitro experiments, rat organotypic hippocampal slices were exposed to a 30 min duration of oxygen-glucose deprivation (OGD): treatment with topiramate (1 μM) and memantine (10–30 μM) or hypothermia (35 °C or 32 °C) significantly attenuated CA1 damage after 24 h. The combination of hypothermia with topiramate and memantine enhanced their protective effect. For the in vivo experiments, we used 7 day-old rat pups subjected to permanent left common carotid artery occlusion followed by 120 min of hypoxia. Administration of topiramate or memantine (i.p., 20 mg/kg) immediately and 2 h after hypoxia or exposure to hypothermia (32 °C for 4 h beginning 1 h after hypoxia) significantly reduced the extent of the resulting infarct. The combination of topiramate or memantine with hypothermia elicited a reduction of the infarct that was greater than that produced by drugs or hypothermia alone. Notably, memantine displayed a higher degree of neuroprotection as compared to topiramate both in vitro and in vivo and, when used alone at 20 mg/kg in vivo, produced a greater reduction in brain damage than observed using topiramate in combination with hypothermia. These results suggest that memantine may be more advantageous than topiramate as a therapeutic agent in neonates with HIE treated with hypothermia.

Subchronic hypoxia pretreatment on brain pathophysiology in unilateral common carotid artery occluded albino rats.

OBJECTIVE:This study was aimed to assess the effect of unilateral common carotid artery occlusion on brain pathophysiology in rats pretreated with subchronic hypoxia.MATERIALS AND METHODS:Rats (200 ± 20 g) were randomized into three groups: Group 1 served as sham, Group 2 were normoxic (21% O2 and 79% N2), and Group 3 were hypoxia preconditioned (10% O2 and 90% N2) for 21 days before left common carotid artery occlusion (LCCAO). The LCCAO was done for 75 min followed by reperfusion for 12 h. Neurological scores were recorded. Serum malondialdehyde (MDA) and nitric oxide (NO) levels at pre- and 12 h post-LCCAO were measured. Brain histopathological assessments were also done.RESULTS:Higher neurological deficits scores in Group 2 as compared to Group 3 rats were noticed. Serum MDA and NO levels at 12 h post-LCCAO in Group 2 rats showed significant elevation as compared to preocclusion levels. Group 3 rats did not show such elevations. On histopathology of left and right cerebral hemispheres of Group 1 (sham) did not show any specific changes. In Group 2 rats, the right cerebral hemisphere (nonoccluded) showed no areas of ischemia-induced brain changes, but in the left side (occlusive), there were features of ischemic brain damage including cerebral edema. In the case of Group 3 rats, there were less ischemic damages in the left occluded side as compared to the left side of the Group 2 rats.CONCLUSION:This study clearly demonstrates that subchronic hypoxia pretreatment can reduce ischemic brain injury by unilateral common carotid artery occlusion in rats.