Relation of supersensitivity to cerebral vasospasm induced by oxyhaemoglobin

Iwai, Ryosei; Kamiyama, K; Nagahori, Takeshi; Ohtsuji, Tsuneo; Endo, Shunro; Takaku, Akira

doi:10.1080/01616412.1988.11739836

Cited by 6 publications

(1 citation statement)

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“…The paracrinal factors are mainly from endothelial cells, such as nitric oxide (NO) and prostaglandins as vasodilators, and endothelins as vasoconstrictors. Oxy-hemoglobin after SAH could be an additional vasoconstrictor (6,8). The neurogenic factors of brain vasculature are all released by the terminals of the trigeminal nerve.…”

Section: Introductionmentioning

confidence: 99%

Intranasal delivery of calcitonin gene-related peptide reduces cerebral vasospasm in rats

Sun

Shen²,

Wu³

et al. 2010

Front Biosci

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Cerebral vasospasm is the primary cause of sequelae and poor clinical conditions of subarachnoid hemorrhage (SAH); therefore, it is imperative to relieve vasospasm and improve cerebral blood supply. Calcitonin gene-related peptide (CGRP) is a potent vasodilator that is normally released by trigeminal sensory fibers but depleted following SAH. We propose that intranasal application may be an effective way to deliver CGRP to the brain and ameliorate vasospasm after SAH. In this study, we intranasally applied CGRP to rats and induced SAH by double-injection of autologous blood into the cisterna magna. Compared to intravenous injection, intranasal delivery led to a 10-fold higher level of CGRP in the brain. Intranasal CGRP significantly ameliorated vasospasm, improved cerebral blood flow, and reduced cortical and endothelial cell death. Moreover, CGRP increased the levels of vascular endothelial growth factor and stimulated angiogenesis. Altogether, our data demonstrate that intranasal CGRP delivery is a promising method for moderating vasospasm and reducing the associated ischemic brain injury after SAH in rats, and suggest that it may be a potential approach in clinic.

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Section: Introductionmentioning

confidence: 99%