Increased platelet-activating factor-induced periventricular brain microvascular constriction associated with immaturity

Hou, Xin; Gobeil, Fernand; Marrache, Anne Marilise; Quiniou, Christiane; Brault, Sonia; Checchin, Daniella; Bernier, Sylvie G.; Sennlaub, Florian; Joyal, Jean‐Sébastien; Abran, Daniel; Peri, Krishna G.; Varma, Daya R.; Chemtob, Sylvain

doi:10.1152/ajpregu.00633.2002

Cited by 8 publications

(7 citation statements)

References 39 publications

(61 reference statements)

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“…L-type voltage-gated calcium channels in the central nervous system and dihydropyridines act on these receptors (19,20,(38)(39)(40). Thus, it is possible that lipophilic dihydropyridines (such as nifedipine and amlodipine) are able to cross the blood-brain barrier in chronic hypertension (21,22) and reduce the generation of reactive oxygen species (41)(42)(43). However, this might not occur with all calcium channel blockers, as nicardipine did not reduce the generation of reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

Amlodipine-Induced Reduction of Oxidative Stress in the Brain Is Associated with Sympatho-Inhibitory Effects in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Amlodipine-Induced Reduction of Oxidative Stress in the Brain Is Associated with Sympatho-Inhibitory Effects in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2006

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“…In ROP, AAs are cleaved off from membrane phospholipids (by cPLA 2 ) to yield lysophospholipids, which in turn can be acetylated and converted to PAF (78). Both vasomotor and cytotoxic effects of PAF in the premature infant are mediated to a large extent by TXA 2 (79,80). Thus, PAF, which is generated concomitantly with TXA 2 during oxidant stress and amplifies formation of TXA 2 , contributes to retinal vasoobliteration in ischemic retinopathies ( Figure 4).…”

Section: Figurementioning

confidence: 99%

Retinopathy of prematurity: understanding ischemic retinal vasculopathies at an extreme of life

Sapieha¹,

Joyal²,

Rivera³

et al. 2010

J. Clin. Invest.

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Retinopathy of prematurity (ROP) is a major complication of preterm birth. It encompasses a spectrum of pathologies that affect vision, from mild disease that resolves spontaneously to severe disease that causes retinal detachment and subsequent blindness. The pathologies are characterized by an arrest in normal retinal vascular development associated with microvascular degeneration. The resulting ischemia and retinal hypoxia lead to excessive abnormal compensatory blood vessel growth. However, this neovascularization can lead to fibrous scar formation and culminate in retinal detachment. Present therapeutic modalities to limit the adverse consequences of aberrant neovascularization are invasive and/or tissue-destructive. In this Review, we discuss current concepts on retinal microvascular degeneration, neovascularization, and available treatments, as well as present future perspectives toward more profound elucidation of the pathogenesis of ROP.Retinopathy of prematurity (ROP) is the major ocular disorder of the neonate (1, 2) and the dominant cause of severe visual impairment in childhood in North America and Europe. ROP is associated with significant sequelae, the most serious being retinal detachment, which results in blindness. However, even milder forms of ROP increase the incidence of pathologies that negatively impact visual acuity, for example, ametropias, refractive errors that reduce visual acuity; strabismus, a condition in which the eyes are not properly aligned, preventing proper binocular vision and adversely affecting depth perception; and disorders of color discrimination (3-6). ROP proceeds following an initial phase of degeneration of the retinal microvasculature (vasoobliteration) (7,8) (Figure 1) that is associated with cessation of progression of vascular growth toward the retinal periphery. In the subsequent phase of the disease, the ensuing retinal ischemia predisposes to abnormal compensatory neovascularization (9, 10). Of the various factors that have been associated with the development of ROP, low birth weight, low gestational age, supplemental oxygen therapy, and its associated relative hyperoxia dominate.The development of the human retinal vasculature commences at approximately the 16th week of gestation and concludes at term (i.e., the 40th week of gestation) (11). Hence, when an infant is born prematurely, its retinal blood supply is incomplete and highly vulnerable to decay. This immaturity in vascular development predisposes the retina to complications. Major advances have been made over the past 30 years in identifying mechanisms implicated in the genesis of ROP. Comprehension of mechanisms underlying this disorder has, in turn, enhanced understanding of the pathogenesis of ischemic retinal vasculopathies in the adult, for example, diabetic retinopathy (a complication of diabetes mellitus) and neovascular forms of age-related macular degeneration (the major cause of visual impairment in adults over 50 years of age).The oxygen-induced retinopathy (OIR) model of ischemic retinop...

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“…In ROP, AAs are cleaved off from membrane phospholipids (by cPLA 2 ) to yield lysophospholipids, which in turn can be acetylated and converted to PAF [40] . Both the vasomotor and cytotoxic effects of PAF in the premature infant are mediated to a large extent by TXA 2 [41,42] . Thus, PAF, which is generated concomitantly with TXA 2 during oxidant stress and amplifies formation of TXA 2 , contributes to retinal vaso-obliteration in ischemic retinopathies ( fig.…”

Section: Vaso-obliterationmentioning

confidence: 99%

Understanding Retinopathy of Prematurity: Update on Pathogenesis

Rivera

Sapieha²,

Joyal³

et al. 2011

Neonatology

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105

103

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Retinopathy of prematurity (ROP), an ocular disease characterized by the onset of vascular abnormalities in the developing retina, is the major cause of visual impairment and blindness in premature neonates. ROP is a complex condition in which various factors participate at different stages of the disease leading to microvascular degeneration followed by neovascularization, which in turn predisposes to retinal detachment. Current ablative therapies (cryotherapy and laser photocoagulation) used in the clinic for the treatment of ROP have limitations and patients can still have long-term effects even after successful treatment. New treatment modalities are still emerging. The most promising are the therapies directed against VEGF; more recently the use of preventive dietary supplementation with ω-3 polyunsaturated fatty acid may also be promising. Other than pharmacologic and nutritional approaches, cell-based strategies for vascular repair are likely to arise from advances in regenerative medicine using stem cells. In addition to all of these, a greater understanding of other factors involved in regulating pathologic retinal angiogenesis continues to emerge, suggesting potential targets for therapeutic approaches. This review summarizes an update on the current state of knowledge on ROP from our and other laboratories, with particular focus on the role of nitro-oxidative stress and notably trans-arachidonic acids in microvascular degeneration, semaphorin 3 operating as vasorepulsive molecules in the avascular hypoxic retina and in turn impairing revascularization, succinate and its receptor GPR91 in neuron-mediated retinal neovascularization, and ω-3 lipids as modulators of preretinal neovascularization.

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Increased platelet-activating factor-induced periventricular brain microvascular constriction associated with immaturity

Cited by 8 publications

References 39 publications

Amlodipine-Induced Reduction of Oxidative Stress in the Brain Is Associated with Sympatho-Inhibitory Effects in Stroke-Prone Spontaneously Hypertensive Rats

Amlodipine-Induced Reduction of Oxidative Stress in the Brain Is Associated with Sympatho-Inhibitory Effects in Stroke-Prone Spontaneously Hypertensive Rats

Retinopathy of prematurity: understanding ischemic retinal vasculopathies at an extreme of life

Understanding Retinopathy of Prematurity: Update on Pathogenesis

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