Transient middle cerebral artery occlusion causes different structural, mechanical, and myogenic alterations in normotensive and hypertensive rats

Jiménez‐Altayó, Francesc; Martín, Abraham; Rojas, Santiago; Justicia, Carles; Briones, Ana M.; Giraldo, Jesús; Planas, Anna M.; Vila, Elisabet

doi:10.1152/ajpheart.00165.2007

Cited by 35 publications

(47 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Focal cerebral ischemia and the surgical protocol were similar to the methods described previously (Jiménez-Altayó et al, 2007). Rats were anesthetized with isoflurane (2-2.5%) vaporized in O 2 and N 2 O (30: 70).…”

Section: Methodsmentioning

confidence: 99%

“…Pressure Myography. The structural, mechanical, and myogenic properties of MCA were studied with a pressure myograph (Danish Myo Tech Model P100; J.P. Trading I/S, Aarhus, Denmark), as described previously (Jiménez-Altayó et al, 2007). In brief, the vessel was placed on two glass microcannulae and secured with surgical nylon suture.…”

Section: Methodsmentioning

confidence: 99%

“…Changes in either vascular remodeling or myogenic tone have been reported in several animal models of vascular diseases such as diabetes (Sachidanandam et al, 2009), hypertension (Touyz, 2000), and cerebral ischemia (Cipolla et al, 1997;Jiménez-Altayó et al, 2007). Furthermore, vascular remodeling is improved by treatment with antioxidants, vitamins, or NADPH oxidase inhibitors in animal experimental models and in clinical trials of hypertension (Lee and Griendling, 2008).…”

mentioning

confidence: 99%

“…It has also been reported that superoxide anion inhibits the opening of K ATP (Lee and Griendling, 2008). Thus, the formation of ROS could also participate in the myogenic response changes of the middle cerebral artery (MCA) induced by ischemia/reperfusion (I/R) (Cipolla and Curry, 2002;Jiménez-Altayó et al, 2007).…”

mentioning

confidence: 99%

See 3 more Smart Citations

Participation of Oxidative Stress on Rat Middle Cerebral Artery Changes Induced by Focal Cerebral Ischemia: Beneficial Effects of 3,4-Dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran (CR-6)

Jiménez‐Altayó¹,

Caracuel²,

Pérez-Asensio³

et al. 2009

The Journal of Pharmacology and Experimental Therapeutics

Self Cite

View full text Add to dashboard Cite

Cerebral ischemia followed by reperfusion alters vessel properties of brain arteries in rats, inducing an inflammatory response and excessive generation of reactive oxygen species. This study investigated the participation of oxidative stress on vessel properties after ischemia/reperfusion and the beneficial effects of 3,4-dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran (CR-6). The right middle cerebral artery was occluded (90 min) and reperfused (24 h). Sham-operated animals were used as controls. Ischemic rats were treated either with CR-6 (100 mg/kg in 1 ml olive oil) or vehicle (1 ml olive oil) administered orally at 2 and 8 h after the onset of ischemia. The structural, mechanical, and myogenic properties of the middle cerebral artery (MCA) were assessed by pressure myography. Superoxide anion (O 2 . ) production was evaluated by ethidium fluorescence, and protein tyrosine nitrosylation was determined by immunofluorescence. Infarct volume was smaller in rats treated with CR-6. In MCA, ischemia/reperfusion increased wall thickness, cross-sectional area, wall/lumen, and decreased wall stress. CR-6 treatment prevented all of these changes induced by ischemia/reperfusion. However, impaired myogenic response and larger lumen diameter in active conditions observed after ischemia/reperfusion were not modified by CR-6. Treatment with CR-6 prevented the increase in O 2 . production and partially prevented the enhanced protein tyrosine nitrosylation that occurred in response to ischemia/reperfusion. Our findings suggest that oxidative stress is involved in the alterations of MCA properties observed after ischemia/reperfusion and that CR-6 induces protection.Stroke is a complex neurodegenerative disorder characterized by interruption of blood flow supply to the brain. There are several mechanisms involved in ischemic brain injury. Increasing evidence indicates that cerebral ischemia and particularly reperfusion are responsible for oxidative stress caused by free radical production. After reperfusion, there is a surge in production of superoxide anion (O 2 . ), nitric oxide (NO), and peroxynitrite (ONOO Ϫ ). Formation of these species in the vicinity of blood vessels plays an important role in reperfusion-induced injury (Doyle et al., 2008). In healthy individuals, antioxidant activity counterbalances free radical production, but in the case of ischemia, the balance between reactive oxygen species (ROS) and antioxidant activity is shifted toward free radicals, causing oxidative stress.All vascular cells can produce ROS through different sources, including NADPH oxidase, mitochondria, cyclooxygenases, and ABBREVIATIONS: ROS, reactive oxygen species; MCA, middle cerebral artery; I/R, ischemia/reperfusion; CR-6, 3,4-dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran; KHS, Krebs-Henseleit solution; DHE, dihydroethidium; SOD, superoxide dismutase; ANOVA, analysis of variance; CSA, cross-sectional area; PEG, polyethylene glycol; WT, wall thickness; D iCa 2ϩ, internal diameter measured in active c...

