Inhibition of polymorphonuclear leukocyte adherence suppresses no-reflow after focal cerebral ischemia in baboons.

Mori, Etsuro; Zoppo, Gregory J. del; Chambers, JD; Copeland, Brian R.; Arfors, K. E.

doi:10.1161/01.str.23.5.712

Cited by 341 publications

(185 citation statements)

References 46 publications

Supporting

Mentioning

179

Contrasting

Unclassified

Order By: Relevance

“…A significant increase (p < 0.001) was seen postoperatively in total white cell count and absolute numbers of PMN leukocytes, followed by a return to baseline levels over 7 days. Baseline values for measurements ob tained from all subjects were in agreement with previously published values (Mori et al, 1992). No substantial changes in the platelet count were noted after the implantation procedure.…”

Section: Resultssupporting

confidence: 89%

“…The surgical preparation of the nonhuman pri mate model for reversible MCA 0 involved implan tation of a Silas tic balloon occlusion device (Mentor Corporation and PS Medical, Goleta, CA, U.S.A.) through an orbital window (delZoppo et al, 1986) with the modifications noted by delZoppo et al, Mori et al, 1992). Following ketamine ana lepsis (10 mg/kg), anesthesia was routinely induced by inhalation of 3.0--5.0% halothane and maintained by halothane at 1.5-2.0%.…”

Section: Methodsmentioning

confidence: 99%

“…These changes may ultimately affect peripheral granulocyte function and leukocyte-mediated events in experimental I. Following experimental middle cerebral artery (MCA) O/R, PMN leukocytes may contribute to mi crovascular defects (delZoppo et al, 1991;Mori et al, 1992) and to the maturation of ischemic neuro nal injury (Garcia et al, 1993). The time frame for O/R in this nonhuman primate model is that which is being exploited in the clinical arena.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Ember¹,

Zoppo

Mori

et al. 1994

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: There is increasing interest in the role of poly morphonuclear (PMN) leukocytes in the evolution of fo cal cerebral infarction. Surgical preparation of focal ce rebral ischemia models may alter leukocyte reactivity and thereby make interpretation of leukocyte function follow ing ischemiaireperfusion difficult. The effects of surgical preparation and of experimental ischemiaireperfusion on granulocyte function have been examined prospectively in a baboon model. Twenty-six adolescent male baboons underwent surgical preparation, of which 21 underwent middle cerebral artery occlusion/reperfusion. Four addi tional animals served as nonsurgical controls. Peripheral venous blood specimens were taken for performing as says of leukocyte function at defined intervals before and after both the surgical preparation (i.e., the overall pro cedure for implantation of the middle cerebral artery oc clusion device) and occlusionlreperfusion. A stress related elevation in total leukocyte number was attributed mainly to an increase in the number of circulating PMN leukocytes. Values rose from 13.9 ± 4.9 x 103 to 27.8 ± S.8 x 103/fLl, (±SD; n = 21) for total leukocyte number, withp < 0.001, and from 4.3 ± 2. 1 x 103 to IS.9 ± 4.7 x 103/fLi (n = 21) for PMN leukocytes, with p < 0.001.Polymorphonuclear (PMN) leukocytes may play an active and significant role in microvascular events (Ernst et aI

show abstract

Section: Resultssupporting

confidence: 89%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Ember¹,

Zoppo

Mori

et al. 1994

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…Experimentally, focal I/R induces recruitment and activation of inflammatory cells, which are thought to be key events causing I/R injury, represented by blood brain barrier (BBB) breakdown brain edema, neural death, and hemorrhagic transformation (Amantea et al, 2009;Jin et al, 2010). Many studies have shown that systemic suppression of neutrophils attenuated I/R injury in a transient middle cerebral artery occlusion (MCAO) model (Matsuo et al, 1994;Mori et al, 1992;Zhang RL et al, 1994;Connolly et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Post-ischemic intra-arterial infusion of liposome-encapsulated hemoglobin can reduce ischemia reperfusion injury

et al. 2014

View full text Add to dashboard Cite

Despite successful revascularization, reperfusion after prolonged ischemia causes ischemia reperfusion (I/R) injury. Recruitment and activation of neutrophils is thought to be a key event causing I/R injury. We examined whether post-ischemic intra-arterial infusion of liposome-encapsulated hemoglobin (LEH), an artificial oxygen carrier without neutrophils, could reduce I/R injury in a rat transient middle cerebral artery occlusion (MCAO) model. Male Sprague-Dawley rats were subjected to 2-hour MCAO and then were divided into three groups: 1) LEH group (n=7) infused with LEH (Hb concentration of 6g/dl, 10ml/kg/h) through the recanalized internal carotid artery for 2 hours, 2) vehicle group (n=8) infused with saline (10ml/kg/h) in the same manner as the LEH group, and 3) control group (n=9) subjected to recanalization only. After 24-hour reperfusion, all rats were tested for neurological score and then sacrificed to examine infarct and edema volumes, myeloperoxidase (MPO) expression, matrix metalloproteinase-9 (MMP-9) expression and activity, and reactive oxygen species (ROS) production. Compared with the control group and the vehicle group, the LEH group showed a significantly better neurological score and significantly smaller infarct and edema volumes. MPO expression, MMP-9 expression and activity, and ROS production in the LEH group were also significantly lower than those in the control and vehicle groups. The results in the present study suggest that post-ischemic intra-arterial infusion of LEH can reduce I/R injury through reducing the effect of MMP-9, most likely produced by 2 neutrophils. This therapeutic strategy may be a promising candidate to prevent I/R injury after thrombolysis and/or thromboectomy. (246 words) 3

show abstract

“…18 The "no reflow" effect can be considerably reduced by the monoclonal antibody IB4, which inhibits neutrophil adhesion to the endothelium. 19 Red blood cell aggregation near the exit of capillaries pushes leukocytes against endothelial cells, thereby increasing leukocyte adhesion. 20 Leukocyte adhesion (and reperfusion damage) is higher in older animals.…”

Section: Blood Vesselsmentioning

confidence: 99%

Vascular and Neuronal Ischemic Damage in Cryonics Patients

Best¹

2012

Rejuvenation Research

View full text Add to dashboard Cite

Cryonics technology seeks to cryopreserve the anatomical basis of mind so that future medicine can restore legally dead cryonics patients to life, youth, and health. Most cryonics patients experience varying degrees of ischemia and reperfusion injury. Neurons can survive ischemia and reperfusion injury more than is generally believed. But blood vessels are more vulnerable, which can impair perfusion of vitrifying cryoprotectant solution intended to eliminate ice formation in the brain. Forms of vascular and neuronal damage are reviewed, along with means of mitigating that damage. Recommendations are also made for preventing such damage.

show abstract

Inhibition of polymorphonuclear leukocyte adherence suppresses no-reflow after focal cerebral ischemia in baboons.

Cited by 341 publications

References 46 publications

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Post-ischemic intra-arterial infusion of liposome-encapsulated hemoglobin can reduce ischemia reperfusion injury

Vascular and Neuronal Ischemic Damage in Cryonics Patients

Contact Info

Product

Resources

About