Effect of atherosclerosis on cerebral vascular responses to activation of leukocytes and platelets in monkeys.

Faraci, Frank M.; Lopez, Antoine-Guy; Breese, Keith; Armstrong, Marc P.; Heistad, D D

doi:10.1161/01.str.22.6.790

Cited by 31 publications

(13 citation statements)

References 28 publications

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“…27 - 28 In hypercholesterolemic monkeys, increased vascular tone was associated with lower cerebral flow in response to infusion of collagen-activated platelets. 29 Our patients with familial hypercholesterolemia had disturbed cerebral blood flow even in the presence of non-flow reducing arterial lesions in the carotid arteries. It is unlikely that the hemodynamic abnormality we have found was due to the aortic gradient that had been demonstrated in hypercholesterolemic patients.…”

Section: Discussionmentioning

confidence: 67%

Premature carotid atherosclerosis: does it occur in both familial hypercholesterolemia and homocystinuria? Ultrasound assessment of arterial intima-media thickness and blood flow velocity.

Rubba

Mercuri

Faccenda

et al. 1994

Stroke

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Homocystinuria due to cystathionine beta-synthase deficiency and familial hypercholesterolemia are inherited disorders of metabolism that are associated with premature development of cardiovascular disease. This study addresses the possibility that different patterns of carotid wall damage and cerebral blood flow hemodynamics are present in these two metabolic diseases. Twelve patients with homocystinuria due to cystathionine beta-synthase deficiency (mean age, 24 years), 10 patients with homozygous familial hypercholesterolemia (mean age, 26 years), and 11 healthy control subjects (mean age, 26 years) underwent a vascular examination by noninvasive methods. B-mode ultrasound imaging was used to obtain measurements of intima-media thickness of common carotid, bifurcation, and internal carotid arteries as an index of atherosclerosis. Cerebral blood flow velocity was estimated from vascular examination of the middle cerebral artery by transcranial Doppler. Systolic, diastolic, and mean velocities were measured. Pulsatility index, a possible indicator of vascular resistance in the cerebral circulation, was also calculated. Mean maximum intima-media thickness was 1.4 mm in patients with familial hypercholesterolemia, 0.6 mm in patients with homocystinuria, and 0.6 mm in control subjects. The difference between hypercholesterolemic and homocystinuric patients or control subjects was statistically significant (P < .001). Diastolic blood flow velocities were significantly reduced in the middle cerebral arteries of hypercholesterolemic patients compared with homocystinuric patients or control subjects (P < .05), whereas systolic or mean velocities did not differ. The pulsatility index, a possible indicator of vascular resistance in the cerebral circulation, was significantly higher in hypercholesterolemic patients compared with homocystinuric patients or healthy control subjects (P < .01). A direct relation was demonstrated between pulsatility index of the middle cerebral artery and mean maximum intima-media thickness of carotid arteries on the same side (P < .001). Familial hypercholesterolemia is responsible for diffuse and focal thickening of carotid arteries and possibly also for hyperlipidemic endothelial dysfunction extending to small resistance arteries and leading to a disturbed cerebral blood flow. Patients with homocystinuria due to homozygosis for cystathionine beta-synthase deficiency seldom have plaques in their carotid arteries. They are similar to healthy control subjects with regard to both intima-media thickness and blood flow velocity in the middle cerebral artery. Therefore, it is unlikely that typical atherosclerotic lesions precede thrombotic events in homocystinuria. However, it is possible that arterial dilatations caused by medial damage lead to thrombosis in homocystinuric patients.

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Section: Discussionmentioning

confidence: 67%

Premature carotid atherosclerosis: does it occur in both familial hypercholesterolemia and homocystinuria? Ultrasound assessment of arterial intima-media thickness and blood flow velocity.

Rubba

Mercuri

Faccenda

et al. 1994

Stroke

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“…Recovery of CBF from this low-flow state, however, is made more rapid by prior PMNL depletion, 84 suggesting that activated leukocytes may sustain blood flow reduction (through either vascular obstruction or vasoconstrictor effects). Intracarotid injection of fMLP produces no effect on CBF or vascular resistance in normal monkeys and no reduction in CBF in rats.…”

mentioning

confidence: 99%

Polymorphonuclear leukocytes and monocytes/macrophages in the pathogenesis of cerebral ischemia and stroke.

Kochanek

Hallenbeck

1992

Stroke

561

310

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Background:The extent to which polymorphonuclear leukocytes and monocytes/macrophages contribute to the pathobiology of cerebral ischemia and stroke is an issue of long-standing contradiction and controversy. Recent developments in the ability to selectively modify leukocyte adhesion with antiadhesion antibodies and the potential clinical application of this therapeutic approach have spurred a resurgence of experimental studies examining the role of leukocytes in cerebral ischemia and stroke.Summary of Review: We review studies examining leukocyte accumulation, initiation of thrombosis, and exacerbation of ischemic brain injury in stroke, and we examine other proposed contributions of leukocytes to cerebrovascular pathophysiology.Conclusions: The importance of specific characteristics of a given ischemia model and of underlying stroke risk factors in determining the degree of leukocyte involvement and effectiveness of therapies directed against these cells is discussed. (Stroke 1992;23:1367-1379)

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“…Although the increased activity of neutrophils is not associated with increased adhesion to microvascular endothelium [78], their increased numbers raise peripheral vascular resistance [110]. One possible explanation is that circulating activated neutrophils in SHRs release vasoactive substances that constrict the small arteries and arterioles; this has been documented for atherosclerosis [114][115][116]. Extensive evidence, however, points to a hemorheological effect of leukocyte activation on microvascular resistance [1,34,36].…”

Section: Impaired Fluid Shear Responses and Downstream Effects On Vasmentioning

confidence: 99%

Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

Zhang¹,

Shin²

2012

Lipoproteins - Role in Health and Diseases

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Effect of atherosclerosis on cerebral vascular responses to activation of leukocytes and platelets in monkeys.

Cited by 31 publications

References 28 publications

Premature carotid atherosclerosis: does it occur in both familial hypercholesterolemia and homocystinuria? Ultrasound assessment of arterial intima-media thickness and blood flow velocity.

Premature carotid atherosclerosis: does it occur in both familial hypercholesterolemia and homocystinuria? Ultrasound assessment of arterial intima-media thickness and blood flow velocity.

Polymorphonuclear leukocytes and monocytes/macrophages in the pathogenesis of cerebral ischemia and stroke.

Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

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