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Participation of Oxidative Stress on Rat Middle Cerebral Artery Changes Induced by Focal Cerebral Ischemia: Beneficial Effects of 3,4-Dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran (CR-6)

Jiménez‐Altayó¹,

Caracuel²,

Pérez-Asensio³

et al. 2009

The Journal of Pharmacology and Experimental Therapeutics

Self Cite

View full text Add to dashboard Cite

show abstract

“…Focal brain ischemia was produced by 90-min intraluminal occlusion of the right middle cerebral artery (MCA) with reperfusion (24 h) as reported previously (Jiménez-Altayó et al, 2007). Sham-operated animals were used as controls.…”

Section: Methodsmentioning

confidence: 99%

Endothelial Dysfunction in Rat Mesenteric Resistance Artery after Transient Middle Cerebral Artery Occlusion

Martínez-Revelles

Jiménez‐Altayó²,

Caracuel³

et al. 2008

The Journal of Pharmacology and Experimental Therapeutics

Self Cite

View full text Add to dashboard Cite

Stroke triggers a local and systemic inflammatory response leading to the production of cytokines that can influence blood vessel reactivity. In this study, we aimed to assess whether cerebral ischemia/reperfusion could affect vasoconstriction and vasodilatation on mesenteric resistance arteries (MRA) from Wistar Kyoto rats. The right middle cerebral artery was occluded (90 min) and reperfused (24 h). Sham-operated animals were used as controls. Plasma levels of interleukin (IL)-6 and IL-1␤ were measured at 24 h. Vasoconstrictor and vasodilator responses were recorded in a wire myograph. Protein expression was determined by Western blot and immunofluorescence, and superoxide anion (O 2 . ) production was evaluated by ethidium fluorescence. In MRA, ischemia/reperfusion increased plasma levels of IL-6, O 2 . production, protein expression of cyclooxygenase-2, and protein tyrosine nitrosylation, but it impaired acetylcholine (ACh) vasodilatation without modifying the vasodilatations to sodium nitroprusside or the contractions to phenylephrine and KCl. Superoxide dismutase (SOD) and indomethacin reversed the impairment of ACh relaxation induced by ischemia/reperfusion. However, N -nitro-L-arginine methyl ester affected similarly ACh-induced vasodilatations in MRA of ischemic and sham-operated rats. Protein expression of endothelial and inducible nitric-oxide synthase, copper/zinc SOD, manganese SOD, and extracellular SOD was similar in both groups of rats. Our results show MRA endothelial dysfunction 24 h after brain ischemia/reperfusion. Excessive production of O 2 . in MRA mediates endothelial dysfunction, and the increase in plasma cytokine levels after brain ischemia/reperfusion might be involved in this effect.

show abstract

Animal models of stroke

Zhang

2021

Anim Models and Exp Med

View full text Add to dashboard Cite

Stroke is a leading cause of morbidity and mortality worldwide and in China. In China, stroke was the leading cause of death and DALYs in 2017. 1 Age-standardized DALYs per 100 000 population decreased by 33.1% for stroke. Of all strokes, up to 80% to 85% are ischemic, 2 which can be subdivided based on the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. 3 Large vessel atherosclerosis of cervical or proximal intracranial vessels comprises a major cause of acute stroke, ranging from 30% to 43%, while 20%-31% is caused by cardioembolism. Approximately 10%-23% of all strokes are lacunar in type, which are mainly caused by diabetes and hypertension. Some additional unusual causes, such as vasculopathy or extracranial artery dissection, account for 2%-11%. 4,5 Approximately 5%-21% of strokes are hemorrhagic, and their common causes are hypertension and vascular malformations. 6 Strokes are heterogeneous diseases, and in vivo models are essential tools to mimic these processes for investigating pathophysiology and therapeutic approaches. Each model has its unique strengths and weaknesses (Tables 1 and 2). Only when we realize their importance can we choose the best one for an investigation, with "best" referring to that which most closely approximates a certain aspect of the multiple facets of strokes.

show abstract

Transient middle cerebral artery occlusion causes different structural, mechanical, and myogenic alterations in normotensive and hypertensive rats

Cited by 35 publications

References 37 publications

Participation of Oxidative Stress on Rat Middle Cerebral Artery Changes Induced by Focal Cerebral Ischemia: Beneficial Effects of 3,4-Dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran (CR-6)

Participation of Oxidative Stress on Rat Middle Cerebral Artery Changes Induced by Focal Cerebral Ischemia: Beneficial Effects of 3,4-Dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran (CR-6)

Endothelial Dysfunction in Rat Mesenteric Resistance Artery after Transient Middle Cerebral Artery Occlusion

Animal models of stroke

Contact Info

Product

Resources

About